This action might not be possible to undo. Are you sure you want to continue?
(Proposal of renal ultrasound in chronic renal failure) Introduction Ultrasound is recognized as an important adjunct to clinical examination in care of patients with many common illnesses. The WHO “goal of health for all” recommended that many of the U/S examinations will be performed at the first referral level ; it is now a routine examination in Obstetrics & Gynaecology. As there is no ionizing radiation, it should be the preferred method of imaging whenever it can aid to reach a diagnosis. Although C/T Scanning has superceded U/S in many aspects of diagnosis, still U/S remains a very useful, easy, safe, quick, non-invasive, available, and relatively inexpensive technique. Chronic renal failure is a common disease nowadays everywhere and appears in U/S with strict criteria ; so it is easily diagnosed by U/S ; and the True Cut Needle Biopsy of the kidney is performed under sonographic guidance. Skill, proper training and experience is mandatory to making an accurate diagnosis from U/S images. The Problem of the study The kidney is affected in a vast variety of diseases e.g. congenital anomalies, calculi, hydronephrosis, solid renal masses, cystic renal diseases, and medical renal diseases such as pyelonephritis, glomerulonephritis, nephrotic syndrome, acute and chronic renal failure. My thesis will be dealing with renal U/S in chronic renal failure. Objectives 1. To find the incidence of CRF in patients coming with different renal complaints in Sudanese population i.e. to sort out CRF patients from one hundred selected different renal disease patients and to show the role of ultrasound in their diagnosis 2. To find out how many of them are already on dialysis ? how many of them need dialysis ? how many need transplantation ?
Hypothesis It is expected that U/S is a good tool in diagnosing CRF which will help in early management.. Methodology It is a field work practical study. I will select one hundred patients with different renal problems and find out how many of them are suffering from CRF and show the classical sonographic appearances of CRF in the selected cases. Different US equipments with varying facilities will be used namely Aloka SSD 500, Toshiba CEE / ECC, Shimadzu SDU-350, Medison 1500 etc… Data Collection Will be done by evaluating one hundred patients, in my full-time private clinic in Sinnar city and in sinnar teaching hospital renal unit and in Gezira renal teaching hospital, who suffer from renal disease especially CRF, and who differ in sex, age, occupation, social status, and economic status. The sources of data collection will be the patients data sheets which will be especially for thesis needs (questionnaire) . In addition to request forms which will include the patient’s complaints and the physician’s clinical findings. The variables of data collection are the kidneys, ureters, and urinary bladder. Scanning technique of the kidney requires : a full bladder, Liberal amount of coupling jell on the upper abdomen, A 3.5 MHz transducer for adults and a 5.0 MHz for children and thin adults, Using the liver as an acoustic window, the right kidney is best seen in supine position in deep inspiration. Scan over right upper abdomen in a longitudinal axis then rotate the patient to the left lateral decubitus position then angle the beam as necessary and adjust the gain to obtain the best image of the renal parenchyma in this coronal view. The left kidney is scanned in a similar sequence using the spleen as an acoustic window. The methods for data analysis will be by computer, summarizing, classifying, and then analyzing the collected data sheets. Complex tables will be used and carried out in the study. The relationship between different variables, and the important statistical indicaters will be drawn from the study. The area for the study will be in the different diagnostic U/S centers at Wadmedani –University of Gezira-Renal Unit, and at the renal unit in Sinnar hospital, and in my full time private clinic
in Sinnar town. The duration of the study will be starting from first September 2005 to the end of April 2006( INSHA-ALLAH.) under the supervision of Dr. Ibrahim Elmahi–senior RadioSonologist and Dr. Suzan Omer Abdalla (consultant sonologist). The study will be classified into chapters : Chapter ONE : Deals with the Proposal ( Synopsis) of the study in which the Problem, Objectives, Hypothesis, Methodology, and the Importance of the study are stated. Chapter TWO : Literature Review including :A ) Anatomy B) Physiology
C) a/ clinical features of CRF b/ normal sonographic appearance of the kidney and technique D) Pathology of the kidney Chapter THREE: Data collection and presentation Chapter FOUR : Data analysis and results Chapter FIVE : Discussion Chapter SIX: A) Conclusion B) Recommendations C) Appendix D) References
A ) Anatomy of the kidney The kidneys are paired retroperitoneal organs situated high up in the posterior abdominal wall in the lumbar region, one on each side of the vertebral column, largely under cover of the costal margins below the diaphragm, between the twelfth thoracic and the fourth lumbar vertebra protected by the lower ribs Each kidney weighs approximately 150 grams in the adult male, and 135 grams in the female. (Fig 1 – 2)
Fig 2-1 The right kidney is usually slightly 1.5 cm inferior than the left due to the large right lobe of the liver. The left kidney is a little longer and narrower and nearer to the median plane. The long axis of each kidney is directed downwards and laterally, the transverse axis posterolaterally. The transpyloric plane passes through the superior part of the hilum of the right kidney, and through the inferior part of the hilum of the left.
Each kidney is 9-13 cm in length, 4-6 cm in breadth, and 2.5-3.5 in anteroposterior thickness. Anteriorly, the upper pole is about 2.5 cm and the lower pole about 7.5 cm from the midline. Posteriorly the centre of the hilum lies opposite the lower border of the spine of the first lumbar vertebra, about 5 cm from the median plane. The lower pole is 2.5 cm above the highest part of the iliac crest. The kidneys lie about 2.5 cm lower in the standing than in the recumbent position and they move inferiorly with inspiration and superiorly with expiration by as much as 2.5 cm due to contraction and relaxation of the diaphragm. The size of the kidneys is affected by age, body size & height, and sex (greater in men). Both kidneys should be about the same size in adult ; and a bilateral difference of more than 2 cm in length is abnormal. The renal volume is a more sensitive indicator of size, and is important in renal transplant patients, and is correlated with the weight of the patient. The median renal volume in adults ranges between 134-150 ml. The renal volume formula is : V = o.49 x L x W x AP-where L represents maximum length of the long axis; W is the average of three width measurements taken at the hilum ; AP is the anteroposterior measurement taken through the hilum. The anterior relations of the right kidney include the adrenal gland, liver, second part of the duodenum, right colic flexure and Morison’s pouch. Posterior to the right kidney lie the diaphragm, the costodiaphragmatic recess of the pleura, the 12th rib, the psoas muscle, quadratus lumborum muscle, the transversus abdominis muscles, the subcostal (T12), iliohypogastric and ilioinguinal (L1) nerves which run downwards and laterally. Anterior to the left kidney lie the suprarenal gland, spleen, stomach, pancreas, left colic flexure, and coils of jejunum. Posterior to the left kidney lie the diaphragm, costodiaphragmatic pleural recess, the11thand12th ribs, psoas, quadratus lumborum, the transversus abdominis muscles, the subcostal (T12), iliohypogastric and ilioinguinal L1 nerves which run downwards and laterally. The superior pole of each kidney is thick, rounded, and nearer the median plane than the lower pole. The inferior pole is smaller, thinner, and extends to within 2.5 cm of the iliac crest. The lateral border is convex ; that of the left kidney is covered superiorly with the greater sac peritoneum which separates it from the spleen; and below this it is in contact with the descending colon. The lateral border of the right kidney is separated from the right lobe of the liver by the peritoneum of the greater sac.
The medial border is convex adjacent to the poles and concave between these curvatures ; it slopes downwards and laterally. In its central part lies the hilum which is a deep vertical fissure opening anteromedially. The hilum is bounded by an anterior and a posterior lip and contains the renal vesseles, nerves, and the funnel- shaped continuation of the upper end of the ureter, named the renal pelvis. The main hilar structures are the renal vein in front , the renal artery in the middle, and the renal pelvis behind. The hilum leads into a central recess named he renal sinus, which is lined by a continuation of the renal capsule, and is almost entirely filled by the pelvis of the kidney and renal vesseles. Numerous nipple-like elevations, termed the renal papillae, indent the wall of the sinus. The renal pelvis extends outside the hilum to become continuous with the ureter. Within the sinus it divides into two and sometimes three large branches, which are named the major calices, each of which divides again into 7-13 short branches, named the minor calices. Each minor calix expands as it approaches the wall of the renal pelvis, and the expanded end is indented and moulded round one to three renal papillae. The wall of the expanded end of each calix is firmly adherent to the capsule lining the renal sinus ; it is perforated by the collecting tubules which open on the summits of the renal papillae. The kidney and its vesseles are embedded in a mass of adipose connective tissue, termed the perirenal ( perinephric) fat, which is thickest at the borders of the kidney and is prolonged through the hilum into the renal sinus. The fibro-areolar tissue surrounding the kidney and perirenal fat is condensed to form a sheath termed the renal fascia, whose two layers are fused at the lateral border of the kidney. The anterior layer is carried medially in front of the kidney and its vessels, and at the level of aorta and inferior vena cava it is a very thin continuation and does not extend higher than the superior mesenteric artery. The posterior layer extends medially behind the kidney and in front of the fascia on the quadratus lumborum and psoas major, and is attached to that fascia at the lateral and medial borders of the psoas, and to the vertebrae and intervertebral discs. There is also a deeper stratum attaching the anterior and posterior layers to one another at the medial border of the kidney and pierced by the renal vessels. This may account for the fact that a peritoneal effusion does not usually extend across to the opposite perirenal space. (Fig 2– 2)
Fig 2 – 2 Above the suprarenal gland the two layers of the renal fascia fuse, and are connected with the fascia of the diaphragm; but below the kidney they remain separate, enclosing the ureter, the anterior layer being gradually in the extra peritoneal tissue of the iliac fossa, while the posterior layer blends with the fascia over the iliacus. The renal fascia is connected to the fibrous renal capsule by numerous trabeculae, which traverse the perirenal fat, and are strongest near the lower pole. The kidney is held in position partly through the attachments of the renal fascia, but principally by the apposition of the neighboring viscera. Structurally, the kidney is invested by a thin capsule that is easily stripped off and consists of white fibrous tissue. The kidneys are composed of two distinct areas: The sinus, the entrance to which is the hilum. The renal parechyma is the second area, and is divided into a dark-brown outer cortex–due to increased blood perfusion-and a light brown inner medulla; total parenchymal thickness approximates 11-18 mm. The renal medulla consists of a series of 8-18 pale striated conical masses termed the renal pyramids, composed almost entirely by parallel bundles of collecting ducts formed by folding of the inner medullary surface into projections conveying urine into the renal pelvis. The bases of the pyramids are directed towards the cortex and periphery of the kidney, while their apices converge towards the renal sinus where they form prominent papillae projecting into the interior of the minor calices, each minor calix receiving from
one to three papillae. Spirally arranged muscles surround the calyces and may exert a milking action on these tubes, aiding the flow of urine into the renal pelvis. The renal pelvis divides into2-3 major calyces each of which is formed by 2-3 minor calyces. The renal cortex lies immediately beneath the fibrous capsule, arches over the bases of the pyramids, and dips in between adjacent pyramids towards the renal sinus as the renal columns, which provide passage of blood vessels and nerves. The inner cortex is divided from the medulla by a line of tangentially running blood vessels-the arcuate arteries and veins. The layers of cortex close to the medulla are termed the juxtamedullary cortex. Histologically, the kidney is composed of a very large number of tortuous, closely packed uriniferous tubules, bound together by a little connective tissue in which run the blood vessels, lymphatics and nerves. Each uriniferous tubule consists of two embryologically distinct parts namely, the nephron or secreting part which elaborates the urine, and the collecting tubule which carries the fluid from a number of renal tubules to a terminal papillary duct or duct of Bellini, which opens into a minor calix at the apex of a renal papilla. The nephron is the structural functional unit of the kidney of which each kidney contains about one million. (Fig 2-3)
The nephron comprises the renal corpuscle, which is concerned with filtration of substances from the plasma; and the renal tubule, which is concerned with selective resorption of substances from the glomerular filtrate until it approaches urine composition. The renal corpuscle (Malpighian) are small rounded masses about 0.2 mm in diameter which are visible in the renal cortex and columns of Bertin. Each is composed of a central glomerulus of vessels, and a membranous envelope termed the glomerular capsule(Bowman's capsule) which is the small pouch-like commencement of a renal tubule. The glomerulus is a lobulated tuft of convoluted, capillary blood vessels, held together by scanty connective tissue. This capillary network is derived from a small afferent arteriole, which enters the capsule at a point opposite to that at which the capsule is connected with the tubule ; the efferent arteriole emerges from the capsule at the same point which is called the vascular pole of the capsule. The glomerular capsule(of Bowman) is the blind, expanded end of the renal tubule, deeply invaginated by the glomerulus. Its outer parietal wall is lined by squamous epithelium, while the visceral (glomerular) wall surrounding the capillaries and fixed to the basement membrane of the glomerulus, is lined by specialised epithelial podocytes. Thus, between the glomerulus and the outer layer of the capsule i.e. between visceral and parietal, there is a flattened cavity (capsular or urinary space) which is continuous with the lumen of the proximal convoluted tubule (PCT). It is the region within the glomerular capsule that collects the filtrate. A distinct basal lamina underlies the cells of the capsule and, in the glomerulus, this fuses with the basal lamina surrounding the capillary endothelial cells. The podocytes which surround the capillary loops consist of flattened stellate cells, the major dendrite-like processes of which are curved around the capillaries, interdigitating tightly with the processes of other podocytes. Where they approach neighbouring capillaries, many end-feet pedicels encroach on the basal lamina leaving narrow gaps between them. Each podocyte contains numerous mitochondria, microtubules, microfilaments, and vessels of various types, indicating a metabolic activity. The endothelium of the glomerulus is of the finely fenestrated type, the only barriers to the passage of fluid from the capillary lumen to the cavity of glomerular capsule are therefore, the fused basal lamina of the endothelium and podocytes. This layer, the glomerular basement membrane is~ 0.33 micrometer thick and is composed of three distinct layers, the first and third are the pale-staining laminae rarae interna and externa, and the middle
dense, fibrous lamina densa. The glomerular slit diaphragm through which the filtrate must pass before it enters the urinary space covers the area between adjacent podocyte end- feet. (Fig 2– 4)
Fig 2-4 The PCT is lined with simple cuboidal cells with highly folded basolateral membrane into numerous microvilli projecting into the lumen of the PCT called brush border. Microvilli are protoplasmic extensions of the plasma membrane and they greatly increase the surface area for absorption. They are permeable to water and solutes Tight junctions are a type of cell to cell connection in which the cell membrane of adjacent cells form a very close binding and permit passage of water but limits escape of large molecules from tubular lumen into the interstitial space. The thin segment or the descending loop of Henle is formed of a single layer of simple flattened epithelium lacking brush border thus permeable ONLY to WATER but not to solutes. The thin segment extends from the PCT to the hair – pin turn in the loop of Henle. The thick segment or the ascending limb of the loop of Henle becomes continuous with the distal or second convoluted tubule which is divisible into a straight and a convoluted section, between which is a special thickened region, the macula densa, after
which the nephron straightens out as the junctional or connecting tubule which ends by joining a collecting or straight duct. (Fig 2– 5)
Fig 2- 5 The collecting ducts commence in the medullary rays of the cortex. They unite at short intervals with one another and finally open into wider tubes termed the papillary ducts or ducts of Bellini, which in turn open on the summit of a papilla, the numerous duct openings giving the tip of the papilla a perforated cribriform appearance. The thick ascending segment and early distal convoluted tubules(DCT) are lined with similar cuboidal epithelium having a glycoprotein covering of the luminal membrane, with more tighter tight junctions than in the PCT, thus being permeable to SOLUTES only like Nacl but IMPERMEABLE to WATER. The DCT extends from the guxtaglomerular apparatus or JGA to the cortical collecting ducts. As the thick ascending loop of Henle transitions into the early DCT the tubule runs adjacent to the afferent and efferent arterioles, and when these structures are in contact, they form the JGA formed by the macula densa or MD and the juxtaglomerular cells, which are modified smooth muscle cells of the afferent and efferent arterioles, namely the afferent. These enlarged cells serve as baroreceptors sensitive to blood pressure changes
within the arterioles. The MD is a plaque of cells containing large tightly packed cell nuclei within the thick segment and is formed by the cells of the thick ascending limb of the loop of Henle in contact with the arterioles. These cells monitor and respond to changes in the osmolarity of the filtrate in the tubule thus serving as osmoreceptors, and allowing changes in the tubule to influence the behavior of the adjacent glomerulus. (Fig 2– 6)
Fig 2- 6 The cuboidal cells of the late DCT and cortical collecting ducts or CCD are of two distinct functional types : the principal and the intercalated cells. The principal cells are sensitive to the hormone ADH which regulates the permeability to water and solutes like urea which is a waste product of protein deamination and it is the chief nitrogenous waste excreted in urine.( Fig 2-7)
Fig 2- 7 The renal arterial blood supply is through the main renal artery which arises as a lateral branch of the aorta just inferior to the superior mesenteric artery at the level of the 2nd lumbar vertebra, and venous blood is conveyed to the inferior vena cava(IVC) via the renal vein. Each renal artery divides into five segmental arteries that enter the hilum, four infront and one behind the renal pelvis, and are distributed to different segments and areas of the kidney. Segmental arteries give rise to lobar arteries, one for each renal pyramid, which again divide just before entering the kidney substance into 2-3 interlobar arteries which run radially to the corticomedullary junction on each side of the renal pyramids, where they give off the arcuate arteries which arch over the bases of the pyramids giving rise to the interlobular arteries that ascend in the cortex as far as the capsule. The afferent glomerular arterioles or AGA arise as branches of the of the interlobular arteries to supply the nephrons and glomerular capillary bed which drains into the efferent glomerular arterioles or EGA. EGA from the outer cortical glomeruli drain into a peritubular capillary network within the renal cortex and thence into increasingly larger and more proximal branches of the renal vein .Blood from the juxtamedullary glomeruli passes via vasa recta in the medulla and then turns back towards the area of the cortex from which the vasa recta originated. Vasa recta vessels possess fenestrated walls which facilitates movement of diffusible substances. Vasa recta drain the nephrons and coalesce to form the arcuate vein. Other small venules flow into the interlobular vein which in turn drains into the arcuate vein. The remainder of the venous drainage of the kidney corresponds to the arteries in the opposite direction. The renal vein emerges from the hilum in front of the renal artery and drains into the IVC. (Fig 2– 8)
Fig 2-8 Approximately 25% of humans possess dual or multiple renal arteries on one or both sides. The main renal arteries are solitary in ~60% of individuals, and multiple and smaller in the remainder. Renal arteries are more commonly multiple when the kidney is malpositioned or malrotated. Supplemental renal arteries may course directly into the polar regions of the kidney without coursing through the renal hilum. Renal veins are usually solitary. The left renal vein is longer than the right, and for this reason the left kidney is usually chosen for live donor transplant nephrectomy. Anomalies of the kidney include: ectopic kidney, congenital fusion(horseshoe kidney), unilateral renal agenesis, hypoplastic kidneys, duplicated collecting system, extra renal pelvis, (persistent)fetal lobation,, junctional parenchymal defect, interrenicular septum, renal sinus lipomatosis, dromedary hump, renal column hypertrophy, medullary sponge kidney, ureteropelvic junction obstruction. Renal variants are those slight alterations in anatomy that may lead the sonographer to suspect that an abnormality is present while it is a normal variation. Renal variants include: Renal column hypertrophy, the dromedary hump, and the junctional parenchymal defect. Renal column hypertrophy is a common anatomic variant also termed hyppertrophy of the septal cortex or a prominent column of Bertin . It is a double layer of renal cortex that is folded towards the centre of the renal medulla, displacing a portion of the renal sinus. The echo texture is same as the adjacent renal cortex ; and the width of the mass is twice as great as the adjacent renal cortical thickness. The dromedary hump is more common in the left kidney and demonstrates a lateral bulge at its mid portion . Sonographically it is identical to the renal cortex. The junctional parenchymal defect is more common in the left kidney. Embryologically, each kidney is formed from upper and lower units of parenchyma that fuse along an oblique line. The junction points of these limits may persist as a prominent indentation of the cortical surface. The parenchymal defect is triangular in shape with echogenic focus best demonstrated on longitudinal scans. It is commonly located anteriorly, at the junction of the upper and middle thirds of the kidney.
B ) RENAL PHYSIOLOGY The principal role of the kidneys is the elimination of waste material and the regulation of volume and composition of body fluids. In addition, the kidney has endocrine and metabolic functions producing erythropoietn, renin, prostaglandins and the metabolism of vitamin D and small molecular weight proteins. The kidney purifies the blood by excreting urine (excess water, salts and toxic metabolites), involving the processes of glomerular filtration, tubular reabsorption, and tubular secretion. The hydrostatic pressure within the glomerular capillaries of ~ 45mm Hg results in filtration of fluid from plasma into Bowmans capsule. This filtrate is identical in its composition with plasma except that it normally contains no fat and very little protein. The filtrate then flows through the various parts of the renal tubule and is modified according to body needs to maintain homoeostasis by tubular selective reabsorption of its constituents and by tubular secretion. About 65% of the water filtered by the glomerulus is reabsorbed by the PCT through active and passive transport processes. The remaining fluid passes through the DCT and collecting ducts. The filtrate is concentrated in the descending limb by reabsorbing (loosing) water and retaining solutes. The filtrate is diluted in the ascending limb where water is retained and solutes lost. This asymmetrical pattern of H2O & Nacl reabsorption in the descending and ascending limbs of the loop of Henle, creates an osmotic gradient within the medullary region. The Vasa recta circulates blood through the medulla to provide nutrients WITHOUT removing solutes, thus not weakening the osmotic gradient. The final processing of the filtrate in the late DCT and collecting ducts comes under direct physiological control, that membrane permeabilities and cellular activities are altered in response to the body needs to retain or excrete specific substances. This variability provides the mechanism for precisely regulating the balance of fluid and solutes returned to the blood. The principal cells of the late DCT and collecting ducts are sensitive to the hormones aldosterone and ADH. They perform hormonally – regulated Na & H2O reabsorption and potassium secretion. Thus Aldosterone precisely regulates the final amount of Na reabsorbed ; aldosteron levels remain low when the levels of Na & K in the blood are balanced. (Fig 2-9)
Fig 2- 9 The Intercalated cells are specialized cells of the collecting ducts that are involved in Acid–base regulation, hence the pH of the blood, by secreting H+ ions into the filtrate through ATPase pumps in the luminal membrane. A decrease in the level of Na+ ions or an increase in K+ ions will trigger the release of Aldosterone which will result in increase in the number and activity of Na / K pumps in the basolateral membrane and Na/K channels in the luminal membrane,( K channels are absent from the basolateral membrane). K+ ions enter the cell trough the basolateral membrane, but instead of diffusing back into the interstitium they diffuse through the luminal membrane and are secreted into the filtrate. Na+ excretion will be reduced leading to increased interstitial osmolarity and high water reabsorption hence reduced urine volume. This permeabilty to water is only possible in the presence of ADH which occurs along with an increase in aldosterone under most normal conditions, that is because when stimulated by ADH, the principal cells quickly insert luminal water channels thereby increasing water permeability. The filtrate composition is altered as it passes up through the differing osmotic environments of the renal cortex and medulla (300 mosmoles in PCT–1200 mosmoles in interstitium) because filtrate concentration in the tubule is related to the interstitial osmolarity. The opposing flow and opposite activities of the descending and ascending
segments of the loop of Henle is called the COUNTER CURRENT MULTIPLIER MECHANISM .The final step in urine formation occurs as the filtrate passes down the medullary collecting duct(MCD). Of the 125 ml / min of glomerular filtrate that entered the PCT from the glomerular capsule,95 % has been reabsorbed back into the peritubular capillaries into the blood, and only 5% (6ml/min) remains to enter the MCD. The medullary osmotic gradient (MOG) Is necessary for determining the final volume and concentration of urine through ADH release, and is constructed by the counter current multiplier mechanism, the chief substances being NaCl and Urea. Normal urine has an osmolarity of 600 mosm i.e. twice the normal body osmolarity. About 99% of the filtrate is reabsorbed into the blood leaving ~ 0.9% of the filtrate or(1.10ml/min) of concentrated urine to continue the passage into the renal pelvis and urinary bladder which equals~1.5liters/day in the normally hydrated person. Blood flowing through the kidneys is first filtered (all blood constituents are filtered except blood cells and plasma proteins) ; secondly the filtrate is modified so that useful substances including most of the filtered water are quickly reabsorbed back into the blood. Thirdly the unwanted substances that escape filtration are actively secreted into the tubular lumen. Filtration, reabsorption and secretion are the renal mechanisms undertaken for various homoestatic functions. The triple filtering membrane is composed of three layers namely the capillary endothelial layer with pores of about 100 micrometers in diameter, the tubular epithelium also called podocytes which contain slits of 25 nm in width and the basement membrane separating them ; it is made of mucopolysaccharides and contains no pores. The filtration membrane allows particles about 8 nm in diameter. The total surface area of the filtering membrane is about 0.4 m2 for each kidney. The PCT is 15 mm long and 5 microns in diameter with a well defined single layered luminal epithelial brush border which reabsorbs useful substances including Na+ and water. The descending limb of the loop of Henle is 12-14 mm in length and 15 microm in diameter, lined with flat epithelial cells. Only 15% of the nephrons have long loops descending into the renal pyramids and called juxta-medullary nephrons which play a major role in the urine concentration mechanism. The ascending limb of the loop of Henle is 12 mm long, the most distal part of which becomes thicker as it joins the DCT where it comes close to the afferent arteriole of the glomerulus and forms the juxtaglomerular apparatus which plays an important role in the regulation of the renin-angiotensin-aldosterone system. The DCTs are 5 mm in diameter, lined with microvilli lacking brush border. They join the collecting
ducts which are 20 mm long and lined with cuboidal epithelium with no brush border. The collecting ducts open at the renal papillae into the minor calyces. Each collecting duct serves about 4000 nephrons ; thus the total length of one nephron is about 45-65 mm. Glomerular filteration is a passive physical process which does not require energy. The glomerular capillaries are 50 times more permeable than skeletal muscle capillaries. Glomerular filteration is controlled by the capillary hydrostatic pressure, capillary permeability, renal blood flow, plasma albumin concentration, pressure in bowman’s capsule and the number of functioning glomeruli. The glomerular capillary pressure is 60 mm Hg i.e twice that in skeletal muscle capillaries. The force of this pressure tends to help filtration of fluid through the filtration membrane into Bowman’s capsular space. There is an autoregulation system for the GFR that it hardly changes with changes of hydrostatic pressure from as little as 75 mm Hg to as high as 180 mm Hg. If GFR is too slow, the glomerular filtrate will flow slowly and most of its constituents will be reabsorbed and thus the kidney will fail to excrete the unwanted waste products. If the GFR is too fast, time will not be enough for tubular cells to reabsorb the vital substances of the glomerular filtrate. GFR is autoregulated by two mechanisms, namely the afferent arteriolar vasodilator feedback mechanism and the efferent arteriolar vasoconstrictor feedback mechanism. They are local myogenic responses of the vascular smooth muscle to the distending force of the blood flow. The renal blood vessels constrict in response to increased blood flow and dilate if blood flow is reduced. The combination of the two feedback mechanisms is called tubuloglomerular feedback, and are controlled by the juxtaglomerular cells(JGCs) which secrete renin, an enzyme which splits a decapeptide called angiotensin 1 from a plasma protein, alpha-2globulin, called angiotensinogen. Angiotensin 1 loses two amino acids in the presence of a converting enzyme to become an octapeptide called angiotensin 11 which is a potent vaso-constrictor and also stimulates the adrenal cortex to secrete aldosterone. Renin secretion by the JGCs cells is stimulated by a high rate of flow in the DCT and a low Na+ concentration in the distal tubular fluid. Renin secretion activates the angiotensinaldosterone system which produces constriction of the afferent arterioles thereby lowering the hydrostatic pressure in the glomerular capillaries resulting in lowering of the GFR. Glomerular and other renal diseases that damage the filtration membrane results in passage of large size molecules in the filtrate.
In severe hemorrhage there is a reduction in systemic blood pressure and renal blood flow which result in serious reduction of GFR leading to acute shutdown and complete failure of urine formation and anuria. Plasma albumin increases in dehydration resulting in reduction of the GFR ; but those with hypoalbuminaemia usually have a high GFR, e.g. renal and liver disease. Passive tubular reabsorption depends on the concentration and/or electrochemical gradient e.g anions and water follow Na+ in the PCT and also 50% of the filtered urea passively diffuse from the tubules into the peri PCT capillaries. Active tubular reabsorption is the transfer of substances against concentration or electrical gradients and requires energy expenditure or specialized transport systems in the tubular cells. All filtered glucose is actively reabsorbed in the PCT. Transport maximum for glucose(Tm) is 300 mg / min i.e > 300 mg of glucose load in diabetes mellitus (DM) exceeds the Tm and the excess will appear in urine. Renal threshold for glucose is the level of glucose in the blood above which the Tm is exceeded resulting in glucosuria. Small amounts of albumin about 30-50 mg/day escape in the glomerular filtrate but reabsorbed in the PCT. Albuminuria may occur in renal diseases which cause an increase in glomerular capillary permeability. Standing for along time results in albuminuria due to increased pressure in the renal vein. 70-75% of the filtered water and sodium is reabsorbed in the PCT; Na+ reabsorption is active against an electrochemical gradient. Na+ and water are also reabsorbed in the DCTs and collecting ducts under the influence of the hormones aldosterone and ADH respectively; this enables the kidney to maintain homeostasis by regulating the excretion of Na+ and water in urine. When the filtrate passes down the descending limb of the loop of Henle, it looses water and regains urea from the surrounding more concentrated medullary interstitium. The fluid keeps it’s urea untill it reaches the collecting ducts where water is reabsorbed under the effect of ADH , resulting in a rise in urea concentration and as a result 40-50% of it diffuses back into the medullary interstitium and the rest is lost in urine. Due to it’s low Tm, phosphate is always found in urine where it acts as a main buffering system. Its absorption is related to glucose reabsorption as their transport mechanisms compete for a common source of energy, phloridzin, which blocks glucose reabsorption and increases phosphate reabsorption. Parathyroid hormone reduces the Tm for phosphate thereby increasing it’s excretion. Tubular secretion refers to the transport of substances from the peritubular blood, interstitium or tubular cells into the tubular lumen. It is a supplement to glomerular
filteration since it removes from peritubular blood those substances which escaped total elimination by filtration at the glomerulus. Ammonia, salicylic acid and quinidine are passively secreted into the lumen. Creatinine, glucuronides, PAH, penicilline, chlorothiazide and diodrast are actively secreted. K+ and H+ ions are actively secreted by the tubular cells into the lumen by a mechanism which does not seem to be Tm- limited. K+ secretion in the DCT is reciprocally associated with the reabsorption of N+, so that when N+ reabsorption increases, K+ secretion also increases by an unknown mechanism. About 65% of K+ is reabsorbed in the PCT, 25% in the loop and 10% in the DCT and collecting ducts. In the PCT and loop, K+ moves in the same direction as Na+ i.e. both Na+ and K+ are reabsorbed. The amount of K+ secreted is directly related to aldosterone secretion and to Na+ reabsorption. A small increase in serum K+ directly stimulates the adrenal cortex to release aldosterone thereby enhancing K+ secretion which stops in the absence of aldosterone but reabsorption continues. Hypokalaemia results in alkalosis due to excess H+ ion secretion instead, indicating that the same carrier system is involved. The intercalated cells in the DCT and collecting ducts balance the blood pH by secreting H+ ions into the filtrate through ATPase pumps in the luminal membrane. The principal cells of the DCT and collecting ducts perform hormonally–regulated Na+ and water reabsorption, and K+ secretion. The loops of Henle of the juxtamedullary nephrons play a key role in the concentration of urine because they are responsible for the creation and maintenance of the high osmotic pressure in the interstitial fluid of the renal medulla. The descending limb is permeable to water which will be lost into the more concentrated medullary interstitium leading to gradual concentration of the fluid passing down the descending limb and becomes hypertonic as it descends. Some Na+ and chloride go into the descending limb adding further to the rise in their concentration. In the thick portion of the ascending limb, which is impermeable to water, chloride is actively pumped out of the tubule followed passively by Na+ into the interstitial fluid resulting in a hypotonic tubular fluid as it reaches the DCT. In the same way there is a similar change in the concentration of the interstitial fluid surrounding the loop. The osmotic pressure becomes progressively higher towards the tips of the renal papillae. This process of concentration is known as the counter–current multiplier mechanism for the concentration of urine. Vasa rectae are capillary loops descending from the cortex to the medulla with similar role as the loops of Henle. In the descending capillaries water escapes into the interstitial fluid while Na+ and urea enter the lumen increasing blood osmolarity as it descends. In the ascending
capillaries water is reabsorbed and very quickly removed towards the cortex, as the capillaries rejoin the cortical circulation; thus the vasa rectae remove any water reabsorbed from the DCT and collecting ducts in addition to being the only blood supply to the medulla transporting oxygen and nutrients to it, and removing C2O and waste products from it. Up to 75% of Na+ in the filtrate, is actively reabsorbed in the PCT, in addition to a further amount in the loop; and only 10% reaching the DCT where fine regulation of Na+ reabsorption occurs under the influence of aldosterone. In the absence of aldosterone, most of the remaining Na+ is lost in the urine, while large amounts of aldosterone lead to reabsorption of almost all the sodium. The amount which passes in the filtrate is about 625 gm/day of which a very large amount is reabsorbed daily by the kidney. Na+ transport is greater than that of K+, which explains the negative intracellular potential. Na+ transport in the DCT is active against a concentration gradient from the tubular cells to the peritubular fluid; this net movement of Na+ creates a negative electrical gradient which tends to draw Na+ into the cell. Active Na+ transport also results in pumping K+ into the cell. Aldosterone acts by stimulating the synthesis of mRNA which is responsible for synthesis of protein carriers or enzymes necessary for the transport of Na+. Aldosterone secretion is regulated by means of the Na+ level in the extra cellular fluid. The GFR and concentration of urea in the blood determine the excretion of urea, which is normally 4060%. Reduced GFR leads to less urea being filtered and more urea reabsorption due to the slow flow rate. The pH of the urine produced by the kidneys varies from 4-8 according to internal environment requirements, where the pH should be constant at 7.4. This is achieved by the ability of the renal tubules to regulate the acid-base balance through secreting acid and reabsorbing bicarbonate. Blood buffers tend to minimize changes in pH while the lungs and kidneys excrete excess acid formed during metabolism. About 85% of the filtered bicarbonate is reabsorbed in the PCT, the rest in the DCT and collecting ducts which also secrete H+ ions. A fall of urine pH to 6.0 is achieved by reabsorption of HCO3 only, but below that requires active secretion of H+ ions. HCO3 is reabsorbed together with Na+. Na+ in the tubular lumen is present in the form of sodium bicarbonate( NaHco3), disodium phosphate (Na2Po4) and sodium chloride( Nacl) and other monovalent salts. Carbonic anhydrase(CA) in the brush border enhances the conversion of carbonic acid (H2CO3) into CO2 +H2O. CO2 diffuses into the tubular cell to combine with H2O forming H2CO3 enhanced by CA. H2CO3 dissociate yielding new HCO3 which is
reabsorbed and added to the blood, while the H+ ion is actively secreted into the tubular lumen and picked up by either phosphate or ammonium buffers. The Tm for HCO3 is 2.9 mmol / min or 2.8 mmol per 10 ml of filtrate, i.e. above this level, it appears in urine indicating alkalosis. Under normal conditions of GFR 125 ml / min, up to 3 mmol / min of HCO3 are filtered and almost all of it is reabsorbed. The rate of formation of H+ ions by tubular cells is directly related to the concentration of CO2 in the extra cellular fluid i.e. the more CO2 is formed, the more of it passes into the tubular cells, and the more H+ is secreted. The excretion of H+ by tubular cells is achieved by means of their acceptance in urine by several buffers namely the combination with HCO3 in the filtrate thus facilitating the reabsorption of filtered HCO3, the conjugation with dibasic phosphate forming monobasic phosphate ions. Since all phosphate is filtered, its quantity is limited and therefore in acidosis it will readily be utilized as a buffer. The third buffer is ammonia (NH3) formed by the tubular cells ; it combines with H+ forming ammonium( NH4); NH3 also combines with chloride forming NH4CL which is excreted in urine. In hypo-natraemia more Na+ reabsorption takes place in exchange for K+, leaving little K+ to exchange with H+, leading to acidosis. In hypokalaemia more K+ is reabsorbed and more H+ is secreted, leading to alkalosis. Hyperkalaemia results in more K+ excretion and retention of H+ with the secretion of alkaline urine leading to acidosis. NH3 is formed in the renal tubular cells from glutamine which is broken down by the enzyme glutaminase to glutamic acid and NH3. NH3 is secreted into the lumen. H+ secreted by tubular cells into the lumen combines with NH3 to form NH4 which is an important buffer because it forms a weak acid, therefore can take large quantities of H+ with little change in pH. About two thirds of the H+ secreted by the renal tubules is excreted in this form. The rate of production of NH3 is proportional to the rate of H+ formation in the renal tubular cells. The more acidic the urine is, the more NH3 is produced; and the kidney can increase its NH3 production up to 50 times when there is excessive need for excretion of H+ Secretion can take place until its concentration in tubular lumen is 900 times that in the extra cellular fluid. This is the maximum transport gradient for H+ and corresponds to a urine pH of 4.5 (limiting pH). The acid excretion by the kidney is about 20-40 meq/day. The endocrine functions of the kidney include production of renin, erythropoietin, vitamin D and prostaglandins . Erythropoietin is produced by peritubular cells in the renal cortex, and released in response to hypoxia. It stimulates the bone marrow stem cells to
promote erythropoiesis. Its half–life is 5 hours thus if large amounts are produced, polycythaemia follows. Low levels of erythropoietin are found in renal damage, which accounts for the anemia associated with kidney disease e.g. CRF. Vitamin D3(1,25dihydroxycholecalciferol) is synthesized in the skin or taken in food in an inactive form. It is hydroxylated in the liver at the C-25 position to give 25-hydroxycholecalciferol( calcidiol) which is the major form of vitamin D in the blood but is not active to act on the gut, kidney or bone. Calcidiol is hydroxylated at the C-1 position by a specific kidney enzyme to give calcitriol (1,25-dihydroxy-cholecalciferol) which is the active form that acts on the gut to regulate calcium and phosphate absorption, on the kidney to regulate calcium and phosphate excretion and on the bone to regulate calcium mobilization and exchange with serum calcium. All these actions are achieved together with the parathyroid hormone. Prostaglandins are a group of 20-carbon unsaturated fatty acids which are rapidly metabolized particularly by the lungs. They act as local hormones due to their short half life which is about few minutes. Renal prostaglandins (PGE) are released in response to renal ischemia due to sympathetic stimulation, catecholamine release or angiotensin11 release. PGE may be involved in the regulation of renal blood flow in these conditions; and may also modify the action of ADH by reducing the sensitivity of renal tubular cells to the effect of ADH.
C-I ) CLINICAL FEATURES OF CRF There are few physical signs of ureamia per se and include: short stature in those with CRF in childhood, increased photosensitive pigmentation which makes the patient misleadingly healthy, scratch marks due to uremic pruritus, signs of fluid overload, pericardial friction rub, flow murmurs namely mitral regurgitation due to annular calcification; aortic and pulmonary regurgitant murmurs due to volume overload, rarely there is glove and stocking peripheral sensory loss. The symptoms and signs which constitute the clinical features of the uremic syndrome are multisystem and include mainly neurological manifestations, hematological disorders, cardiovascular disorders, pulmonary disorders, gastrointestinal manifestations, bone and calcium and phosphorous disorders, skin disorders, psychological disorders, and fluid and electrolyte disorders. In the majority of patients suffering from chronic renal failure, symptoms and signs are not referred to the anatomical site of the kidneys; clinical features commonly arise from abnormalities in the chemical composition of the body or from hypertension, anemia, metabolic bone disease manifestations; the origin of these manifestations may be suspected only after detection of urinary abnormalities. In the CNS, CRF causes an unusual combination of depressed cerebral function and decreased seizure threshold. However convulsions in CRF are caused by accelerated hypertension, drug accumulation and thrombocytopenic purpura. Patients suffer from fatigue, lethargy, sleep disturbances, peripheral neuropathy including the restless leg syndrome. Anemia and bleeding tendency is a common manifestation which is due in part to platelet dysfunction and abnormal coagulation. Anemia is universal as the glomerular filtration rate falls below 25 ml/min. Several factors contribute to the anemia namely depressed production of erythropoietin leading to reduced heme synthesis resulting in reduced end-organ response to erythropoietin; shortened red cell survival due to uremic toxins; marrow space fibrosis occurs with osteitis fibrosa of secondary hyperparathyroidism resulting in decreased erythropoiesis. Pericarditis, hypertension, congestive heart failure, coronary artery disease, and myocarditis constitute the cardiovascular manifestations. Hypertension occurs in 80-90% of those with renal insufficiency and is due to expansion of extra cellular fluid volume
from the reduced ability of the kidney to excrete ingested sodium; increased activity of rennin-angiotensin system; dysfunction of the autonomic nervous system with increased sympathetic tone and insensitive baroreceptors; diminished presence of vasodilators such as prostaglandins. Patients also develop pleuritis and uremic lung. Anorexia, nausea, vomiting gastroenteritis, gastrointestinal bleeding, and peptic ulcer are the main manifestations in the gastrointestinal tract. Metabolic–endocrine disorders manifest as glucose intolerance, hyperlipidemia, hyperuricemia, malnutrition, sexual dysfunction, and infertility. Fluid and electrolyte disorders consist of hyponatremia, hyperkalemia, hypermagnesemia, metabolic acidosis, and volume expansion or depletion. Skin features of uremia include pruritus, pigmentation, easy bruising, and uremic frost. The kidneys are usually impalpable unless enlarged as a result of polycystic disease, obstruction, diabetes mellitus, amyloid, myeloma or tumours ; in addition to the physical signs of the underlying diseases which may have caused the CRF. An assessment of the central venous pressure and blood pressure are also made. CRF is a permanent reduction in GFR sufficient to produce detectable alterations in well-being and organ function. This usually occurs at GFR below 25ml/min. There are four stages : Stage 1(silent) : GFR is up to50 ml/min Stage11( renal insufficiency): GRF is 25-50 ml/min Stage111( renal failure) : GFR 5-25 ml/min Stage1V(end-stage renal failure): GFR less than 5ml/min Uraemia (azotaemia) implies the manifestations of organ dysfunction seen in stages 111&1V. Azotemia, the accumulation of nitrogenous waste products, chiefly UREA, in the blood IS THE HALL MARK of renal failure. It is a clinical syndrome resulting from multiple factors namely Retained metabolic products, Overproduction of counterregulatory hormones e.g. parathyroid hormone in response to hypocalcaemia and the natriuretic hormone in response to volume overload, Underproduction of renal hormones e.g. decreased erythropoietin causes anaemia and the decreased 1-hydroxylation of vitamin D3 contributes to bone disease. Anaemia is universal as GFR falls below 25ml/min ; it is due to reduced erythropoietin production, reduced red cell life span, blood loss from decreased platelet function and
abnormal coagulation, marrow space fibrosis from osteitis fibrosa of secondary hyperparathyroidism resulting in decreased erythropoiesis. Hypertension occurs in 80-90% of patients with renal insufficiency and is produced due to reduced ability to excrete ingested Na+ leads to expansion of extra cellular fluid volume; Increased activity of the renin–angiotensin system; Autonomic dysfunction occurs with insensitive baroreceptors leading to increased sympathetic tone; Decreased renal generation of prostaglandins and other vasodilators of the kallikrein– kinine system. As GFR decreases there is a slight retention of phosphorus which leads to hypocalcaemia which stimulates PTH. This causes phosphaturia till eventually the renal tubule can no longer respond to higher levels of PTH with a further decrease in phosphorus reabsorption .When this occurs hyperphosphatemia develops, hypocalcaemia becomes prominent and PTH increases to very high levels which can cause bone disease with severe osteitis fibrosa. Altered vitamin D metabolism occurs secondary to decreased renal mass or to phosphorus retention, with decreased synthesis of 1,25(OH)2 D3. Eventually these events can lead to secondary hyperparathyroidism and osteomalacia. Therefore on mangement always be in the look up for reversible factors and their correction, mainly, hypertension, urinary tract infections, urinary tract obstruction, reduced renal perfusion due to water and salt depletion in addition to cardiogenic and septic shock and hemorrhage, infections which increase urea production, and nephrotoxic medication. When plasma creatinine consistently exceeds 300micromol/l, dietary protein should be restricted to 40 gm per day in adult with adequate intake of carbohydrate(250 gm) and 60 gm of fat thus providing energy value of at least 1700 kcal. Fluid restriction is necessary only when the glomerular filtration rate is less than 5 ml/min or with congestive heart failure. The excretory function of the kidney can be partially replaced by dialysis, but dialysis cannot replace the endocrine and metabolic functions of the failing kidneys which can be achieved by a successful renal transplantation. When creatinine level is consistently exceeding 600 micromol/l an arteriovenous fistula is performed in the forearm to go for hemodialysis for 4-6 hours three times weekly. There will be gradual reduction of uremic symptoms during the first six weeks of dialysis, but plasma creatinine and blood urea do not return to normal.
C-II) NORMAL RENAL SONOGRAPHY AND TECHNIQUE Sonography is used primarily for anatomy, the IVU,CT for anatomy and function and nuclear medicine for function. Evaluating kidneys with U/S is a non-invasive approach. It delineates retroperitoneal masses or fluid collections such as haematomas or abscesses. It rules out hydronephrosis in those with renal failure since U/S is supreme in showing fluid filled structures. It determines the renal size and parenchymal detail, detects hydroureter, and images renal congenital abnormalities. Patients are given nothing by mouth except water to fill the bladder before examination. If over hydrated, the internal collecting system will become also distended. If dehydrated, the infundibula and renal pelvis will be collapsed. The examination begins with the patient in the supine or decubitus position.. Scans are performed in the sagittal and transverse planes from the anterior approach using the liver and spleen as acoustic windows for the right and left kidneys respectively. Scanning is always done in deep suspended inspiration.. Start with a longitudinal scan over the right upper abdomen and then follow with a transverse scan. Next, rotate the patient to the left lateral decubitus position, to visualize the right kidney in this coronal view. To visualize the left kidney, scan in the left upper abdomen in a similar sequence. If the left kidney cannot be seen (usually due to excess bowl gas), try the right decubitus position. Bowl gas can also be displaced by drinking 3-4 glasses of water. The left kidney can then be visualized through the fluid-filled stomach with the patient in the supine position. If the kidneys have not been imaged adequately, scan through the lower intercostal spaces. Turn the patient prone and apply enough gel to the left and right renal areas and perform longitudinal and transverse scans. Both kidneys can be also examined with the patient sitting or standing erect. When examining any part of renal area, compare both kidneys in different projections. Variations in size, contour and internal echogenicity may indicate an abnormality. For adults use a 3.5MHz transducer, for children and thin adults use a 5.0 MHz transducer. Start by placing the transducer over the right upper abdomen, then angle the beam as necessary and adjust the time gain compensation (TGC) with adequate sensitivity settings to allow uniform acoustic pattern, thus obtaining the best image of renal parenchyma. Gain is the amplification of the reflected U/S waves by the U/S unit. The “
near gain” control amplifies echoes returning from tissues above the focal point of the beam, while the “far gain” control amplifies echoes returning from beyond the focal point of the beam i.e. echoes coming from deeper tissues need more amplification. These controls can be adjusted to allow proper comparison of echogenicity at different levels. Renal detail may be obscured if there is a significant amount of perirenal fat, hepatocellular disease, gall stones, rib interference or other abdominal masses or collections between the liver and kidney. When scanning it is better to identify: the renal capsule, the cortex, macula, sinus, ureters, renal arteries and veins . The kidneys are imaged by U/S as organs with smooth outer contours surrounded by highly echogenic peri-renal fat. The renal capsule appears as a bright, Smooth, echogenic line surrounding the renal cortex which is homogeneous with smooth contour. Its echogenicity is moderate (mid to low-level echoes) in an even texture that is less echogenic than normal liver or spleen but more echogenic than the adjacent renal medullary pyramids. The renal medulla contains the pyramids which appear as triangular or blunted hypo-echoic to anechoic areas (it should not be mistaken for renal cysts or tumors ). (Fig 2 -10)
Fig 2 - 10 The renal columns(septal cortex or the columns of Bertin) are projections of cortex that extend between the pyramids. They are sonographically identical to the peripheral cortex. It is easier to visualize the pyramids in children and young adults. The central echo complex (the renal sinus) is imaged as a very highly hyperechoic(very echogenic) area normally occupying about one third of the kidney and includes the collecting system
(pelvis and calyces), fat, and vessels. It is the innermost part of the kidney and has the greatest echogenicity due to the fat deposition. The sinus is surrounded by parenchyma (the area from renal sinus to outer renal surface whose thickness is 11-18 mm in males and 11-16 mm in the female). The pelvis is not visualized unless urine filled when it appears unechoic. It is scanned through the renal sinus in an anterior transverse view. The renal arteries and veins are best seen at the hilus. They enter the kidney at different levels and may be multiple. The arcuate vessels are demonstrated as intense specular echoes in cross section or oblique section at the corticomedullary junction. The renal arteries are best seen in supine and lateral decubitus views. The right renal artery can be seen in a longitudinal scan as a circular structure posterior to the inferior vena cava. The right renal vein extends from the central renal sinus directly into the IVC. Both vessels appear as tubular structures in the transverse plane. The renal arteries have an echo –free central lumen with highly echogenic borders that consist of the vessel wall and the surrounding retroperitoneal fat and connective tissue. They lie posterior to the veins and can be demonstrated with certainty if their junction with the aorta is seen. The left renal artery flows from the posterolateral wall of the aorta to the central renal sinus. An extra-renal pelvis may be seen as a fluid-filled structure medial to the kidney on transverse scans. Differentiation of the normal variant from obstruction is made by noting the absence of intra-sinus distension of the renal pelvis and infundibula. Dilatation of the collecting system has also been noted in pregnancy (the right kidney is generally involved with mild degree of hydronephrosis which reverts to normal after delivery). Normally in the non-hydrated subject, the renal pelvis is collapsed and therefore not demonstrated on the scan, the renal pelvis is influenced by bladder distension, diuretics and the state of hydration. Distension of the renal pelvis is seen in 50% of non hydrated and in 90% of hydrated subjects examined with a full bladder. The normal renal pelvis in the hydrated patients is between 2-14 mm. If two separate collections of renal sinus fat are identified, a double collecting system should be suspected. Ability to visualize the kidney does not mean that it is functioning. To assess renal function, use contrast urography, a radionuclide study or laboratory tests.. Injury to a kidney may result in temporary loss of function. Normal ureters are not always seen. They should be sought where they leave the kidney at the hilus. They may be multiple and are often seen in the coronal projection . Generally, echogenicity from higher to decreasing order is : renal sinus, spleen, liver renal cortex, renal medulla. (Fig 2 – 11)
Fig 2 - 11 In adult, the thickness of the renal parenchyma decrease at about 10% per decade after 20 years of age. The corticomedullary ratio is 1:1.6 up to 30 years old ; 1:1.2 up to 50 years old ; I:1 above 50 years old with thinning of cortex with age. The overall size decreases with age and only apparent in the elderly. The fetal kidney size in cm equals the gestational age in weeks plus or minus 3 mm. Infantile kidneys are large compared to overall body size (typically 4- 5 cm long at birth) and may be imaged from 12- 14 weeks onwards but clearly seen after 16 weeks. In transverse section they appear hypoechogenic, circular structures on either side of the spine. Within them can be seen the strongly echogenic renal pelvis ; the capsule is also echogenic. The renal papillae are hypoechogenic and can appear large. Some dilatation of the renal pelvis (less than 5mm) may sometimes be seen but is a normal finding. It is important to assess renal size by comparing the renal circumference with the abdominal circumference, the normal ratio being 0.27- 0.3. The fetal urinary bladder can be recognized as a small ovoid cystic structure within the fetal pelvis as early as 14- 15 weeks. The normal urinary production at 22 weeks is 2 ml per hour, whereas at full term it is 26 ml per hour. Until the age of 6 month. neonatal kidneys differ acoustically from adult kidneys in that: the difference between cortex and medulla is less marked in the infant; pyramids are relatively hypoechogenic and may resemble cysts; cortex is less echogenic than liver parenchyma. for the first 3 years of life .Its pyramids appear large because the cortex is relatively thin and hyperechoic. During the first year of life the cortex gradually develops to assume the adult corticomedullary proportions. The pediatric renal sinus is poorly echogenic because it contains little fat.
Fat deposition and accumulation occurs gradually to achieve adult proportions by about age 10 years. The majority of infants have a slight separation of the central echo complex, reflecting the presence of a small amount of urine of unknown cause. (Fig 2 – 12)
Fig 2There is no absolute measurement to separate normal distension from hydronephrosis; 10 mm separation is considered the upper limit of normal. Unlike in adult practice, detection of children with vesicoureteric reflux is important and may only be reflected by minor separation of the central sinus echoes without renal scarring. Normal renal length of the pediatric kidney is determined using this guide: Renal length (over one year) in cm = 6.79 +(0.22x age in years); in those less than one year = 4.98 +(0.155 x age in months). Asymmetry in renal lengths exceeding 5mm in infants and 10 mm in older children should raise the suspicion of an underlying problem even if both kidneys are within the normal range. D) RENAL PATHOLOGY The kidney is affected by a vast multitude of pathological disorders including congenital and hereditary lesions e.g. congenital cystic kidneys; Acute renal trauma; Vascular disorders e.g. renal artery stenosis and thrombosis; Renal cystic diseases; Renal calculus disease; Renal calcifications e.g. nephrolithiasis involving the collecting system and nephrocalcinosis which affects the cortex in 5% and the medulla in 95%; Hydronephrosis; Renal obstructive disorders ; Neoplastic kidney disease the benign type of which include intra-renal medullary fibroma, cortical adenomas, angiomyolipomas, pelvis villous papillary tumors and renin-producing tumors. The malignant group comprises: renal cell carcinoma (adenocarcinoma) nephroblastoma, transitional cell tumors, renal lymphoma leukaemia, metastasis to the kidney. The medical renal diseases include: Urinary tract infection and Pyelonephritis, Glomerulonephritis, Nephrotic syndrome, Collagen renal disease, Amyloidosis; Sickle cell disease, tubulointerstitial 12
diseases (acute renal and acute tubular necrosis, tubulointerstitial injury due to drugs, toxins, systemic diseases and chronic renal failure) tubuloinerstitial nephritis is the interstitial inflammation with tubular damage. It is a regular feature of bacterial pyelonephritis but rarely to severe renal damage .The causes also include metabolic conditions like urate nephropaty or Gout, nephrocalcinosis, hypokalaemic nephropathy and oxalate nephropathy. Other miscellaneous causes include multiple myeloma, Sjogrens syndrome, SLE, radiation nephritis, secondary to glomerulonephritis and/or vascular disease and idiopathic interstitial nephritis. In acute tubular necrosis (the most important cause of acute renal failure) there is a profound decrease in GFR resulting in the pathological changes which include enlarged kidneys with bulging cut surface due to dilatation of tubules and interstitial oedema. The cortical vessels contain little blood and the cortex appears pale; the medulla is dark and congested leading to accentuated corticomedullary differentiation. Microscopically the tubular changes are variable and non specific. The tubular necrosis tends to be focal involving segments of the PCT and DCT and the ascending limb of the loop of Henle. Rupture of the basement membrane (tubulorrhexis) is seen with an accompanying inflammatory reaction in the interstitial tissue. An early change seen by the electron microscope is the loss of the normal brush border from the proximal tubular cells. Proteinaceous, eosinophilic, granular casts are conspicuous in the DCT. In cases of haemoglobinuria, cells containing granules of pigmented material are prominent. There is interstitial edema. In Mercuric chlorideinduced acute tubular necrosis (ATN), the whole of the PCT may be involved. Oliguria is common in ATN and during the initial phase, both renal blood flow and GFR are markedly reduced which leads to retention of nitrgenous products that are aggravated by endogenous protein breakdown resulting from tissue damage. The oliguria itself leads to fluid overload unless fluid intake is restricted. Fluid overload results in oedema in young persons, while it predisposes to cardiac failure in the elderly. Tubular function is also impaired leading to an inability to concentrate the urine. There is acidosis and hyperkalaemia in the oliguric phase which may be life threatening, because of reduced renal excretion and a shift of potassium from within the cells to the extra cellular fluid. In the recovery phase when urine concentrating power is still reduced, increased electrolyte loss may occur leading to hypokalaemia and/or hyponatremia. In renal tubular acidosis, deficient tubular function is partly responsible for the acidosis which complicates chronic renal failure. The renal lesion of K+ deficiency is
associated with an intense hydropic vacuolation chiefly in the cells of descending straight portion of the PCT. It is also associated with marked loss of concentrating power, but only minimal proteinuria and no urea retention. In chronic interstitial nephritis, NSAIDs and other analgesics lead to analgesic nephropathy which comprise interstitial fibrosis and papillary necrosis. There is interference with the urine concentrating ability, and pyuria is common. Progressive renal function impairment follows with metabolic acidosis and anaemia being prominent features. Sloughing of the necrotic papillae occurs at the distal part of some or all of the papillae, demarcated from living tissue by a red line of congestion. It appears white or yellow, structure less with patchy calcification. Atrophy of the overlying cortex ensues so that the gross appearance of the kidney resembles that of chronic pyelonephritis with intervening patches of more normal and sometimes hypertrophied renal tissue Microscopically the junction between the dead and living papillary tissue is often indistinct and there may be a zone of partial necrosis. The cortex shows tubular loss and atrophy. A distinctive microangiopathy occurs, characterized by the presence of PAS positive material in the vessel wall leading to marked narrowing of the lumen. The resultant ischemia is an important factor in the pathogenesis of the papillary necrosis. Papillary necrosis may also be found as a complication of urinary tract obstruction or in diabetes mellitus .In those with longstanding analgesic nephropathy there is an increased incidence of transitional cell carcinoma of the renal pelvis. The very uncommon condition of diffuse bilateral cortical necrosis with sparing of medulla leads to failure of renal function or to incomplete recovery. It is more frequently associated with pre-eclampsia, but may also occur in the haemolytic uraemic syndrome and septic shock. It is due mainly to intravascular coagulation. In the cellular dysfunction in uremia, hypometabolism and an abnormally low body temperature may be seen in patients with advanced, uncomplicated uremia. A characteristic feature of nearly every normal cell in the body is a very low concentration of sodium ions in the intracellular water compartment, for example in the muscle cells, about 10 mmol/l or less. In contrast the concentration outside the cell is 140 mmol/l. Under normal conditions sodium ions leak through the cellular membrane into the cell which increases sodium concentration inside the cell which activates the enzyme adenosine triphosphate which promptly moves sodium from the cell into the extra cellular space.
Two important events allow sodium transport, namely, burning of glucose and consumption of oxygen. Removal of positively charged sodium ions from the cell accounts for the production of a substantial portion of the body’s heat. This process also leaves in its wake a negative charge, which in turn attracts and holds potassium ions inside the cell. Potassium is important for the proper functioning of a number of enzymes. The transport of sodium thus helps to concentrate potassium ions in the cell and to maintain normal body temperature. Certain of the abnormal characteristics in the muscle cells of patients with advanced uremia can be reversed simply by removing protein from the diet and replacing it with optimal quantities of essential amino acids. Besides the retention of salt and water in the extra cellular fluid, there is marked retention inside the cell. Although patients with end-stage renal disease may show no evidence of edema, one of the early changes commonly following the initiation of dialysis therapy is a sharp decline in total body weight, which matches the loss of cellular salt and water. This loss corresponds in timing to correction of the derangement in sodium transport in nearly all cells. In the pathophysiology, the most intriguing aspect of chronic renal failure is that compensatory mechanisms allow loss of 90% of glomerular filtration rate before the manifestations of the uremic syndrome are evident. Thus a variety of adaptations compensate for the decreased glomerular filtration rate and allow a new steady state of external balance to exist, but on the other hand contribute to the uremic syndrome. In spite of these adaptations, the HALLMARK of chronic renal failure is the loss of flexibility in responding to challenges in external load of solutes and water. The adaptations include intact nephron hypothesis, the magnification phenomenon and the trade-off hypothesis. Nephrons functioning in diseased kidneys maintain glomerulo-tubular balance. That is, filtration and net excretion of various substances are coordinated; for example with normal renal function, usually 50-60% of filtered urea is reabsorbed from the tubules. In chronic renal failure it may fall to 30% to maintain balance. Although nephrons in diseased kidneys function homogeneously, they alter their handling of given solutes as needed to maintain balance of these solutes. That is, nephrons can magnify their excretion of a given solute; for example tubular creatinine excretion is less than 10% with normal renal function. In chronic renal failure it may increase to 30%.
The mechanisms that are magnified to maintain individual solute control may have deleterious effects on other systems. This trade-off is seen in the increased parathyroid hormone(PTH) secretion seen in chronic renal failure which enhances renal phosphorous excretion. Parathyroid hormone has been implicated in the pathogenesis of many disturbances of uremia namely sleep, sex, bone, anemia, lipidemia, and vascular disease. The corollary of the trade-off hypothesis is the concept of proportional reduction of solute, that is, reduction of solute intake(e.g. phosphorous) in proportional to decrements in glomerular filtration rate could prevent the compensatory changes(e.g. increased parathyroid hormone) which may contribute to the development of uremia. In order to maintain sodium balance, the fraction of sodium reabsorbed must be decreased, thereby increased excretion of sodium fraction because of decreased glomerular filtration rate. A humoral natriuretic factor in chronic renal failure helps to increase sodium excretion. In chronic renal failure, the kidneys are unable to reduce sodium excretion rapidly in response to a sudden decrease in intake or external losses for example gastrointestinal losses. Thus major increase in sodium intake results in edema, and major decreases in intake or increases in external loss result in volume depletion. THE HALLMARK of chronic renal failure is the loss of flexibility in responding to challenges to external load of solutes and water. While normal subjects can excrete sodium promptly following a sodium load with minimal effect on the extra cellular fluid, in chronic renal failure subjects delayed excretion results in extra cellular fluid expansion. While normal subjects on salt restricted diet reduce urine sodium to 20 mEq in 48 hours, chronic renal failure patients may require one to two weeks for similar sodium conservation and thus are prone to sodium depletion. Deranged Na+ transport in advanced uremia results in accumulation of Na+ &Cl inside the cell leading to accumulation of water and a fall in K+ concentrations with consequent defects in metabolic processes and a defect in heat production and thus this type of cell is referred to as the SICK CELL OF UREMIA. These changes can be reversed by adequate dialysis or successful renal transplantation. Besides retention of salt and water in the extra cellular fluid, there is marked retention inside the cell which will be lost following dialysis thus explaining the sharp decline in total body weight after dialysis despite no evidence of edema. In spite of the adaptations compensating or the decreased GFR, the HALL MARK OF CRF is the
loss of flexibility in responding to challenges to external load of solutes and water. With normal renal function, usually 50-60% of filtered urea is reabsorbed from the tubules, but in CRF it may fall to 30% or less to maintain balance. With normal renal function tubular creatinine excretion is less than 10%, but in CRF it may increase to 30% i.e. the nephrons can magnify their excretion of a given solute. Although creatinine is secreted and urea is reabsorbed through tubules, balance depends on their rates of filtration. Balance (rate of filtration) is maintained by allowing plasma concentrations to rise until renal excretion equals production. Urea reabsorption falls with the solute diuresis per nephron and thus the blood urea nitrogen (BUN) need not rise as much as expected to maintain balance. Creatinine secretion is enhanced and thus excretion also is balanced to production at a plasma concentration less than anticipated. In addition, urea is metabolized in increased amounts by gut bacteria as the blood urea nitrogen rises and creatinine production is reduced by metabolic suppression. In order to maintain water balance, the fraction of water reabsorbed by the kidney must decrease leading to increased flow per nephron. With progressive CRF, the ability to excrete a water load is compromised leading to hypo-osmolarity and the urine concentrating ability of the kidney becomes fixed around 300 mosm/kg of water rendering the patient susceptible to dehydration if water intake is lowered. Thus, a CRF is prone to both excess and deficit of water. Nocturia develops early in CRF because of decreased concentrating ability of urine during sleep. In order to maintain Na+ balance, the fraction of Na+ reabsorbed must be decreased , thereby increased excretion of Na+ fraction because of decreased GFR. A humoral natriuretic factor in CRF helps to increase Na+ excretion. Increased tubular secretion of K+ helps maintain its balance until renal failure is severe when fecal excretion of K+ increases to 50% of K load (in normal subjects, 90% of K+ is excreted in urine and 10% in stool), however the patient is susceptible to hyperkalaemia from sudden K+ loads. CRF is associated with a continuous positive balance of hydrogen ions (retention) due to a decrease in tubular ammonia production. Retained anions such as SO4 and PO4 contribute to acidosis. A variety of chronic renal diseases progress to end-stage renal failure, including chronic glomerulonephritis, diabetic nephropathy, and polycystic kidney disease. The progression may be due to secondary factors that are unrelated to the activity of the initial disease. These include Systemic and Intraglomerular hypertension, Glomerular hypertrophy, Intrarenal precipitation of calcium phosphate, hyperlipidaemia,
and altered prostanoid metabolism. The major histologic manifestation of these secondary causes is FOCAL SEGMENTAL glomerulosclerosis, thus glomrular damage and proteinuria typically occur with progressive renal failure. As the number of functioning nephrons declines, each remaining nephron excretes more acid (primarily as ammonia). The local accumulation of ammonia can directly activate complement, leading to secondary tubulointerstitial damage . Increased tubular secretion of potassium helps maintain potassium balance until renal failure is severe. In normal subjects, 90% of potassium is excreted in urine and 10% in stool. In advanced chronic renal failure, fecal excretion of potassium increases to 50% of the potassium load. Thus, plasma potassium and body potassium are maintained on normal dietary intake. However the patient is susceptible to hyperkalemia from sudden potassium loads. Decreased glomerular filtration rate leads to a sequence of events, for example a trade-off occurs in the development of secondary hyperparathyroidism in that the elevated parathyroid hormone increases phosphate excretion but contributes to bone disease and perhaps other system dysfunction. Chronic renal failure is associated with a continuous positive balance(retention) of hydrogen ions due to a decrease in the tubular ammonia production to excrete hydrogen. Retained anions such as sulphates and phosphates contribute to acidosis. Bone serves as a sump for excess hydrogen ion and plasma bicarbonate concentration is preserved at only a modestly reduced concentration(about 15 mmol/l). However, flexibility is lost and severe acidosis may occur from small challenges. A variety of chronic renal diseases progress to end-stage renal disease, including chronic glomerulonephritis, diabetic nephropathy, and polycystic kidney disease. Although the underlying problem often cannot be treated, extensive studies in experimental animals and preliminary studies in humans suggest that progression in chronic renal disease may be largely due to secondary factors that are unrelated to the activity of the initial disease. These include systemic and intraglomerular hypertension, glomerular hypertrophy, the intrarenal precipitation of calcium phosphate, hyperlipidemia especially in the nephrotic syndrome, metabolic acidosis, proteinuria, tubulointerstitial disease, retained uremic toxins and filtered iron in the nephritic syndrome. The major histologic manifestation of these secondary causes of renal injury is focal segmental glomerulosclerosis. Thus glomerular damage and proteinuria typically occur with progressive renal failure.
A rise in intraglomerular pressure, due either to the compensatory response to nephron loss or to primary renal vasodilatation(as in diabetes mellitus) appears to play an important role in the progressive glomerular scarring. At least two factors may be involved in the incompletely understood mechanisms by which intraglomerular hypertension might promote glomerular injury, namely, direct endothelial cell damage (similar to that induced by systemic hypertension) and increased pressure-induced movement of circulating macromolecules(such as IgM and fibrinogen and complement metabolites) through the fenestrated endothelial cells into the sub endothelial space in the glomerular capillary wall. The characteristic accumulation of these hyaline deposits can progressively narrow the capillary lumens, thereby decreasing glomerular perfusion and filtration. An increase in glomerular size, as well as intraglomerular pressure, also may occur in these settings. This change can contribute to glomerular injury both by increasing wall stress and by causing detachment of the glomerular epithelial cells from the glomerular capillary wall. Non-hemodynamic factors also may be important in the development of secondary glomerulosclerosis. Marked nephron loss in experimental animals can lead to glomerular cell proliferation, macrophage influx and accumulation of extra cellular matrix components( leading to narrowing of the capillary lumens). How these changes occur is not well understood, but cytokines such as platelet-derived growth factor and transforming growth factor-beta(TGF-beta) may play a contributory role. Experimental studies, for example, suggest that TGF-beta may contribute to increased extra cellular matrix production and the development of glomerulosclrosis in a variety of renal diseases. Thus glomerulosclerosis results from the glomerular hypertension itself or from increased glomerular capillary flow and filtration. In addition to processes affecting the glomeruli, secondary tubulointerstitial disease also is commonly seen. Both the glomerular filtration rate and long-term prognosis are more closely related to the degree of tubulointerstitial, rather than glomerular injury. A tendency to phosphate retention is an early problem in renal disease, beginning as soon as the glomerular filtration rate starts to fall. In addition to promoting bone disease, the excess phosphate also may contribute to the progression of the renal failure. This may occur at least in part by phosphate precipitation with calcium in the renal interstitium, leading to an increase in renal calcium content even before the plasma creatinine
concentration exceeds 1.5 mg/dL(132 micromole per liter). The calcium phosphate salts may then initiate an inflammatory reaction, resulting in interstitial fibrosis and tubular atrophy. These problems can be minimized by decreasing phosphate intake or by the use of oral phosphate binders. It has been suggested that the efficacy of protein restriction may be related in part to a concurrent decline in phosphate intake. Glomerular prostaglandin production tends to be increased in glomerular disease. This response may represent an appropriate intra-nephronal adaptation, since the ensuing vasodilatation helps to maintain the glomerular filtration rate in the presence of an often marked reduction in glomerular capillary permeability induced by the underlying disease. This adaptation is reversed by an NSAIDs, leading to renal vasoconstriction and a subsequent fall in intraglomerular pressure. These changes are manifested clinically by reduction in glmerular filtration rate(usually by about 20%) and protein excretion(often by more than 50%) in many patients with chronic glomerular disease. Non-randomized studies suggest that long term therapy in responders(those with a substantial decline in proteinuria) may be associated with a lesser rate of progression to end-stage renal disease. Hyperlipidemia is common in patients with chronic renal disease, particularly those with nephrotic syndrome. In addition to accelerating the development of systemic atherosclerosis, experimental studies suggest that high lipid levels also may promote progression of renal disease. The major evidence in support of this hypothesis are the observations in experimental animals that cholesterol loading enhances glomerular injury and that reducing lipid levels with a drug such as livostatin slows the rate of progressive injury. The factors responsible for the lipid effects are incompletely understood. In different animal models, a high cholesterol intake may be deleterious in association with a rise in intraglomerular pressure, while lipid-lowering agents may beneficial without affecting glomerular hemodynamics. These disparate observations suggest that mechanisms other than intraglomerular pressure alone may play a contributory role. It has been shown experimentally, for example, that hyperlipidemia activates the mesangial cells(which have LDL receptors), leading to increased production of fibronectin(a component of the extra cellular matrix) and for a chemo-attractant for monocytes. Both of these changes could contribute to glomerular injury. In addition HMG CoA reductase inhibitors such lovastatin may act independent of plasma lipid levels by directly inhibiting mesangial cell proliferation.
The applicability of these findings to human disease is unproven, since there are no studies evaluating the possible protective effect of lowering lipid levels. However, both increased mesangial lipid deposition and enhanced expression of LDL-receptors on mesangial and epithelial cells have been demonstrated in patients with chronic glomerular disease. Mesangial phagocytosis and increased traffic of macromolecules through the more permeable glomerular capillary wall could be responsible for the lipoprotein deposition; in addition, the increase in receptors could promote lipid accumulation even in the absence of hyperlipidemia. Whether the deposited lipid contributes to the glomerular injury is uncertain. As the number of functioning nephrons declines each remaining nephron excretes more acid(primarily as ammonia). The local accumulation of ammonia can directly activate complement, leading to secondary tubulointerstitial damage(at least in experimental animals). On the other hand, buffering the acid with alkali therapy prevents the increases in ammonium production and minimizes the renal injury. Although the renal protective effect of alkali therapy is unproven in humans, there are other reasons(prevention of osteopenia and muscle wasting) why correction of the academia might be desirable. Sodium bicarbonate is preferred to sodium citrate in this setting, since citrate leads to marked increase in intestinal aluminum absorption, possibly promoting the development of aluminum toxicity; this is most likely to occur in those patients treated with aluminum-containing antacids to bind dietary phosphate. The effect of phosphate may be mediated both by keeping aluminum soluble( via the formation of aluminum citrate) and by binding of calcium in the intestinal lumen; the ensuing fall in free calcium then may lead to increased permeability of the tight junctions between the cells and the rise in passive aluminum absorption. Bicarbonate, on the other hand, does not produce these effects and therefore does not increase aluminum transport. Progressive anemia, due largely to erythropoietin deficiency, is a common complication of advanced renal disease. Experimental studies suggest that this may be a protective adaptation, since anemia leads to reduced vascular resistance which lowers both systemic and intraglomerular blood pressure. Prevention of anemia in animals is associated with reversal of these changes and enhancement of glomerular injury. These observations may have clinical relevance, since anemia can now be corrected in predialysis patients by the administration of recombinant erythropoietin. Preliminary observations on a relatively small number of patients suggest that, although the correction
of the anemia with erythropoietin does raise the systemic blood pressure in advanced renal failure, there does not seem to be any acceleration of the rate of progression. It has been suggested that proteinuria itself may contribute to disease progression, both by overloading the mesangium with macromolecules and by promoting tubulointerstitial disease. It is possible, for example, that a marked increase in protein filtration and subsequent proximal tubular reabsorption leads to tubular cell injury and the release of lysozymes into the interstitium. Thus reversing the intraglomerular hypertension with protein restriction or antihypertensive therapy may be beneficial both by diminishing hemodynamic injury to the glomeruli and by reducing protein filtration(which is in part dependent upon the intraglomerular pressure) . All forms of chronic renal failure are associated with marked tubulointerstitial injury (tubular dilatation and interstitial fibrosis), even if the primary process is a glomerulopathy. Furthermore, the degree of tubulointerstitial disease is a better predictor of the glomerular filtration rate and long term prognosis than is the severity of glomerular damage. Almost all are chronic progressive glomerular diseases, including IgA nephropathy, membranous nephropathy, membranoproliferative glomerulonephritis, and lupus nephritis. The mechanism by which the tubulointerstitial disease occurs is not well understood. Both calcium phosphate deposition and metabolic acidosis with secondary interstitial ammonia accumulatation may play a contributory role. There is also evidence that an active immunologic process is involved, beginning early in the course of the disease and in some cases being an extension of the inflammatory process in the glomeruli. In some experimental models of renal disease, corticosteroid therapy can ameliorate the tubuloiterstitial damage( without effect on the glomerular injury). However, even effective therapy of the interstitial inflammation may not prevent progressive injury. In this setting, healing may be associated with interstitial fibrosis mediated in part by the release of cytokines such as transforming growth factor-beta. Dialysis of non uremic animals with glomerulosclerosis preserves the glomerular filtration rate and slows the rate of further glomerular damage. This observation suggests that retention of ultrafiltrable toxins during the course of progressive renal disease contributes to secondary glomerular injury; but the mechanism is not clear. Increased glomerular permeability can result in the filtration of the normally non filtered iron-transferrin complex. Dissociation of this complex in the tubular lumen leads
to the release of free iron which can promote tubular injury by promoting the formation of hydroxyl radicals. The diseases which can damage the kidneys in a progressive and irreversible way, leading to chronic renal failure (CRF) include: Glomerulonephritis; Diabetic glomerulosclerosis; Chronic pyelonephritis; Obstructive uropathy; Hypertensive nephrosclerosis; Polycystic kidneys ;Drugs and Toxins. CRF is the major cause of death from renal disease. The healthy kidney has a large reserve of function, and only when around 75% of renal function has been lost that the symptoms of CRF make themselves manifest, while the biochemical evidence of renal insufficiency will occur earlier. Normal kidney tissue adapts to loss of nephrons to maintain a normal internal body environment by hypertrophy and increased blood flow to the remaining healthy glomeruli, accompanied by an increase in their individual GFR. Prostaglandins may play a role to compensate for the overall drop in the total GFR. Hypertrophy of the tubules is more prominent in PCT. Electrolyte loss from diarrhea will not be followed by the necessary increase in tubular electrolyte reabsorption and so electrolyte depletion will result. Compensatory tubular hypertrophy affects adversely the ability to vary urine concentration and to excrete an acid load. The increased volume of glomerular filtrate Combined with a decrease in tubular cell mass, results in a decrease in Na+ and Cl reabsorption in the thick ascending limb. this in turn results in a reduced hypertonicity in the medulla on which the urine concentrating mechanism depends. Also contributing are an osmotic diuresis due to high blood urea and decreased responsiveness of the collecting tubule to ADH. The decrease in acidification of the urine is mainly due to reduced ammonia production because of the reduced tubular mass. The compensatory process of hyperfiltration will have a deleterious sclerosing effect on the glomerulus. Atheroma occurs to a much greater degree in CRF due to a combination of hypperlipidaemia and hypertension in addition to calcification. Cardiomegaly, LVF and later heart failure are common and are due to hypertension, anaemia and coronary artery disease. Fibrinous pericarditis may occur in CRF which may be complicated by a pericardial effusion and when there is bleeding pericardial tamponade ensues. Renal osteodystrophy includes osteomalacia, osteitis fibrosa cystica and osteosclerosis. One of the two most important primary factors is a deficiency of 1,25(OH)2D3 which results from a lack of the enzyme 25-hydroxyvitamin D3 1-alpha-
hydroxylase within the kidney. The main consequences are reduced calcium absorption from the intestine and hypocalcaemia which may lead to osteomalacia (in adults) or rickets in childhood. The hpocalcaemia stimulates the parathyroid glands leading to secondary hyperparathyroidism which manifests itself as osteitis fibrosa cystica. Phosphate retension leads to hyperphosphataemia which contributes to the parathyroid stimulation and to the high Ca X P product in the blood causing metastatic calcification, mainly in the blood vessels and around joints. The main haematlogical consequence in CRF is anaemia which is due mainly to deficiency of the hormone erythropoietin which is synthesized by the kidney. Synthetic recombinant erythropoietin is now available. CRF is accompanied by a variable degree of immunodeficiency, both cell mediated and humoral which predisposes to infection although it does have the compensating advantage of reducing the strength of the rejection reaction following transplantation. Uraemic oesophagitis, gastritis and duodenitis are the commonest GIT pathological changes in CRF.
E ) TECHNIQUES USED IN DIAGNOSIS OF CRF The approach to the patient with CRF starts with the history, examination, and investigations. Particular attention is paid to the duration of symptoms, drug ingestion including NSAIDs and herbal remedies; also previous medical and surgical history e.g. multisystem disease like SLE or chemotherapy, in addition to previous occasions on which urinalysis or creatinine and urea measurements might have been performed. Family history of renal disease is very important. Urinalysis may show heamaturia and proteinuria suggesting glomerular disease, glycosuria with normal blood glucose is common in CRF. Sterile pyuria suggests papilary necrosis or renal tuberculosis. Granular casts are formed from abnormal cells within the tubular lumen, and indicate active renal disease especially acute tubular necrosis and rapidly progressive glomerulonephritis ;while red cell casts are highly suggestive of glomerulonephritis (more than 2/mm3 is abnormal). Early morning estimation of urine albumin: creatinine ratio
predicts death and renal failure from diabetes mellitus ; It is positive if the ratio is above 3 or 30-200 microgram albumin per 24 hour. Urine biochemistry include: 24-hour creatinine clearance which is useful in assessing the severity of the renal failure; low urine osmolality ( N.R 350-1000 mosml/kg)when there is hypovolaemia or hypotension indicates deranged kidney ability to concentrae urine. Urinary electrolyte measurements are of no help in CRF. Urine electrophoresis is necessary for the detection of light chains, which can be present without a detectable serum paraprotein. Urine culture should always be performed in addition to ASOT, anti DNAase B which suggest poststreptococcal glomerulonephritis, antibodies to hepatitis B (may point to membranous nephropathy or polyarteritis), antibodies to hepatitis C suggest cryoglobulinaemic renal disease, antibodies to HIV raise the possibility of HIVassociated renal disease. Malaria is a major cause of glomerular disease in the tropics. Serum biochemistry is performed to evaluate urea, creatinine and electrolytes. Electrphoresis should be done for myeloma. Extreme elevation of creatine kinase and a disproportionate elevation in serum creatinine and K+ compared to urea suggest rhabdomyolysis. Eosinophilia suggests vasculitis, allergic tubulointerstitial nephritis, or cholesterol embolism. Markedly raised viscosity or ESR suggests myeloma or vasculitis. Fragmented red cells and/or thrombocytopenia suggests intravascular haemolysis due to accelerated hypertension, haemolytic uremic syndrome or thrombotic thrombocytopenic purpura.Sickling test should be done when relevant. Complement components may be low in active renal disease due to SLE, mesangiocapillary glomerulonephritis, poststreptococcal glomerulonephritis, and cryoglobulinemia. Autoantibody screening is useful in detection of SLE, scleroderma, Wegener’s granulomatosis and microscopic polyangiitis, and Goodpasture’s syndrome. CryoGlobulins should be sought in those with unexplained glomerular disease particularly mesangiocapillary glomerulonephritis. Laboratory findings in chronic renal failure include low hemoglobin, low PCV, high creatinine levels, high blood urea values, hypocalcemia, hyponatremia, hypokalemia (due to polyuria), hyperuricemia, hyper or normal phosphate levels. While the BLOOD UREA level ( normal range is 2.5 – 6.7 mmol/l ) will reflect the degree of renal failure, it is also affected by dietary protein and rate of tissue breakdown, the serum CREATININE (normal range is 70- 150 micromol/l ) is a more accurate guide to renal function. Other nitrogenous products whose blood levels are elevated include uric acid. Serum sodium is often NORMAL but may be low due to decreased tubular capacity
to conserve Na+. The same applies to potassium although in very advanced cases the blood level may become high once the GFR falls to very low levels, or in association with oliguria or severe acidosis. The acidosis is of metabolic type and is characterized by a lowering of the pH, CO2 and bicarbonate. The serum phosphate rises due to the decrease in phosphate filtered and this is usually associated with a fall in serum calcium. The ability of the glomeruli to perform their function in health and disease may be estimated by measurement of the renal clearance. It is an arbitrary, but quantitatively valid measurement which relates the amount of a substance present in the urine, produced over a unit of time, to its concentration in the plasma. It is measured from the following equation: C = UXV/P i.e. renal clearance(C) equals, the concentration of the substance in the urine(U) multiplied by the volume of urine in ml secreted per minute(V) and divided by the concentration of the substance in the plasma(P). If a substance in the plasma passes freely through the glomerular filter, and is neither absorbed nor excreted by the tubules, the quantity excreted in the urine (UV), is identical with the quantity filtered by the glomeruli. The clearance of such a substance is therefore equal to the rate of glomerular filtration. Endogenous creatinine and the polysaccharide, inulin, appear to be excreted in this way and their clearances are used to estimate the rate of glomerular filtration, which for the average adult is about 120 ml/min. Since urea is partly reabsorbed by the tubules its clearance is less than that of creatinine or inulin. The clearance of creatinine is determined by collecting urine over a 24-hour period and withdrawing one sample of blood during the day. It is important to remember that neither plasma creatinine nor blood urea rise above the accepted normal maximum until renal function is reduced by at least 50% and the patient with chronic renal failure may remain asymptomatic till the glomerular filtration rate is 15 ml/min or less. The ranges of creatinine clearance are as follows: 90-130 ml/min is the normal range( it is lower in females); 15-50 ml/min in chronic renal failure( >15&<50); >50&<90 in renal impairment; up to 30 ml/min in chronic renal failure type 1; it is up to 15ml/min in chronic renal failure type 11 with diabetes mellitus, and up to 10ml/min in non-diabetics; in end-stage renal disease, creatinine clearance is 15ml/min & below in diabetics, and 10ml/min & below in nondiabetics. Note that those with creatinine clearance of 10ml/min and below are CANDIDATES FOR DIALYSIS. The majority of patients with CRF lose their renal function ( i.e. GFR) at a constant rate. Creatinine is produced at a fairly constant rate and rises on a hyperbolic curve as
renal function declines. The reciprocal creatinine plot is thus a straight line, parallel to the fall in GFR. This is widely used to monitor renal function and to predict when end-stage renal failure requiring dialysis will occur. Rapid decline in renal function greater than that expected may be due to infection, dehydration, uncontrolled hypertension, metabolic disturbance e.g. hypercalcaemia, obstruction and nephrotoxins (injudicious use of drugs). IMAGING OF THE KIDNEYS INCLUDE : Ultrasonography( US), intravenous Urography(IVU), computerized tomography(CT), and radionuclide studies are the four basic procedures undertaken in evaluation of renal disease. Every patient should undergo Ultrasonography ( for renal size and echogenicity which is typically small( i.e. shrunken) and hyperechoic, but is large if obstructed, DM, polycystic amyloid or myeloma ).U/S is also used to exclude hydronephrosis, solid and cystic structures and extension of tumors into renal vein or inferior vena cava or nodes or the liver; it also detects calculi but very small stones may be missed; cortical thickness and perinephric hematoma are also assessed by US. Cyst puncture, renal biopsy, and ante grade pyelography are all best performed under US guidance. US is quick, portable, harmless, safe, noninvasive, inexpensive tool which is not an ionizing radiation. Sonography does not require renal function in order to be effective, and it is used primarily for anatomy. Plain abdominal radiography is done to exclude low-density renal stones or nephrocalcinosis which may be missed in U/S. IVU is seldom diagnostic in advanced renal disease ( it relies on function ). A contrast medium is injected intravenously. IVU provides both functional and anatomic information and has the advantage of demonstrating the entire urinary tract and it is considered an ideal method of demonstrating calculi. Its major limitation is its reliance on renal function. CT utilizes radiation to create a series of thin body sections which supply three dimensional cross sectional views of the kidneys as well as the adjacent organs. The sections are taken before and after an intravenous contrast medium. Functioning kidneys will collect and excrete the contrast agent thus enabling an evaluation of renal function. CT provides exquisite anatomical detail and function is able to differentiate between types of masses based on differences in their radio density. CT disadvantages include limited
facilities, expensive, hazard of ionizing radiation to young children and the pregnant, contrast collection and excretion rely on renal function. It is useful for the diagnosis of retroperitoneal fibrosis and some other causes of urinary obstruction, and may also demonstrate cortical scarring. Nuclear medicine assesses function and perfusion of organs. It involves administration of intravenous radionuclide substance which is filtered through the kidneys at a specific rate and concentration. A series of films document the effectiveness of renal perfusion and function. The disadvantages include reliance on renal function and they demonstrate only gross anatomy. RENAL BIOPSY is considered in those with UNEXPLAINED renal failure and normal-sized kidneys, unless there are strong contraindications. Sonographically-guided fine-needle aspiration and core biopsy of a solid renal mass can be performed safely. In many cases, a definitive diagnosis can be made on the basis of fine-needle aspiration alone, but may ultimately require core biopsy, for which 18-gauge core needles would be more reliably diagnostic than 20-gauge needles. It is performed also to diagnose diffuse parenchymal renal disease and it is the most important instrument in the diagnosis of medical renal disease. The lower pole as it is the least vascular portion of the parenchyma and contains the least number of large blood vessels. The patient lies prone, and using local anesthesia a real time needle guide is performed. The depth is measured from the skin to the renal capsule within the guide path, and once the needle reaches the renal capsule, the guide and transducer are removed and the biopsy is performed free-hand. Routine coagulation studies are done prior to biopsy. Hemorrhage and gross hematuria are the most frequent complications of renal biopsy.
Original study Data collection and presentation
3.1 Study design: The study will follow the scientific methods to collect the related information from different sources namely references, textbooks, intrenet service, scientific magazines and patient's data collection sheets. 3.2 Study period: Data collection was started on first September 2005 and completed on the first of May 2006, about six hours daily six days per week. 3.3 Study area: The study had been done in two Sudanese states (Sinnar and Gezira states). The first area is my full-time private clinic in Sinnar city the capital of sinnar state. It is a very busy famous clinic with good reputation since 18.12.1979. It is attended by more than seventy patients day and evening with different medical problems. The second area is Sinnar teaching hospital and its specialized renal unit. Sinnar city lies on the west bank of sinnar dam about three hundred kilometers south east of Khartoum. The third area is Gezira teaching renal hospital in Wadmedani , the capital city which lies one hundred and ten kilometers north of Sinnar(I used to drive every Wednesday to Wadmedani to attend the very busy referred renal clinics and technique training) 3.4 Study populaton: All patients complaining of renal symptoms were included in the study. 3.5 Research team: The team consisted of me( the author), Dr. Suzan Omer Abdallah (sonologist) , Dr. Hadeel (my daughter) , Hasan Abdulgadir Mohammed ( my clinic lab technician) ,Khalid Elfadul Farag Elham,(lab technician), Abdalla Gaafar(medical engineer), Moawya Mohammed Ahmed(statistician), and Dr. Ibrahim Elmahi-consultant radiosonologist(the regional supervisor). 3.6 Research methodology: This is field work practical study in which one hundred patients with different renal problems were selected. Those found to suffer from chronic renal failure were determined, and the classical sonographic appearances were shown.
3.6.1 Questionnaire: A structured questionnaire was completed to one hundred patients complaining of different renal problems. It provided an account to their age , sex , residence, occupation (i.e. socioeconomic status), the symptoms and history of previous exposure to risk factors. Dr. Hadeel shared in the completion of the questionnaire with a good sum of cases. The physical examination and the ultrasound evaluation were performed by the author. All these patients were firstly scanned by me( the author) and secondly by a competent sinologist ( all by Dr. Suzan the sinologist) to confirm the diagnosis. 3.6.2 Lab. Data: Serum creatinine and blood urea levels were performed on those suspected to have chronic renal disease especially renal failure. 3.6.3 US evaluation: All patients included in the study were scanned by me( the author) , and all positive renal U/S finding( pathology) was rescanned by the sinologist to confirm the diagnosis, and the images were stored in a flash disc, and the relevant image samples were programmed in the appendix. 3.6.4 Equipment: The equipments used in the study included: Medison 1500 Shimadzu SDU 350 Aloka SSD-500 convex probe T-A3.5 and 5MHz Toshiba
Urinalysis was performed by both lab technicians for all the patients included in the study.
Other machines with varying facilities. Data analysis: The data was statistically performed using computerized programs namely SPSS
Analysis of Results
Part One: The descriptive statistics of socioeconomic and demographic
characteristics of patients
1. The groups of the patients
Table 1 illustrates that 18 % of the patients have chronic renal failure. The rest, 82% have other renal diseases.
The groups of the patient Chronic Renal Failure Other Renal diseases Total Frequency 18 82 100 Percent 18 82 100
90 80 70 60 50 40 30 20 10 0 Frequency 18
Percent Other Renal diseases
Chronic Renal Failure
2. The age of the patients
Table 2 illustrates that 10 % of the patients in the age group (16 -25), 30 % of the them in the age group (26 -40), 48 % of the patients in the age group (41 -65) and 12 % of the patients in the age group more than 65 years.
Age in year 16-25 years 26-40 years 41- 65 years > 65 years Total Frequency 10 30 48 12 100 Percent 10 30 48 12 100
50 45 40 35 30 25 20 15 10 5 0 10 30
Frequency 16-25 years 26-40 years 41- 65 years
Percent > 65 years
3. The sex of the patients
Table 3 illustrates that 67 % of the patients are males and 33 % of the them are females.
The sex of the patient Male Female Total
Frequency 67 33 100
Percent 67 33 100
70 60 50 40
33 30 20 10 0 Frequency Male Female Percent
4. The residence of the patients
Table 4 illustrates that 83% of the patients are from Sinnar, 7 % are from Gezira state and 10 % of the them are from Blue Nile state.
The residence Sinnar state Gezira state Blue Nile state Total
Frequency 83 7 10 100
Percent 83 7 10 100
90 80 70 60 50 40 30 20 10 0
7 Frequency Sinnar state
Blue Nile state
5. The Occupations of the patients
Table 5 illustrates that 25 % of the patients are housewives, 37 % of the patients are farmers, 12 % of the patients are labors, 1 % of the patients are non-skilled employees, 5% of the patients are skilled employees, 10 % of the patients are business men and 10 % of the patients have other different jobs.
The occupation Housewife Farmer Labors Non-skilled employee Frequency 25 37 12 1 Percent 25 37 12 1
Skilled employee Business man Others Total
5 10 10 100
5 10 10 100
40 37 37 35 30 25 20 15 12 12 10 5 0
Housew ife Farm er Labours
10 10 5 5 1 1
Skilled em ployee Business m an
Non-skilled em ployee
Part Two: The descriptive statistics of clinical symptoms of patients
Table 6 illustrates that 81% of the patients have burning micturition and 19 % of the patients have no burning micturition.
Burning micturition Yes No Total 7.
Frequency 81 19 100
Percent 81 19 100
Table 7 illustrates that 81% of the patients have dysuria and 19 % of the patients have no dysuria.
Symptoms: Dysuria Yes No Total 8. Frequency 81 19 100 Percent 81 19 100
Table 8 illustrates that 15% of the patients have haematuria and 85 % of the patients have no haematuria.
Haematuria Yes No Total Frequency 15 85 100 Percent 15 85 100
9. Reddish urine
Table 9 illustrates that 74% of the patients have reddish urine and 24 % of the patients have no reddish urine.
Reddish urine Yes No Frequency 76 24 Percent 76 24
80 70 60 50 40 30 20 10 0
Table 10 illustrates that 91 % of the patients have hot flushes and 9 % of the patients have no hot flushes.
Hot flushes Yes No Total Frequency 91 9 100 Percent 91 9 100
100 90 80 70 60 50 40 30 20 10 0
Frequency Yes No Percent
Table 11 illustrates that 47 % of the patients have polyuria and 53 % of the patients have no polyuria.
Polyuria Yes No Total Frequency 47 53 100 Percent 47 53 100
Table 12 illustrates that 49 % of the patients have urgency and 51 % of the patients have no urgency.
Urgency Yes No Total 12. Frequency 49 51 100 Percent 49 51 100
Table 13 illustrates that 72 % of the patients have epigastric pain and 28% of the patients have no epigastric pain.
Eepigastric Pain Yes No Total
Frequency 72 28 100
Percent 72 28 100
80 70 60 50 40 30 20 10 0
Table 14 illustrates that 92 % of the patients have Lions pains pain and 8 % of the patients have no Lions pains.
Lions pains Yes No Total 14. Frequency 92 8 100 Percent 92 8 100
Table 15 illustrates that 43 % of the patients have vomiting and 57 % of the patients have no vomiting.
Vomiting Yes No Total Frequency 43 57 100 Percent 43 57 100
60 50 40 30 20 10 0 43
Table 16 illustrates that 75 % of the patients have suprapubic pain and 25 % of the patients have no suprapubic pain .
Suprapubic pain Yes No Total 16.
Frequency 75 25 100
Percent 75 25 100
Table 17 illustrates that 22 % of the patients have cough pain and 78 % of the patients have no cough.
Cough Yes No Total
Frequency 22 78 100
Percent 22 78 100
80 60 40 20 0
Frequency Yes No
Table 18 illustrates that 7 % of the patients have hiccough and 93 % of the patients have no hiccough.
Hiccough Yes No Total
Frequency 7 93 100
Percent 7 93 100
100 90 80 70 60 50 40 30 20 10 0 7
Frequency Yes No
18. Face puffiness
Table 19 illustrates that 20 % of the patients have face puffiness and 80 % of the patients have no face puffiness.
Face puffiness Yes No Total
Frequency 20 80 100
Percent 20 80 100
80 70 60 50 40 30 20 20 10 0
Frequency Yes No
Lower limb edema
Table 20 illustrates that 24 % of the patients have Lower limb edema and 76 % of the patients have no Lower limb edema.
Lower limb edema Yes No Total Frequency 24 76 100 Percent 24 76 100
Table 21 illustrates that 82 % of the patients have Malaise and 18 % of the patients have no Malaise.
Malaise Yes No Total
Frequency 82 18 100
Percent 82 18 100
90 80 70 60 50 40 30 20 10 0
patients have no Table 22 illustrates that 38 % of the patients have Bone aches and 62 % of the Bone aches.
Bone aches Yes No Total 22. Frequency 38 62 100 Percent 38 62 100
Loss of concentration
Table 23 illustrates that 1 % of the patients have Loss of concentration
and 99 % of the patients have no Loss of concentration.
Loss of concentration Yes No Total Frequency 1 99 100 Percent 1 99 100
Table 24 illustrates that 60 % of the patients have anorexia and 40 % of the patients have no anorexia.
Anorexia Yes No Total Frequency 60 40 100 Percent 60 40 100
60 50 40 30 20 10 0
24. Diabetes mellitus
% Table 25 illustrates that 8 % of the patients have diabetes mellitus, 91 of the patients have no diabetes mellitus and 1 % do not know his symptoms.
Diabetes mellitus Not know Yes No Total
Frequency 1 8 91 100
Percent 1 8 91 100
Table 26 illustrates that 17 % of the patients have hypertension and 83 % of the patients have no hypertension.
Hypertension Yes No Total Frequency 17 83 100 Percent 17 83 100
26.Polycystic kidney disease
Table 27 illustrates that 1 % of the patients have polycystic kidney disease, 31 % of the patients have no polycystic kidney disease and 68 % do not know their symptoms.
Polycystic kidney disease Not know Yes No Total Frequency 68 1 31 100 Percent 68 1 31 100
Table 28 illustrates that 15 % of the patients have stones and 75 % of the patients have no stones, 10% do not know.
Stones Not know Yes No Total
Frequency 10 15 75 100
Percent 10 15 75 100
Table 29 illustrates that 2 % of the patients have BPH and 98 % of the patients have no BPH.
BPH Yes No Total
Frequency 2 98 100
Percent 2 98 100
Table 30 illustrates that 19 % of the patients have schistosomiasis, 71 % of the patients have no schistosomiasis and 10 % do not know their symptoms.
Schistosomiasis Not know Yes No Total Frequency 10 19 71 100 Percent 10 19 71 100
Table 31 illustrates that 36 % of the patients have jaundice, 63 % of the patients have no jaundice and 1 % do not know their symptoms.
Jaundice Frequency Percent
Not know Yes No Total
1 36 63 100
1 36 63 100
Table 32 illustrates that 92 % of the patients have NSAIDS medication and 8 % of the patients have no NSAIDS.
NSAIDS Yes No Total Frequency 92 8 100 Percent 92 8 100
Table 33 illustrates that 8 % of the patients have Aminoglycosides and 92 % of the patients have no Aminoglycosides.
Aminoglycosides Yes No Total Frequency 8 92 100 Percent 8 92 100
33. Hair dye
Table 34 illustrates that 1 % of the patients have hair dye and 99 % of the patients have no hair dye.
Hair dye Yes
Family history of renal disease
Table 35 illustrates that 15 % of the patients have family history of renal disease, 43 % of the patients have no family history of renal disease and 15 % do not their family history of renal disease.
Family history of renal disease Not know Yes No Total
Frequency 42 15 43 100
Percent 42 15 43 100
35.obstetrical history of PIH
Table 36 illustrates that one female, exactly 1 % of the patients have obstetrical history of PIH and 99 % of the patients have no obstetrical history of PIH.
Obstetrical history of PIH Yes No Total Frequency 1 99 100 Percent 1 99 100
Table 37 illustrates that 36 % of the patients have pallor and 64 % of the patients have no pallor.
Pallor Yes No Total Frequency 36 64 100 Percent 36 64 100
70 60 50 40 30 20 10 0 36
Frequency Yes No
Table 38 illustrates that 74 % of the patients have suprapubic tenderness and 26 % of the patients have no suprapubic tenderness.
Suprapubic tenderness Yes No Total 38.
Frequency 74 26 100
Percent 74 26 100
Table 39 illustrates that 19 % of the patients have dyspnoea and 81 % of the patients have no dyspnoea.
Yes No Total
19 81 100
19 81 100
90 80 70 60 50 40 30 20 10 0 19
Frequency Yes No
90 80 70 60 50 40 30 20 10 0 19
Frequency Yes No
Table 40 illustrates that 9 % of the patients have flow murmurs and 91 % of the patients have no flow murmurs.
Flow murmurs Yes No Total
Frequency 9 91 100
Percent 9 91 100
100 90 80 70 60 50 40 30 20 10 0 9
Table 41 illustrates that 5 % of the patients have pleural effusion and 95 % of the patients have no pleural effusion.
Pleural effusion Yes No Total
Frequency 5 95 100
Percent 5 95 100
100 90 80 70 60 50 40 30 20 10 0
Frequency Yes No
Table 42 illustrates that 6 % of the patients have pericardial rub and 94 % of the patients have no pericardial rub.
Pericardial rub Yes No Total 42. Frequency 6 94 100 Percent 6 94 100
The Tender epigastrium
Table 43 illustrates that 64 % of the patients have tender epigastrium and 36 % of the patients have no tender epigastrium.
Tender epigastrium Yes No Total Frequency 64 36 100 Percent 64 36 100
Table 44 illustrates that 83 % of the patients have tender lions and 17 % of the patients have no tender lions.
Tender lions Yes No Total
Frequency 83 17 100
Percent 83 17 100
Table 46 illustrates that 14 % of the patients have ascitis and 86 % of the patients have no ascitis.
Ascitis Yes No Total
Frequency 14 86 100
Percent 14 86 100
90 80 70 60 50 40 30 20 10 0 14
Frequency Yes No
Table 47illustrates that 9 % of the patients have hepatomegaly and 91 % of the patients have no hepatomegaly.
Hepatomegaly Yes No Total
Frequency 9 91 100
Percent 9 91 100
100 90 80 70 60 50 40 30 20 10 0 9
Frequency Yes No
46.Lower limb edema
Table 48 illustrates that 21 % of the patients have lower limb edema and 79 % of the patients have no lower limb edema.
Lower limb edema Yes No Total
Frequency 21 79 100
Percent 21 79 100
80 70 60 50 40 30 21 20 10 0
Frequency Yes No
Albumin in urine
Table 49 illustrates that 73 % of the patients have albuminuria and 27 % of the patients have no albuminuria.
Albumin Yes No Total Frequency 73 27 100 Percent 73 27 100
Pus cells in urine
Table 50 illustrates that 90 % of the patients have pus cells in urine and 10 % of the patients have no pus cells.
Pus cells Yes No Total
Frequency 90 10 100
Percent 90 10 100
Red blood cells in urine
Table 51 illustrates that 69 % of the patients have red blood cells in urine and 31 % of the patients have no red blood cells.
Red blood cells Yes No Total 50.
Frequency 69 31 100
Percent 69 31 100
Casts in urine
Table 52 illustrates that 12 % of the patients have casts in urine and 88 % of the patients have no casts.
Casts Yes No Total Frequency 12 88 100 Percent 12 88 100
Table 53 illustrates that 24 % of the patients have high serum creatinine and 76 % of the patients have normal serum creatinine.
Serum creatinine Normal
Table 54 illustrates that 72 % of the patients have normal blood urea and 28 % of the patients have high blood urea.
Blood urea Normal High Total Frequency 72 28 100 Percent 72 28 100
Table 54 illustrates that 82% of the patients have normal blood pressure, and 18% have high blood pressure
Blood pressure Normal High Total 54.
Frequency 82 18 100
Percent 82 18 100
The Right kidney: size
Table55 illustrates that 18 % of the patients their right kidney size is and 58 % of them their right kidney is normal, 26 % of them their right kidney is larger.
Right kidney: size Frequency 18 58 24 100 Percent 18 58 24 100
Normal ( 9-13 cm long ) Larger ( > 13 cm long ) Total 55.
Echogenicity of the kidneys
Table 56 illustrates that 18 % of the patients have hyperechoic kidneys, 82% have normal kidney echogenicity.
kidney echogenicity Hyperechogenic kidneys Normal Total
Frequency 18 82 100
Percent 18 82 100
Cortical thickness of the kidneys
Table 57 illustrates that 82 % of the patients their kidneys cortical thickness normal, 18 % of them their kidney cortical thickness is thin.
Right kidney: Cortical thickness Normal Thin Total
Frequency 82 18 100
Percent 82 18 100
57. Associated US findings Right kidney Stones
Table 58 illustrates that 26 % of the patients their right kidney associated US findings shows stones, 74 % of them their right kidney associated US findings shows no stones.
Right kidney : Associated US findings: Stones Yes No Total 58. Frequency 26 74 100 Percent 26 74 100
hydronephrosis in the right kidney
Table 59 illustrates that 20 % of the patients their right kidney associated US findings shows hydronephrosis, 80 % of them their right kidney associated US findings shows no hydronephrosis.
Right kidney : Associated US findings: Hydronophrosis Yes No Total
Frequency 20 80 100
Percent 20 80 100
80 60 40 20 0 20
Frequency Yes No
Cysts in the right kidney
Table 60 illustrates that 13 % of the patients their right kidney associated US findings shows cysts, 87 % of them their right kidney associated US findings shows no cysts.
Right kidney : Associated US findings: Cysts Yes No Total Frequency 13 87 100 Percent 13 87 100
The left Kidney Size
Table 61 illustrates that 18 % of the patients their left kidney size is shrunken, 59 % of them their left kidney is normal, 23 % of them their left kidney is larger.
Left kidney: size shrunken Normal ( 9-13 cm long ) Larger ( > 13 cm long ) Total Frequency 18 59 23 100 Percent 18 59 23 100
Stones in the left kidney
Table 62 illustrates that 26 % of the patients their left kidney associated US findings shows stones, 74 % of them their left kidney associated US findings shows no stones.
Left kidney : Associated US findings: Stones Yes No Total
Frequency 26 74 100
Percent 26 74 100
hydronephrosis in the left kidney
Table 63 illustrates that 19 % of the patients their left kidney associated US findings shows hydronephrosis, 81 % of them their left kidney associated US findings shows no hydronephrosis.
Left kidney :Associated US findings: Hydronephrosis Yes No Total Frequency 19 81 100 Percent 19 81 100
90 80 70 60 50 40 30 20 10 0 19
Frequency Yes No
Cysts in the left kidney
Table 64 illustrates that 8 % of the patients their left kidney associated US findings shows cysts, 92 % of them their left kidney associated US findings shows no cysts.
Left kidney : Associated US findings: Cysts Yes No Total Frequency 8 92 100 Percent 8 92 100
The Final Diagnosis
Table 77 illustrates that
Final Diagnosis Chronic Renal Failure Nephrotic syndrome Acute pyelonephritis Recurrent Renal stones L.R.S R.R.S Acute glomerulo nephritis R.Polycystic Kidney Acute pyelonephritis Multiple R.R.S Bilateral Renal cysts U.Bladder Mass plus Cysts A.R.F R.Cysts L.Ureteric Stone Bilateral Renal Stones Multiple L.R.S Rt.Ureteric Stone Focal segmental UTI L.R.Cysts Acute Renal Failure Reccurent L.Renal Stones Hydronephrosis (Bilateral) Total 100 Frequency 18 5 5 7 11 7 1 1 3 4 1 3 6 4 2 2 5 1 2 6 4 4 1 1 100 Percent 18 5 5 7 11 7 1 1 3 4 1 3 6 4 2 2 5 1 2 6 4 4 1 1
The Final Diagnosis
Table 78 illustrates that 7 % of the patients are on dialysis, 10 % of them need treatment and only one patient (1 %) did the transplantation.
Stage On Dialysis Needs treatment Transplanted Total
Frequency 7 10 1 18
Percent 7 10 1 18
The study demonstrated that U/S is a very practical and useful imaging modality in the workup of patients with suspected chronic renal failure. In this study one hundred symptomatic patients with different renal diseases were evaluated descriptively with ultrasound. I found that the range of age group accumulation for chronic renal failure was between 32 years and 50 years. i.e. the productive age group has got a very high significance. Occupation and residence in this study carried a very high significance with respect to the very high percentage of chronic renal failure among farmers and wives of farmers( 18 %). This probably relates to the wide areas of agriculture and the chemicals used by the protection department. Most patients present late due to poor socioeconomic status and illiteracy. Only one out of the 18 patients suffering from CRF has undergone a successful renal transplantation in Cairo on 22.12.2005 and now he is fairly well; 5 of them were already on dialysis( only one is a female); 3 of them need dialysis( all are males); and 9 of them need medical treatment and close observation(all are males). Due to the large and increasing number of chronic renal failure patients referred to Wadmedani daily for dialysis, the ministry of health decided and established Sinnar hospital renal unit three years ago. The four dialysis machines work at full capacity of four patients daily all through the year. Those with chronic renal failure who present early (serum creatinine less than 5 mg/dl, blood urea less than 100mg/dl,and mild to moderate symptoms) will continue on medical treatment for a variable length of time before they reach the end stage renal failure.. The other renal diseases in the study (82%) comprised a spectrum ranging from renal stones 39%, renal cysts14 %, acute pyelonephritis 6%, nephrotic syndrome 5%, acute renal failure 3%, UTI 2%, and two cases of acute glomerulonephritis. All patients with CRF complained of hot flushes, malaise, anorexia, nausea, puffiness, shortness of breath, cough, and showed variable derees of pallor, dyspnea, pleural effusion, flow murmurs, ascitis, lower limb edema, and hypertension. All patients of CRF showed variable degrees of albuminuria, pus & RBCs in their urine, and casts (4%); but showed significantly high levels of serum creatinine and blood urea. Their renal ultrasound findings include shrunken, hyperechoic kidneys, with loss of corticomedullary
differentiation, and thin cortex. Some of them showed other associated sonographic findings mainly renal cysts, stones, and hydronephrosis. Only 5 of them complained of hiccough. All patients included in the study have history of NSAIDs treatment without medical advice. No one of the patients in the study showed any scratch marks or history of SLE or heavy metal medication Hair dye poisoning contributed to causation of one case with acute renal failure. Post cesarean section bilateral ureteric ligation was the cause of acute renal failure in one case. One case presented with hematuria , dysuria, burning micturition, loin and suprapubic pain, with normal chemistry turned to be a bladder mass on sonography. One case of severe Diabetic septic foot developed acute renal failure post below knee amputation. It worth noting that nine cases were diagnosed by me just on ultrasound scanning directly after the history and physical examination; one case acute renal failure, two cases of ureteric stones; two cases of chronic renal failure; four cases of multiple large renal cysts. No one of the patients with CRF was diabetic; while hypertension was a contributing factor in 13 % of chronic renal failure patients(7%) were known hypertensive before being uremic.
The incidence of chronic renal failure patients in Sudanese population coming with different renal diseases is 18%. 9 cases needed medical treatment, 3 cases needed dialysis; 5 patients were already on dialysis; and one patient had undergone successful renal transplantation in Egypt on 22.12.2005. According to this study Ultrasound proved to be the most accurate, non-invasive, inexpensive, available, easily diagnostic imaging modality for evaluating patients with different renal diseases especially chronic renal failure.
All farmers must have an annual free medical examination with a special attention to the renal system. Fully equipped specialized teams should have several field visits. The availability of portable ultrasound machines made things more easy. The operators should update their knowledge about techniques and any information regarding Ultrasound. All sonologists and sonographers should take utmost care of their patients and machines. Governmental hospitals and private centers should provide excellent advanced machines.
Fig. (10) Fig. (4)
Fig. (28) Fig. (27)
Fig. (34) Obstructed non functioning left kidney
Fig. (46) CRF
QUESTIONNAIRE DATA COLLECTION SHEET RENAL ULTRASOUND IN CHRONIC RENAL FAILURE
IF ANSWERE IS YES WRITE 1 ; NO WRITE 2 ; DONOT KNOW = 0 1/ NAME and address--------------------------------------------------------------------------2/ Code number 3/ Age in years 1 for age group 0-15 ; 2 for 16-25 ; 3 for 26-40 ; 4 for 41-65 ; 5 for >65-------------4/ Sex - if male write 1 ; if female write 2 ----------5/ Residence 1 for Sinnar state ; 2 for Gezira state ; 3 for Blue nile state ; 4 for others ----------------------
6/ Occupation 1 for housewife ; 2 for farmer ; 3 for labourer ; 4 for non-skilled employee; 5 for skilled employee ; 6 for buisiness ; 7 for others ----------------7/ Symptoms - 1 for yes ; 2 for no a/ burning micturition --------- b/ dysuria -------- c/ haematuria -------d/ reddish urine --------- e/ hot flushes --------- f/ polyuria --------- g/ urgency -----h/ epigastric pain ---------- i/ loins pains ----------- j/ vomiting ------------k/ suprapubic pain-------------- l/ cough --------------- m/ hiccough ------------ n/ face puffiness --------------- o/ lower limb oedema ------------ p/ malaise ---------q/ bone aches ------------ r/ loss of cocentration ------------ s/ anorexia --------------8/ In the history ,detailed inquiry about : 1 for yes ; 2 for no ; 0 for don’t know A) Past medical history ? diabetes mellitus -----------; hypertension ---------------polycystic kidney disease ------------; stones ----------------- ; BPH ---------------------schistosomiasis ---------------; jaundice-------------- ; SLE --------------B) Drug history : NSAIDs -----------; aminoglycosides -----------; hair dye-----------Heavy metals --------------; others ----------C) family history of renal disease -----------------; obstetrical history of PIH -------9/ Physical findings O/E : A) 1 for yes, 2 for no Pallor ----------; suprapubic tenderness --------; dyspnoeic ----------; flow murmurs --------pleural effusion ---------; pericardial rub----------; tender epigastrium ----Tender loins -------------; palpable loin mass ----------; ascitis --------; hepto-megaly -------lower limb oedema ----------; scratch marks --------B) The blood pressure recording ------------10/ Laboratory results : A) The presence in urine of : 1 for yes; 2 for no a/ albumin ------- b/ pus cells ------ c/ red blood cells -------- d/ casts ------------------
B) 1 for normal; 2 for high; 3 for low a/serum creatinine (N.R is 62-124 micromol / l=0.7-1.4 mg / 100 ml) ---------; b/ blood urea (N.R is 2.66.6 mmol / l= 15-40 mg / 100 ml)-----------11/ US FINDINGS: A ) Right kidney a/ position (1 for normal 2 for abnormal (ectopic) ; 0 for absent -----------------b/ size( 1 for normal=9-13 cm long); 2 for larger( > 13 cm long); 0 for shrunken(< 9 cm long) -----------------------c/ echogenicity (1 for normal; 2 for hyperechoic;0 for hypoechoic) -------------------d/ cortical thickness (1 for normal ; 2 for thin) --------------e/CMD(1 for normal;2 for poor;0 for lost) -----------f/ associted US findings: yes(1); no(2) : stones ------ ; hydronephrosis ---------; cysts --------------focal lesions --------; others ---------B) Left kidney a/ position( 1 for normal; 2 for abnormal (ectopic) ; 0 for absent ---------b/ size (1 for normal=9-13 cm long); 2 for larger(> 13 cm long); 0 for shrunken(< 9 cm long) -----------c/ echogenicity(1 for normal; 2 for hyperechoic ; 0 for hypoechoic) --------d/ cortical thickness(1 for normal ; 2 for thin) ---------e /CMD(1 for normal;2 for poor; 0 for lost) -----------f/ associated US findings : yes (1 no (2) : stones -------; hydro-nephrosis ----------; cysts --------; focal lesions ---------; others ---------12/ Final Diagnosis Candidat’s signature Dr.Kamal Sayed Ismail M, B; B, S ( U OF K) Co-supervisor’s signature Dr.Elijah Maluk M, B; B, S( U OF G) M D Medicine U OF G Consultant physician Sinnar hospital Renal unit
Gray's anatomy for students. Richard. Drake-Wayne Vogl-Adam W.M. Mitchell. 36th Edition 1980. Pages 1387-1400 Clinical anatomy by Ritchard S. Snell 5th edition 1995. Pages 224-231 A.D.A.M. Benjamin /Cummings CDs of interactive anatomy and physiology. By Marvin J . Branstrom, PhD.Published 1997. Pages 1-22. Concise Human Physiology. 2nd edition 2000. By: M.Y. Sukkar, prof. of physiology,PhD (Edinburge); H.A.Elmunshid, PhD(Newcastle), MD(Lund), prof. of physiology; M.S.M.Ardawi, FRCPath(UK), prof. of clinical Biochemistry and Immunology. Pages 233-251
Burwin abdominal ultrasound part two, module two. By Chris Harrington, RTNM, RDMS, RDCS. Pages 1-86. Kumar& Clark clinical medicine 5th edition. 2002. By Parveen kumar & micheal Clark. Pages 642-658 Oxford hand book of clinical medicine 6th edtion. 2004 By R.A. Hope & Hodgetts. Pages 256-289. Muir's text book of pathology. By Roddie M.N.MacSWEEN Keith Whaley.Thirteenth edition. 1992. Pages 893-945. Manual of diagnostic ultrasound . By P.E.S. Palmer. WHO publication 1995. Pages 152-186 Guidelines and protocols of medical diagnostic ultrasound. Ist edition By Dr.Syed Amir Gilani , M,B; B,S (Pb) M.Sc(Canada) PhD(Swiss). Pages 101-118. Abdominal & Retroperitoneal ultrasound By : Dr. Syed Amir Gilani. Published 2003. Pages 81-86. www.umhc.sunysb.edu/internalmed/nephro/webpages/partghtm. www.aaimsonline.com
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.