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Renal Pathophysiology Normal Anatomy and Physiology
1. Introduction: The primary function of the kidney is to maintain a stable internal environment for optimal cell and tissue metabolism. The kidneys accomplish these life-sustaining tasks by balancing solute and water transport, excreting metabolic waste products, conserving nutrients, and regulating acids and bases. The kidney also has an endocrine function, secreting the hormones rennin, erythropoietin, and 1,25-dihydroxyvitamin D3 for regulation of blood pressure, erythrocyte production, and calcium metabolism, respectively. In times of severe fasting, the kidney also can synthesize glucose from amino acids, performing the process of gluconeogenesis. The formation of urine is achieved through the processes of filtration, reabsorption, and secretion by the glomeruli and tubules within the kidney. The bladder stores the urine that it receives from the kidney by way of the ureters. Urine is then removed from the body through the urethra. 2. General Gross Anatomy Review: a. Kidneys: are paired organs located on the posterior abdominal wall outside the peritoneal cavity. They lie on either side of the vertebral column with their upper and lower poles extending from the twelfth thoracic to the third lumbar vertebrae. Each kidney is approximately 11 cm long, 5 to 6 cm wide, and 3 to 4 cm thick. A tightly adhering capsule (the renal capsule) surrounds each kidney, and the kidney then is embedded in a mass of fat. The capsule and fatty layer are covered with a double layer of renal fascia, fibrous tissue that attaches the kidney to the posterior abdominal wall. The cushion of fat and the position of the kidney between the abdominal organs and muscles of the back protect it from trauma. The right kidney is slightly lower than the left; it is displaced downward by the overlying liver. A medial indentation (the hilum) contains the entry and exit for the renal blood
The major calyces join to form the renal pelvis. an extension of the upper end of the ureter. ii. called Bowman capsule. The wall of the glomerular capillary serves as a filtration membrane (the glomerular filtration membrane) and has three layers: (1) an inner capillary endothelium. The gross structure of the kidney can be identified when it is divided from top to bottom in a coronal plane. The proximal tubular lumen consists of one layer of cuboidal cells with a surface layer of microvilli that increases reabsorptive surface area. The glomerulus is supplied by the afferent arteriole and drained by the efferent arteriole. with an outer zone close to the cortex and an inner zone. Tubules: The proximal tubule continues from Bowman space and has an initial convoluted segment and then a straight segment that descends toward the medulla. The major components are the outer renal cortex and the inner renal medulla. The cortex contains all the glomeruli and portions of the tubules. The apexes of the pyramids project into a minor calyx (a cup-shaped cavity). called renal pyramids. which joins together to form a major calyx. and ureter. The medulla consists of a series of wedges. lymphatic vessels. a hairpin loop composed of thick and thin portions of a descending segment that goes into the medulla. i. like fingers pushed into bread dough. Nephron: The nephron is the functional unit of the kidney. The proximal tubule joins the loop of Henle.000. Approximately 1. with the exception of blood cells and plasma proteins with a molecular weight greater than 70. (2) a middle basement membrane. Each layer has unique structural properties that allow all components of the blood to filter through. nerves. Renal columns extend from the cortex down between the renal pyramids. the site at which blood is filtered. b. that loop into a circular capsule. The tube then loops Renal Pathophysiology (2) . The nephron is a tubular structure that consists of a tuft of capillaries termed the glomerulus.2 million nephrons are contained in each kidney.ProSono copyright 2008 vessels. the glomerular capillaries. The different structures of the epithelial cells lining various segments of the tubule facilitate the special functions of secretion and reabsorption. and (3) an outer layer of capillary epithelium (also called podocytes or visceral epithelium). Glomerulus: The glomerulus is a tuft of capillaries. and a renal tubule from which water and salts in the filtrate are reclaimed.
with downward propulsion of urine. The interlobar arteries are further subdivisions that travel down the renal columns and between the pyramids. interlobar arteries branch into the arcuate arteries. Ureters: The urine formed by the nephrons flows from the distal tubules and collecting ducts through the renal papillae (projections of the ducts). The thin segment is composed of thin squamous cell’ with no active transport function. and the resulting peristaltic activity propels urine into the bladder. At the renal hilum. Inferiorly. When urine flow is slow. it lies in the true pelvis. Peristaltic activity is affected by urine volume. providing easy access for percutaneous aspiration. Bladder and Urethra: The bladder is a bag composed of a basket weave of smooth muscle fibers that forms the detrusor muscle and its smooth lining of transitional epithelium. the bladder sits on the prostate in men and on the anterior vagina in women. the bladder rises above the symphysis pubis. Blood Vessels: The blood vessels of the kidney closely parallel nephron structure. d. urine is funneled into the ureters. they divide into anterior and posterior branches and then subdivide into lobar arteries that supply blood to the lower. Increasing flow rates increase peristalsis. As the bladder fills with urine. and into the calyces and is collected in the renal pelvis. The close approximation of muscle cells permits the direct transmission of electrical stimulation. Contraction of the bladder during micturition (urination) compresses the lower end of the ureter. The lower ends of the ureters pass obliquely through the posterior aspect of the bladder wall. In infants and young children. it distends and the layers of transitional epithelium slide past each other and become thinner as the volume of the bladder increases. which arch over the base of the pyramids and run parallel to the surface of the kidney. surgery. The cells of the thick segment are cuboidal and actively transport several solutes. The position of the bladder varies with age and gender. The distal tubule has straight and convoluted segments and extends to the collecting duct that then empties into a minor calyx. The interlobular arteries arise from the arcuate arteries and extend through the cortex toward the periphery and form the afferent glomerular arterioles. At the cortical medullary junction. e. preventing reflux. In adults. c. in front of the rectum and in front of the uterus in women. The urethra extends from the inferior side of the bladder to the outside of Renal Pathophysiology (3) . middle. the contraction is segmented. Peristalsis is maintained even when the ureter is denervated. From the renal pelvis. and upper thirds of the kidney. Each adult ureter is approximately 30 cm long and is composed of long. accounting for the bleeding that readily occurs with trauma. The bladder has a profuse blood supply.ProSono copyright 2008 and becomes the thickening-ascending segment that extends toward the cortex. intertwining muscle bundles. The renal arteries arise as the fifth branches of the abdominal aorta. so ureters can be transplanted. The trigone is a smooth triangular area lying between the openings of the two ureters and the urethra. or inflammation.
From the renal plasma flow. and ammonium. The external urethral sphincter is composed of striated muscles and is under voluntary control. ii. 20% (approximately 120 to 140 ml/min) is filtered at the glomerulus and passes into Bowman capsule. promoting an increase in blood volume and thus an increase in systemic pressure. With a normal hematocrit of 45%. Two muscles called sphincters control excretion of urine from the bladder through the urethra. Blood flow to the kidneys is regulated by: i. iii.ProSono copyright 2008 the body. When systemic pressure decreases. Renal Pathophysiology (4) . Normal urine is 95% water but also contains urea. Hormonal regulation: Hormonal factors can alter the resistance of the renal vasculature by stimulating vasodilation or vasoconstriction. A ring of smooth muscle forms the internal urethral sphincter at the junction of the urethra and bladder. A major hormonal regulator of RBF is the renin-angiotensin system. Autoregulation: a local mechanism within the kidney that tends to keep the rate of blood flow and GFR fairly constant over a range of arterial pressures between 80 and 180 mmHg. The secretion of hydrogen ions is important in maintaining blood pH. Tubular reabsorption: a process where much of the glomerular filtrate passes out of the nephron tubule and returns to the blood. and other organic and inorganic substances in minute amounts. Production of Urine: Urine is the fluid secreted from the blood by the kidneys. 2. chloride. Urine is produced by: i. medications. The filtration of the plasma per unit of time is known as the glomerular filtration rate (GFR). The entire urethra is lined with mucus-secreting glands. 1. which can increase systemic arterial pressure and change RBF. Other molecules secreted include: food preservatives. iii. and the GFR is directly related to the perfusion pressure in the glomerular capillaries. ii. or about 20% to 25% of the cardiac output. Tubular secretion: substances not removed from the blood during glomerular filtration are transported from the peritubular capillaries directly into the nephron tubule. Renal Blood Flow (RBF): The kidneys are highly vascular organs and usually receive 1000 to 1200 ml of blood per minute. and creatinine. 2. RBF decreases. about 600 to 700 ml of blood flowing through the kidney per minute is plasma. As much as 99% of material in the filtrate is returned to the blood. creatinine. sodium. b. Neural regulation: the sympathetic nervous system innervates the kidney and regulates RBF related to systemic arterial pressure. hydrogen. This reduced blood flow reduces GFR and diminishes the excretion of sodium and water. Physiology a. Glomerular filtration: filtration of the blood through the epithelial walls of the glomerulus produces glomerular filtrate. pesticides. Ions removed from the blood by tubular secretion include: potassium.
a person produces more acidic urine after awakening. cocaine. Laboratory tests for serum creatinine provide an indicator or glomerular filtration rate (GFR). Marijuana. Because sleep is accompanied by intermittent hypoventilation. and the foam is yellow or orange when the urine contains bile pigments. so hydration status should be evaluated before making a diagnosis. The application of this principle is useful for monitoring progressive changes in renal function. Urine is more alkaline after eating and then declines before the next meal. heroin. protein. turbidity. which controls water reabsorption in the collecting ducts. light yellow color because of urochrome and other pigments. When formed substances (crystals. the cause is usually a malfunction of the renal tubules or inappropriate ADH secretion by the posterior pituitary gland. This determination is helpful for differentiating Renal Pathophysiology (5) . Because urea is filtered at the glomerulus. specific gravity.0 and 6. urinary tract obstruction. and other drugs are also removed by tubular secretion. Specific gravity: Specific gravity is an estimated measure of the solute concentration of the urine. When GFR is impaired. given a stimulus. Serum creatinine: normal values: 0. Urinalysis includes evaluation of color. Protein in the urine creates marked foaming when shaken. but it may vary from 4. Urinalysis: Urinalysis is a noninvasive and relatively inexpensive diagnostic procedure.5. or casts) are in the urine. the BUN rises in states of dehydration and acute and chronic renal failure when passage of fluid through the tubules is slowed. Urine normally has a clear. c. Specific gravity of any solution is measured by comparing the weight of the solution with an equal volume of distilled water.7-1. pH.5 to 8. The final urine osmolality is primarily a function of anti-diuretic hormone (ADH). BUN also varies because of altered protein intake and protein catabolism and therefore is a poor measure of GFR. cleanly voided specimen. which makes it possible to perform urine drug testing. because decay permits changes in the composition of urine. d. Serum creatinine is elevated in acute or chronic renal insufficiency. Because urea is reabsorbed by the blood through the permeable tubules. blood urea nitrogen (BUN) levels increase as glomerular filtration drops. and impairment of renal function induced by some drugs. The state of hydration also affects the urine specific gravity. less creatinine is excreted by the glomerulus causing serum levels to rise. and supernatant. If the kidney is unable to concentrate or dilute urine.0. Urine pH normally ranges between 5.2 mg/dL Creatinine is a substance that is produced by muscle and released into the blood at a relatively constant rate. The best results are obtained from a fresh. Tests of Renal Function a. sediment. b. 3. blood cells. Blood Urea Nitrogen (BUN): normal values: 10-20 mg/dL The concentration of urea nitrogen in the blood reflects glomerular filtration and urine-concentrating capacity. it appears turbid.ProSono copyright 2008 3.
Crystals tend to form in concentrated acidic or alkaline urine. Immunologic alterations are most frequently responsible for glomerular injury. Glomerulonephritis: Glomerulonephritis is an inflammation of the glomerulus that can be caused by a variety of factors. Glomerular disease is the most common cause of chronic and end-stage renal failure. and casts. including immunologic abnormalities. they are not clinically significant. h. crystals. The type of cast identified suggests the disease process occurring in the kidney. Urine then will be positive for hemoglobin. g. They may be composed of cystine. or phosphate. uric acid.ProSono copyright 2008 e. In some cases. vascular disorders. Glomerulonephritis and nephrotic syndrome also may demonstrate pyuria. because these casts are not formed in the bladder or prostate. Epithelial cell casts indicate degeneration of the tubular lumen or necrosis of the renal tubules. If a large number of red cells are present. white cell casts are associated with an inflammatory process. oliguria caused by intrinsic renal disease from hypovolemia as a result of dehydration. so that the cells will not be seen. red cells. The finding of WBC casts reflects a kidney infection. Red cell casts indicate bleeding into the tubules. but as the urine cools. particularly when bacteria are present. They are cylindrical with distinct borders. from which they take their shape. crystals will form. Urine sediment: The urine sediment is examined microscopically and may contain cells. effects of drugs or toxins. and systemic diseases. Crystals: Numerous kinds of crystals can be observed in the urine. or a metabolic disorder. usually indicating inflammation. All casts have a precipitated microprotein matrix and arise primarily from the ascending limb of the distal tubule. however. An alkaline or hypotonic urine causes lysis of red cells. f. calcium oxalate. Glomerular Disorders 1. Hematuria can occur with the administration of anticoagulants and with several renal diseases. Crystal formation is diagnostically significant. Casts: Casts (accumulations of cellular precipitates) originate in the renal tubules. Epithelial cells may be seen in the microscopic field because they are shed naturally throughout the urinary tract. but usually in combination with proteinuria. If WBCs are present in the urine. a culture should be done for specific identification of bacteria and sensitivity of bacteria to antibiotics. the exact cause of glomerular injury may be unknown. and the specific gravity will be elevated. and bacteria. White blood cells: White blood cells (WBCs) in the urine (a condition termed pyuria) are primarily indicative of urinary tract infection. Red blood cells: Normal urine contains few or no red blood cells. this is known as hematuria and the sediment may be red. infection. Renal Pathophysiology (6) . i. Generally. They may not be initially observable. casts.
Symptoms usually occur 10 to 21 days after infection and include hematuria. Hypercholesterolemia also has been associated with progressive glomerular injury. altering membrane permeability and leading to proteinuria. The proposed mechanism is related to glomerulosclerosis.ProSono copyright 2008 a. edema. Proliferation of mesangial cells (cells in connective tissue supporting the glomerular capillaries) may be focal or diffuse with segmental fibrosis and glomerular deterioration. proteinuria. Secondary tubular dilation and atrophy may develop. b. c. Activated complement attacks epithelial cells. There may be no history of renal disease before the diagnosis. which alters IgG with binding of anti-IgG to the glomerulus. ascites or pleural effusions develop. although several years of proteinuria and hematuria may have preceded the diagnosis. which may be associated with streptococcal or staphylococcal organisms. Renal Pathophysiology (7) . Insulin-dependent diabetes mellitus and lupus erythematosus are secondary causes of chronic glomerular injury. but there is no specific treatment for the glomerulonephritis. More severe renal disease is observed after a prolonged infection before antibiotic therapy. Occasionally. Sporadic occurrences have been observed after bacterial endocarditis. Deposition of circulating soluble antigen-antibody complexes ii. Streptococcal release of neuramidase. oliguria. or after viral diseases such as varicella and hepatitis B. red blood cell casts. The disease has an abrupt onset and usually occurs 7 to 10 days after a streptococcal infection of the throat (5% to 10% incidence) or skin (25% incidence). decreased GFR. recover without significant loss of renal function or recurrence of disease. The thickening of the glomerular membrane contributes to the decreased GFR. Immunofluorescent findings from renal biopsy indicate the presence of immune complex deposits in the glomerulus and neutrophil and macrophage recruitment and activation. Formation of antibodies specific against the glomerular basement membrane iii. Various pathologic changes are evident in the glomerulus. Serum complement levels are usually low because they are consumed by the initial infection. Most individuals. with diffuse mesangial cell and capillary endothelial cell proliferation of the entire glomeruli. Acute glomerulonephritis: Acute glomerulonephritis is frequently associated with a group A (nephritogenic strain) post-streptococcal infection (acute post-streptococcal glomerulonephritis (APSGN). The primary cause may be difficult to establish because advanced pathologic changes may obscure specific disease characteristics. Pathophysiology: Three types of immune mechanisms contribute to glomerular injury: i. especially children. commonly in children. Chronic glomerulonephritis: Chronic glomerulonephritis encompasses several glomerular diseases with a progressive course leading to chronic renal failure. and hypertension. The edema of acute glomerulonephritis tends to be around the eyes but may involve dependent areas such as the feet and ankles.
location (focal or diffuse). iii. especially nitrogen retention. red blood cell casts. d. which has a brownish color and no blood clots. and swelling reduce renal blood flow and depress glomerular filtration. Clinical manifestations: i. The neutrophils and monocytes further the inflammatory reaction by releasing lysosomal enzymes. Glomerular damage generally occurs from activation of biochemical mediators of inflammation (complement. Concurrent systemic vasculitis or hypersensitivity reaction. mild hypertension. contributing to crescent formation (deposition of substances in Bowman space). History of preceding streptococcal or. which begins after the antibody or antigen-antibody complexes have localized in the glomerular capillary wall. The characteristics of hematuria from red blood cells escaping through the glomerular membrane include a smoky brown-tinged urine. mesangial proliferation. duration of exposure. v. Changes in membrane permeability and electrical charge permit the passage of protein molecules or red blood cells into the urine. Complement is deposited with the antibodies. fibrin). and type of antigen-antibody complexes. granular and hyaline casts. iv. Malaise. ii. which damage glomerular cell walls. The immune-mediated inflammatory response with cellular infiltration decreases GFR. number. Urine changes: Several disorders may produce hematuria because bleeding can occur anywhere along the urinary tract. Bleeding from sites lower in the urinary tract may produce a pinkor red-colored urine. Glomerular bleeding provides prolonged contact with the acidic urine and transforms hemoglobin to methemoglobin. These processes alter membrane permeability and may cause loss of the negative electrical charge across the glomerular filtration membrane. Membrane proliferation. rarely. whereby platelets release vasoactive amines such as serotonin or histamine. protein. Evidence of impaired renal function. The history and physical examination may disclose Renal Pathophysiology (8) . Gross hematuria. and an accompanying proteinuria. Complement activation can serve as a chemotactic stimulus for attraction of neutrophils and monocytes. Membrane damage can lead to platelet aggregation and degranulation. leukocytes. vi. contributing to fluid volume expansion and hypertension. Mild generalized edema. retinal hemorrhages. white cells. which leads to fluid retention. followed by a sequence of metabolic events that initiate an attack on the glomerular membrane. red cell casts. low-grade fever. The coagulation system also may be activated and lead to fibrin deposition in Bowman space. Salt and water are reabsorbed. anorexia. other infection. headache. deposits in the membrane.ProSono copyright 2008 The severity of glomerular damage and renal insufficiency is related to the size. causing proteinuria or hematuria or both. 1. These substances then increase glomerular permeability. and renal epithelial cells in urine.
and vascular disorders. or physiochemical. The large amount of urine protein is characteristic of glomerular injury. which may be metabolic. membranous glomerulonephritis. and lipiduria. amyloidosis. and serum creatinine concentration is elevated. c. Disturbances in the glomerular basement membrane. white blood cells. Hypoalbuminemia < 3g/dL iv. red blood cells. and Henoch-Schönlein purpura. Free fat.5g or more of protein in the urine per day. and hyperlipidemia. hypertension. biochemical. Microscopic evaluation from renal biopsy provides a specific determination of renal injury and type of pathology. Massive edema ii. Albumin is lost in the greatest quantity because of its high plasma concentration and low molecular weight. hyperlipidemia. 2.5g/day iii. Systemic diseases often implicated in secondary nephrotic syndrome include diabetes mellitus. oval bodies. lead to increased permeability to protein. Secondary forms of nephrotic syndrome occur as a result of other organic pathologic processes.ProSono copyright 2008 findings that differentiate glomerular disease from another source of urinary tract bleeding. occurs across the injured glomerular filtration membrane. Proteinuria > 3. hyperkalemia. Hypoalbuminemia results from urinary loss of albumin combined with a diminished synthesis of replacement albumin by the liver. When present as a secondary complication with renal diseases. Hyperlipidemia with cholesterol >300mg/dL v. Nephrotic Syndrome: Nephrotic syndrome is the excretion of 3. Clinical Manifestations: i. Nephrotic syndrome also is seen in association with certain drugs. systemic lupus erythematosus. particularly albumin and some immunoglobulins. Creatinine clearance evaluates the extent of glomerular damage. Serum complement is decreased. and focal glomerulosclerosis are directly related to nephrotic syndrome. b. Management principles for treating glomerulonephritis are related to treating the primary disease. although these conditions can occur with other types of glomerular disease. fatty casts in urine Renal Pathophysiology (9) . edema. and correcting accompanying problems such as edema. Specific treatment regimens are necessary for particular types of glomerulonephritis. nephrotic syndrome often signifies a more serious prognosis. infections. Evaluation and Treatment: The diagnosis of glomerular disease is confirmed by the progressive development of clinical manifestations and laboratory findings of abnormal urinalysis with proteinuria. Other findings include hypoalbuminemia. malignancies. Pathophysiology: Loss of plasma proteins. a. e. preventing or minimizing immune responses. Lipoid nephrosis (minimal change disease). and casts .
The GFR declines because of the decrease in filtration pressure. and neurologic changes. or inadequate cardiac output. deficiency states. or severe glomerular disease.ProSono copyright 2008 Renal Failure Classification: The terms renal insufficiency. or post-renal. Renal insufficiency or renal failure causes azotemia. Intra-renal acute renal failure: Intra-renal acute renal failure may result from pre-renal acute renal failure (e. intra-renal. Poor perfusion can result from renal vasoconstriction. this is termed end-stage renal failure (ESRF).. Azotemia means increased serum urea levels and frequently increased creatinine levels as well. azotemia. Levels of serum creatinine and urea are mildly elevated. a common characteristic that explains the overlap in definitions of terms. Acute renal failure is usually associated with oliguria (urine output of less than 30 ml/hr or less than 400 ml/day). and uremia are all associated with decreasing renal function. anorexia. Acute renal failure can be caused by different clinical conditions. including retention of toxic wastes. hypovolemia. Acute Renal Failure: Acute renal failure (ARF) is an abrupt reduction in renal function with elevation of BUN and plasma creatinine levels. severe hypotension including vascular obstruction. although urine output may be normal or increased. disseminated intravascular coagulation. Azotemia and uremia are sometimes incorrectly used interchangeably. Renal failure may be acute and rapidly progressive. although with some distinctions. Uremia is a syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue. although the process may be reversible. acute tubular necrosis or cortical necrosis) or many other diseases. Most types of acute renal failure are reversible if diagnosed and treated early. Acute pre-renal failure may occur when chronic renal failure exists if a sudden stress is imposed on already marginally functioning kidneys. hemorrhage. Pre-renal acute renal failure: Pre-renal acute renal failure is caused by impaired renal blood flow. When less than 10% of renal function remains. they are used synonymously. and electrolyte disorders. hypotension. renal failure. progressing to ESRF over a period of months or years . vomiting. Failure to restore blood volume or blood pressure may cause acute tubular necrosis or acute cortical necrosis b. Generally. Renal failure often refers to significant loss of renal function. a. A combination of ischemic or hepatotoxic factors may produce acute renal failure. 1.g. Both azotemia and uremia indicate an accumulation of nitrogenous waste products in the blood. nausea. pruritus. Uremia represents the numerous consequences related to renal failure. Often. including acute glomerulonephritis. Renal failure also can be chronic. and renal vasculitis. Acute tubular Renal Pathophysiology (10) . malignant hypertension. commonly it is classified as pre-renal. renal insufficiency refers to a decline in renal function to about 25% of normal or a GFR of 25 to 30 ml/min.
sulfonamides. vii. advanced age. renal disease. surgical shock.010 -1. prostatic hypertrophy. Infectious diseases. hemorrhagic fever. Radiocontrast media (x-ray media) also may be nephrotoxic. Traumatic shock due to severe injury. Renal Pathophysiology (11) . and diabetes mellitus tend to enhance nephrotoxicity from either aminoglycosides or radiocontrast media. but ATN is also associated with sepsis. phenytoin. urine volume 20-200 mL/day. Immunologic mechanisms induced by methicillin. Clinical Manifestations i. gramnegative bacteremia with shock. or multiple myeloma. Other substances such as excessive myoglobin (oxygentransporting substance in muscles).. Sudden onset of oliguria. They include: i. peritonitis. iv. arsenic. Dehydration. heavy metals (mercury. Post-renal acute renal failure: Post-renal acute renal failure usually occurs with urinary tract obstruction that affects the kidneys bilaterally (e. toxic shock syndrome. amphotericin B. diabetic nephropathy. a procedure that may cause edema of the tubular lumen. penicillin. and other drugs. burns. Nephrotoxic ATN can be produced by numerous antibiotics. carbon tetrachloride. or severe burns.g.016. Causes: There are many possible causes of ARF. e. ii. arsenic).. c. e. but the aminoglycosides (neomycin. Complications of pregnancy. Disseminated intravascular coagulation. incompatible blood transfusion). vi. concurrent renal insufficiency.. or bilateral ureteral obstruction). Necrosis caused by nephrotoxins is usually uniform and limited to the proximal tubules. liver failure. v. gentamicin. and mushroom poisoning. bilateral cortical necrosis.. or methoxyflurane anesthesia may promote renal failure. ii. Tissue destruction due to crushing injury. Ischemic necrosis tends to be patchy and may be distributed along any part of the nephron. iii.g. Proteinuria and hematuria. d. and ischemia associated with surgery on the abdominal aorta (vasomotor nephropathy).g. aminoglycoside antibiotics. (Oliguria may not occur). carbon tetrachloride. or myocardial infarction.ProSono copyright 2008 necrosis (ATN) is the most common cause of acute renal failure. rhabdomyolysis. Xray contrast materials are hazardous in patients with dehydration. tobramycin) are the major culprits. diethylene glycol. mercury bichloride. e. bladder outlet obstruction. ATN caused by ischemia occurs most frequently after surgery (40% to 50% of cases). specific gravity of 1. A pattern of several hours of anuria with flank pain followed by polyuria is a characteristic finding. obstetric complications. This type of renal failure can occur after diagnostic catheterization of the ureters. e. intravascular hemolysis (transurethral resection of the prostate.g. Toxic agents. leptospirosis. methoxyflurane.
regardless of the cause. Cysts may be found in the liver and pancreas. blood pressure. Pathology: Polycystic kidney disease is familial (autosomal dominant) and often involves not only the kidney but the liver and pancreas as well. v. Etiology: May be due to systemic infections from bacteria. New cysts do not form. Enlargement of the kidneys are commonly demonstrable. affects these vital processes with changes manifest throughout all organ systems. nausea and vomiting. phosphate. Polycystic Kidneys i. urea. lethargy. b. 2. and symptomatic changes resulting from increased creatinine. potassium. including antibiotics. iv. exhibit remarkable adaptive abilities. Renal Parenchymal Disease 1. v. iv. creatinine. elevation of blood pressure. acute renal failure may occur. but those present enlarge and. and others. diuretics. and secretion of hormones that regulate red blood cell production. calcium. and calcium metabolism. by pressure. however. The kidneys. cause destruction of adjacent tissue.ProSono copyright 2008 iii. nonsteroidal anti-inflammatory agents. and eosinophilia. Signs of uremia. Spontaneous recovery in a few days to 6 weeks. The formation of cysts in the cortex of the kidney is thought to result from failure of union of the collecting tubules and convoluted tubules of some nephrons. Pathology: Diffuse inflammation of the interstitial tissue (non-glomerular) tissue of the kidney. potassium. Progressive and irreversible loss of renal function (chronic renal failure). Cystic Disease of the Kidney a. Signs and Symptoms: i. Interstitial Nephritis a. The Renal Pathophysiology (12) . arthralgia. and alterations in salt and water balance usually do not become apparent until the renal function declines to less than 25% of normal. Progressive increase in serum urea nitrogen. acid-base balance. Anorexia. Hematuria ii. sulfate. Some patients will show other signs of hypersensitivity such as rash. decrease in sodium. excretion of waste products. Chronic Renal Failure: The kidney has many important regulatory functions. including body fluid volume. viruses. c. Occasionally. solute concentration and dilution. Proteinuna iii. and spirochetes and sensitivity to drugs. Recovery may be complete 2. bicarbonate. fever.
or there may be evidence of infection of an organ. although there is often an inability to produce concentrated urine. Infection in any part of the urinary tract may spread to any other part of the tract. Signs and Symptoms: Cases of polycystic disease are discovered during the investigation of hypertension. Infections of the Urinary Tract a. flank pain due to hemorrhage into a cyst will call attention to a kidney disorder. b. The term relapse implies recurrence of infection with the same organism. Many small cysts are scattered through the renal medulla. by diagnostic study in patients presenting with pyelonephritis or hematuria. ii.ProSono copyright 2008 incidence of cerebral vessel (“berry”) aneurysms is higher than normal. 3. At any given time. The latter occurs during bacteremia (e. irregular kidneys are easily palpable b. Far commoner is ascending infection. but azotemia. Renal transplantation is indicated by the usual criteria for the operation. At times. Symptomatic urinary tract infection may be acute or chronic. acidosis. the term re-infection implies infection with another organism. any one of these organs may be asymptomatic or symptomatic. i. Introduction: The term urinary tract infection denotes a wide variety of clinical entities in which the common denominator is the presence of a significantly large number of microorganisms in any portion of the urinary tract. where bacteria are introduced into the urethra (from fecal flora on the perineum or the vaginal vestibule.g. The urine is not remarkable. urethritis.. and only symptomatic therapy for ureteral impaction of a stone or for infection is required. prostatitis. Otherwise. Many small calculi often occupy the cysts. Pathogenesis: Urine secreted by normal kidneys is sterile until it reaches the distal urethra. and hyperphosphatemia soon become evident. the symptoms and signs are those commonly seen in hypertension or renal insufficiency. Enlargement of the papillae and calices and small cavities within the pyramids are demonstrated by the contrast media in the excretory urogram. Anemia is usually the initial manifestation. cystitis. On physical examination. Medullary Cystic Disease: Medullary cystic disease is a familial disease (either autosomal dominant or recessive) that may become symptomatic during adolescence. e. pyelonephritis. Hypertension may develop. Medullary Sponge Kidney: Sponge kidney is asymptomatic and is discovered by the characteristic appearance of the urogram. Bacteria can reach the urinary tract by the ascending route or by hematogenous spread. the enlarged. Life expectancy is not affected. and infection may be troublesome. with staphylococci) and results in abscess formation in the cortex or the perirenal fat.g.. Microorganisms may be evident only in the urine (bactericidal). or by investigating the families of patients with polycystic disease. or by instrumentation) and travel up the urinary tract to reach Renal Pathophysiology (13) .
often with turbid. in diabetics) may lead to slough of papillae and ureteral obstruction. Cystitis. and. Pyuria e. malaise. ii. Laboratory Findings: 1. In most patients with these pathologic findings. or renal pelvis. scarring. In these patients. chronic suppression of infection may stabilize renal function. and acid pH are important antibacterial defenses. Bacteriuria 2. chills and fever. rarely. Lower Urinary Tract (Urethritis. and nephrectomy may be curative. Pyelonephritis): Manifestations include burning pain on urination. progressive renal failure. Acute Urinary Tract Infection i. Free flow. use of analgesics). and suprapubic or lower abdominal discomfort. Chronic pyelonephritis may lead to widespread fibrosis and scarring of functional cortical and medullary tissue. costovertebral angle pain and tenderness. Upper Urinary Tract: (Pyelonephritis) Manifestations include: headache. in the absence of anatomic abnormalities. Some women have chronic bacteremia. chronic bacterial pyelonephritis may progress to inflammation of interstitial tissue. Chronic Urinary Tract Infection (Cystitis. c. i. “chronic pyelonephritis” is in fact not caused by infection but instead represents interstitial nephritis of immunologic or toxic cause. Papillary necrosis (e. or dark urine. however. Pathology: Acute urinary tract infection shows inflammation of any part of the tract and sometimes intense hyperemia or even bleeding of the mucous membranes. which may progress to frank suppuration and patchy necrosis. With bilateral nephritis. vomiting. ureter. ureteral stricture). resulting in renal insufficiency: it appears unlikely that repeated urinary tract infection causes renal insufficiency unless there is concomitant obstruction.g. chronic infection is due to a unilateral structural abnormality (e. Pyelonephritis): Chronic or recurrent episodes of urinary tract infection usually produce no permanent harm unless obstruction is present.. large urine volume. which is asymptomatic. The most important factor in aiding or perpetuating ascending infection is anatomic or functional obstruction to free urine flow. Signs and Symptoms Renal Pathophysiology (14) .. foul-smelling. and abdominal pain. Occasionally. hypersensitivity. The absence of upper tract signs does not exclude bacterial invasion of the upper tract.ProSono copyright 2008 the bladder. The prominent lesion in the kidney is acute inflammation of the interstitial tissue.. d. iii. frequency. complete emptying of the bladder. atrophy. There are usually no positive physical findings unless the upper tract is involved also. the prognosis for preservation of renal function appears to be good.g. Chronic interstitial nephritis may result from bacterial infection or from other causes (e.g. vasculitis. Recurrent urinary tract infection may cause only minimal changes or progressively more severe scarring in any part of the tract.
In chronic prostatitis. Signs and Symptoms: These include perineal pain.ProSono copyright 2008 1. signs. Prostatitis is thus commonly associated with urethritis. Elevated serum BUN and creatinine 2. frequency. but persistent asymptomatic bacteriuria. may occur in sponge kidney. Urinary Stones a. Even gentle palpation of the prostate results in expression of copious purulent discharge. Palpation reveals a symmetrically enlarged. mild dysuria and frequency. and destruction of bone by metastatic carcinoma. boggy. and slightly tender prostate. 3. Signs and Symptoms: The symptoms. Prostatitis: Bacteria may reach the prostate from the bloodstream or from the urethra. or may be idiopathic. Obstruction or other anatomic abnormality in the urinary tract is consistently found in men. Absence of symptoms or signs referable to the urinary tract. or with active bacterial infection of the lower urinary tract. Anemia 3. occasionally in women. fluctuation occurs only if an abscess has formed. In acute prostatitis. or papillary necrosis. i. ii. the de Toni-Fanconi syndrome. Bacteriuria may or may not be present f. Impairment of renal function rare unless obstruction is present. boggy. 4. 4. tuberculosis of the kidney. Pathology: Chronic hypercalciuria and hyperphosphaturia may result in precipitation of calcium salts in the renal parenchyma (nephrocalcinosis). dysuria. fever. 2. True renal stones may be present as well in these patients. the prostate feels enlarged. Laboratory Findings: 1. and scanty urethral discharge. Recurrent episodes of lower or upper tract involvement. and urethral discharge. may be secondary to infection in the urinary tract. renal tubular acidosis. and very tender. Renal Pathophysiology (15) . ii. Other causes include acute osteoporosis following immobilization. Nephrocalcinosis: Urinary stones and calcification in the kidney may be associated with metabolic disease. The incidence of urinary tract calculus is higher in men i. sarcoidosis. and excess calcium and alkali intake. The diagnosis is usually established by x-ray demonstration of calcium deposits in the kidney. which appear as minute calcific densities with linear streaks in the region of the renal papillae. and laboratory findings are those of the primary disease. hypervitaminosis D (particularly with associated high calcium intake). there may be dull lumbo-sacral and perineal pain. Chronic interstitial nephritis predisposes to nephrocalcinosis. The commonest causes are hyperparathyroidism.
bladder stones are associated with urinary stasis due to bladder neck or urethral obstruction. blood clots. may serve as a nucleus for stone formation 4. Horseshoe kidney. a. 4. Gastrointestinal symptoms common. i. Proteus. staphylococci). Congenital or acquired deformities of the kidneys. 2. 5. Signs and Symptoms: 1. Obstruction of ureter produces severe colic with radiation of pain to regions determined by the position of the stone in the ureter. particularly in the presence of stasis or infection. 3.ProSono copyright 2008 b. d. 3. Oxalate c. a. Ureteral Stone: Ureteral stones are formed in the kidney but produce symptoms as they pass down the ureter. Foreign bodies in the bladder act as foci for stone formation. Uric acid 2. Urine usually contains fresh red cells. diverticula. Uricosuria—Crystals of uric acid or sodium hydrogen urate may initiate precipitation of calcium oxalate from solution. Nausea. and clumps of bacteria. Changes in urine pH 3. 4. with flank pain and colic. Exacerbations of infection when obstruction occurs. b. Chills and fever and bladder irritability if infection is present. ii. Local caliceal obstruction or defect. vomiting. Thus. Etiologies: 1. The pathologic changes may be modified by ischemia due to pressure or by infection. and cystocele. Ulceration and bladder inflammation predispose to stone Renal Pathophysiology (16) . May be asymptomatic. c. Excessive excretion of relatively insoluble urinary constituents. Physical changes in urine a. c. abdominal distention. Sponge kidney. Often asymptomatic. Renal Stone: The location and size of the stone and the presence or absence of obstruction determine the changes that occur in the kidney and caliceal system. Hematuria. b. neurogenic bladder. Signs and Symptoms: 1.g.organisms (e. Calcium b. Bits of necrotic tissue. 5. Symptoms of obstruction of calix or ureteropelvic junction. 2. Increased concentration of urine solute as a consequence of low intake of fluid and low urine volume b. i. Nucleus (nidus) for stone formation a. Bladder Stone: Vesical stones occur most commonly when there is residual urine infected with urea-splitting.
3. Obstructive Uropathy: Obstruction of the urinary tract can result in serious damage to the kidneys. Renal papillae become flattened. with dysuria. urgency. Renal blood flow is reduced. 4. Interruption of urinary stream as stone occludes urethra. and frequency. Extrinsic tumors. Neuromuscular disorder related to the spinal cord or peripheral nerve lesions c. 5. Hematuria and pyuria. which then become dilated. Destruction of the kidney results within a few weeks. involuntary voiding. Acute and complete obstruction of a ureter will produce pain in the flank or groin associated with distention of the renal capsule or ureteral colic. or urethral stricture) ii. If a neurologic lesion is the cause of bladder dysfunction. and the complication of urinary tract infection determine the presenting manifestations a. the duration of obstruction. Renal Pathophysiology (17) . tumor. Acute obstruction of the urethra by an enlarged prostate. ureteropelvic. Signs and Symptoms: 1. Signs and Symptoms: The site of obstruction and rapidity of onset determine the presentation. Stone. and glomerular filtration is impeded. and frequency with incomplete emptying of the bladder. Partial obstruction produces lesser impairment of renal function. The site and degree of obstruction. postoperative bladder dysfunction. Pathology: Complete obstruction to the flow of urine produces increase in pressure in the ureters and in the renal pelvis. Functional impairment of tubule function affects the excretion of solute. Most vesical stones are composed of calcium phosphate. or fibrosis iv. or stone will produce painful distention of the bladder. the renal tubules dilate. or clot that obstructs a ureter or the bladder neck iii. there may be overflow dribbling from a distended bladder. or magnesium ammonium phosphate. and the secretion of hydrogen ion. Bladder irritability. Etiology: Obstructive uropathy is the result of: i. Chronic urethral obstruction may result in a distended bladder with “overflow” dribbling. the reabsorption of sodium.ProSono copyright 2008 formation. b. Benign prostatic hypertrophy is occasionally present in men. Uric acid stones are common in the presence of an enlarged prostate and uninfected urine. early detection and treatment are required to prevent irreversible function and anatomic damage. Congenital anatomic abnormalities (eg. bands. calcium oxalate. Chronic or low-grade obstruction is usually asymptomatic. 2. ureterovesical. i.
the cells resemble renal tubule cells arranged in cords and varying patterns. Enlarged kidney may be palpable Renal Pathophysiology (18) . Testicular Torsion: Testicular torsion (torsion of the spermatic cord) is most common in adolescent males and young men under age 25. Chronic orchitis may be due to syphilis. Testicular torsion must be differentiated from epididymitis. made worse by elevation of the scrotum. ii. Orchitis: Acute orchitis is usually due to mumps and occurs during the years just following adolescence. It is most often unilateral but may be bilateral. Destruction of the testis usually leaves some hormonal cell function. It rarely occurs before age 35 and more commonly after age 50. and schistosomiasis haematobia. Epididymitis i. Elevation of the scrotum provides some relief. spermatic cord. Pathology: Acute epididymitis is caused by bacterial infection ascending from the urethra or prostate. filariasis. Hypernephroma) i. Orchiopexy of the other testis is desirable because of the high incidence of the bilateral anatomic abnormality associated with torsion 7. rapid unilateral scrotal enlargement. Pathology: The commonest malignant tumor of the kidney is adenocarcinoma. An anomaly of the tunica vaginalis or of the relationship of the epididymis to the testis is usually present. tender. 3.ProSono copyright 2008 6. 2. which occurs more frequently in men. Mumps may produce acute oophoritis as well. orchitis. leprosy. In older men. and retracted. and groin are the characteristic manifestations. tuberculosis. b. Signs and Symptoms 1. and long bones. Adenocarcinoma of the Kidney (Renal cell carcinoma. Signs and Symptoms: Sudden pain in the scrotum. and marked tenderness of the testes. It invades blood vessels early. Fever. On microscopic examination. it usually follows urinary tract obstruction and infection or instrumentation of the lower genitourinary tract ii. painful testicle may occur . Secondary orchitis with a swollen. groin. and trauma to the testis. This tumor metastasizes early to the lungs. The testis is swollen. or lower abdomen. Testicular Disease a. liver. The characteristic presentation is with a sudden onset of unabating pain in the scrotum. Gross hematuria with or without flank pain. Adenocarcinoma of the kidney apparently arises from renal tubule cells or adenomas. Tumors of the Genitourinary Tract a. Treatment consists of immediate surgery to remove the infarcted testis. c.
Tumors of the Bladder i. reduced force and caliber of the urinary stream. Elevated serum acid phosphatase in 85% of patients with extension of the cancer beyond the prostatic capsule. Benign Prostatic Hyperplasia (BPH) i. 5. epidermoid tumors. 2. 4. liver. which is often of low-grade malignancy. Metastases involve regional lymph nodes. The common tumor is transitional cell carcinoma. Malignant cells by urine cytology. the serum acid phosphatase is increased. Metastases to bone produce pain. gross or microscopic. Hard consistency of the prostate. and sarcomas are rare. c. Pathology: Hyperplasia of the prostatic lateral and subcervical lobes that are invaded by periurethral glands results in enlargement of the prostate and urethral obstruction. Uremia follows prolonged obstruction d. The prostatic tissue is rich in acid phosphatase. Enlarged prostate. At least 75% of bladder tumors occur in men over age 50.ProSono copyright 2008 b. The growth of the tumor is increased by androgens and inhibited by estrogens. 3. 4. ii. 3. particularly in the low back. bone. 2. Tumors usually arise at the base of the bladder and involve ureteral orifices and the bladder neck. Visualization of tumor at cystoscopy. 3. and when cancer has extended beyond the prostate to the periprostatic tissue or to bone. The serum acid phosphatase concentration thus provides a good index of extension and growth of the tumor ii. Signs and Symptoms 1. Pathology: Cancer of the prostate is rare before age 60. It metastasizes early to the bones of the pelvis and locally may produce urethral obstruction with subsequent renal damage. Carcinoma of the Prostate i. adenocarcinomas. Prostatism: hesitancy and straining to initiate micturition. Hematuria. Signs and Symptoms 1. 2. 4. Elevated PSA (prostate specific antigen) Renal Pathophysiology (19) . Signs and Symptoms 1. Suprapubic pain and bladder symptoms associated with infection. and lungs ii. Prostatism. nocturia. Acute urinary retention. Pathology: Bladder tumors are the second most common urinary tract tumors.
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