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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

Renal Pathophysiology


like fingers pushed into bread dough. which joins together to form a major calyx. The glomerulus is supplied by the afferent arteriole and drained by the efferent arteriole. ii. The nephron is a tubular structure that consists of a tuft of capillaries termed the glomerulus. The medulla consists of a series of wedges. the glomerular capillaries. and (3) an outer layer of capillary epithelium (also called podocytes or visceral epithelium). called renal pyramids. Glomerulus: The glomerulus is a tuft of capillaries. a hairpin loop composed of thick and thin portions of a descending segment that goes into the medulla. The gross structure of the kidney can be identified when it is divided from top to bottom in a coronal plane. (2) a middle basement membrane. with an outer zone close to the cortex and an inner zone. The wall of the glomerular capillary serves as a filtration membrane (the glomerular filtration membrane) and has three layers: (1) an inner capillary endothelium. Renal columns extend from the cortex down between the renal pyramids. that loop into a circular capsule. Tubules: The proximal tubule continues from Bowman space and has an initial convoluted segment and then a straight segment that descends toward the medulla. Each layer has unique structural properties that allow all components of the blood to filter through. The proximal tubular lumen consists of one layer of cuboidal cells with a surface layer of microvilli that increases reabsorptive surface area. nerves. i. The major calyces join to form the renal pelvis.ProSono copyright 2008 vessels. The tube then loops Renal Pathophysiology (2) .2 million nephrons are contained in each kidney. and a renal tubule from which water and salts in the filtrate are reclaimed.000. an extension of the upper end of the ureter. The proximal tubule joins the loop of Henle. The cortex contains all the glomeruli and portions of the tubules. Nephron: The nephron is the functional unit of the kidney. the site at which blood is filtered. lymphatic vessels. and ureter. with the exception of blood cells and plasma proteins with a molecular weight greater than 70. called Bowman capsule. The apexes of the pyramids project into a minor calyx (a cup-shaped cavity). The different structures of the epithelial cells lining various segments of the tubule facilitate the special functions of secretion and reabsorption. Approximately 1. The major components are the outer renal cortex and the inner renal medulla. b.

interlobar arteries branch into the arcuate arteries. At the renal hilum. providing easy access for percutaneous aspiration. The distal tubule has straight and convoluted segments and extends to the collecting duct that then empties into a minor calyx. so ureters can be transplanted. Contraction of the bladder during micturition (urination) compresses the lower end of the ureter. the bladder sits on the prostate in men and on the anterior vagina in women. 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. In adults. which arch over the base of the pyramids and run parallel to the surface of the kidney. The thin segment is composed of thin squamous cell’ with no active transport function. accounting for the bleeding that readily occurs with trauma. Inferiorly. Peristalsis is maintained even when the ureter is denervated. The urethra extends from the inferior side of the bladder to the outside of Renal Pathophysiology (3) . it distends and the layers of transitional epithelium slide past each other and become thinner as the volume of the bladder increases. The renal arteries arise as the fifth branches of the abdominal aorta. From the renal pelvis. In infants and young children. Blood Vessels: The blood vessels of the kidney closely parallel nephron structure. and the resulting peristaltic activity propels urine into the bladder. Increasing flow rates increase peristalsis. urine is funneled into the ureters. surgery. The interlobar arteries are further subdivisions that travel down the renal columns and between the pyramids. with downward propulsion of urine. The close approximation of muscle cells permits the direct transmission of electrical stimulation. or inflammation. they divide into anterior and posterior branches and then subdivide into lobar arteries that supply blood to the lower. Each adult ureter is approximately 30 cm long and is composed of long. and upper thirds of the kidney. Peristaltic activity is affected by urine volume. the contraction is segmented. The bladder has a profuse blood supply. the bladder rises above the symphysis pubis. c. At the cortical medullary junction. in front of the rectum and in front of the uterus in women. middle. The cells of the thick segment are cuboidal and actively transport several solutes. The position of the bladder varies with age and gender. intertwining muscle bundles. and into the calyces and is collected in the renal pelvis. d. The interlobular arteries arise from the arcuate arteries and extend through the cortex toward the periphery and form the afferent glomerular arterioles. it lies in the true pelvis. e. When urine flow is slow. The trigone is a smooth triangular area lying between the openings of the two ureters and the urethra.ProSono copyright 2008 and becomes the thickening-ascending segment that extends toward the cortex. As the bladder fills with urine. Ureters: The urine formed by the nephrons flows from the distal tubules and collecting ducts through the renal papillae (projections of the ducts). The lower ends of the ureters pass obliquely through the posterior aspect of the bladder wall. preventing reflux.

2. and ammonium. Neural regulation: the sympathetic nervous system innervates the kidney and regulates RBF related to systemic arterial pressure. promoting an increase in blood volume and thus an increase in systemic pressure. sodium. The secretion of hydrogen ions is important in maintaining blood pH. hydrogen. 2. Renal Pathophysiology (4) . Two muscles called sphincters control excretion of urine from the bladder through the urethra. Urine is produced by: i. Renal Blood Flow (RBF): The kidneys are highly vascular organs and usually receive 1000 to 1200 ml of blood per minute. and other organic and inorganic substances in minute amounts. The entire urethra is lined with mucus-secreting glands. The external urethral sphincter is composed of striated muscles and is under voluntary control. Glomerular filtration: filtration of the blood through the epithelial walls of the glomerulus produces glomerular filtrate. When systemic pressure decreases. RBF decreases. medications. iii. pesticides. Hormonal regulation: Hormonal factors can alter the resistance of the renal vasculature by stimulating vasodilation or vasoconstriction. The filtration of the plasma per unit of time is known as the glomerular filtration rate (GFR). 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. which can increase systemic arterial pressure and change RBF. 1. ii. Physiology a.ProSono copyright 2008 the body. b. creatinine. As much as 99% of material in the filtrate is returned to the blood. A ring of smooth muscle forms the internal urethral sphincter at the junction of the urethra and bladder. ii. With a normal hematocrit of 45%. Other molecules secreted include: food preservatives. Normal urine is 95% water but also contains urea. A major hormonal regulator of RBF is the renin-angiotensin system. This reduced blood flow reduces GFR and diminishes the excretion of sodium and water. or about 20% to 25% of the cardiac output. 20% (approximately 120 to 140 ml/min) is filtered at the glomerulus and passes into Bowman capsule. From the renal plasma flow. about 600 to 700 ml of blood flowing through the kidney per minute is plasma. Production of Urine: Urine is the fluid secreted from the blood by the kidneys. Tubular reabsorption: a process where much of the glomerular filtrate passes out of the nephron tubule and returns to the blood. Tubular secretion: substances not removed from the blood during glomerular filtration are transported from the peritubular capillaries directly into the nephron tubule. and the GFR is directly related to the perfusion pressure in the glomerular capillaries. chloride. and creatinine. Blood flow to the kidneys is regulated by: i. Ions removed from the blood by tubular secretion include: potassium. iii.

This determination is helpful for differentiating Renal Pathophysiology (5) .0 and 6.7-1. b. cleanly voided specimen.5 to 8. Urine is more alkaline after eating and then declines before the next meal. If the kidney is unable to concentrate or dilute urine. Because urea is reabsorbed by the blood through the permeable tubules. a person produces more acidic urine after awakening. blood urea nitrogen (BUN) levels increase as glomerular filtration drops. turbidity. Specific gravity of any solution is measured by comparing the weight of the solution with an equal volume of distilled water. and impairment of renal function induced by some drugs. because decay permits changes in the composition of urine. Specific gravity: Specific gravity is an estimated measure of the solute concentration of the urine. urinary tract obstruction. cocaine. Laboratory tests for serum creatinine provide an indicator or glomerular filtration rate (GFR). c.0. The state of hydration also affects the urine specific gravity. BUN also varies because of altered protein intake and protein catabolism and therefore is a poor measure of GFR. Protein in the urine creates marked foaming when shaken. the cause is usually a malfunction of the renal tubules or inappropriate ADH secretion by the posterior pituitary gland. and supernatant. and other drugs are also removed by tubular secretion. 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. Because urea is filtered at the glomerulus. Urinalysis includes evaluation of color. the BUN rises in states of dehydration and acute and chronic renal failure when passage of fluid through the tubules is slowed. and the foam is yellow or orange when the urine contains bile pigments. Urinalysis: Urinalysis is a noninvasive and relatively inexpensive diagnostic procedure. When GFR is impaired. 3.2 mg/dL Creatinine is a substance that is produced by muscle and released into the blood at a relatively constant rate. specific gravity. light yellow color because of urochrome and other pigments. d. Marijuana. it appears turbid. Serum creatinine: normal values: 0. but it may vary from 4. When formed substances (crystals. sediment.5. The best results are obtained from a fresh. which controls water reabsorption in the collecting ducts. The application of this principle is useful for monitoring progressive changes in renal function. Serum creatinine is elevated in acute or chronic renal insufficiency. heroin. Urine normally has a clear. Because sleep is accompanied by intermittent hypoventilation. Urine pH normally ranges between 5. protein. Tests of Renal Function a. blood cells. given a stimulus. pH.ProSono copyright 2008 3. less creatinine is excreted by the glomerulus causing serum levels to rise. or casts) are in the urine. which makes it possible to perform urine drug testing. so hydration status should be evaluated before making a diagnosis. The final urine osmolality is primarily a function of anti-diuretic hormone (ADH).

Immunologic alterations are most frequently responsible for glomerular injury. Glomerular Disorders 1. uric acid. but as the urine cools. Renal Pathophysiology (6) . Glomerular disease is the most common cause of chronic and end-stage renal failure. Glomerulonephritis and nephrotic syndrome also may demonstrate pyuria. the exact cause of glomerular injury may be unknown. Hematuria can occur with the administration of anticoagulants and with several renal diseases. Glomerulonephritis: Glomerulonephritis is an inflammation of the glomerulus that can be caused by a variety of factors. casts. white cell casts are associated with an inflammatory process. Casts: Casts (accumulations of cellular precipitates) originate in the renal tubules. so that the cells will not be seen. and the specific gravity will be elevated. this is known as hematuria and the sediment may be red. however. All casts have a precipitated microprotein matrix and arise primarily from the ascending limb of the distal tubule. They are cylindrical with distinct borders. The finding of WBC casts reflects a kidney infection. and bacteria. An alkaline or hypotonic urine causes lysis of red cells. Red cell casts indicate bleeding into the tubules. h. The type of cast identified suggests the disease process occurring in the kidney. Urine then will be positive for hemoglobin. Crystals tend to form in concentrated acidic or alkaline urine. because these casts are not formed in the bladder or prostate. Red blood cells: Normal urine contains few or no red blood cells. crystals. but usually in combination with proteinuria. red cells. including immunologic abnormalities. and casts. crystals will form. They may not be initially observable. a culture should be done for specific identification of bacteria and sensitivity of bacteria to antibiotics. infection. f. or a metabolic disorder. vascular disorders. from which they take their shape. and systemic diseases. Urine sediment: The urine sediment is examined microscopically and may contain cells. In some cases. Generally. or phosphate. Epithelial cell casts indicate degeneration of the tubular lumen or necrosis of the renal tubules. oliguria caused by intrinsic renal disease from hypovolemia as a result of dehydration. effects of drugs or toxins. calcium oxalate. Crystal formation is diagnostically significant. particularly when bacteria are present. They may be composed of cystine. usually indicating inflammation. Epithelial cells may be seen in the microscopic field because they are shed naturally throughout the urinary tract.ProSono copyright 2008 e. i. g. White blood cells: White blood cells (WBCs) in the urine (a condition termed pyuria) are primarily indicative of urinary tract infection. they are not clinically significant. If WBCs are present in the urine. If a large number of red cells are present. Crystals: Numerous kinds of crystals can be observed in the urine.

Deposition of circulating soluble antigen-antibody complexes ii. Streptococcal release of neuramidase. Secondary tubular dilation and atrophy may develop. The proposed mechanism is related to glomerulosclerosis. especially children. Acute glomerulonephritis: Acute glomerulonephritis is frequently associated with a group A (nephritogenic strain) post-streptococcal infection (acute post-streptococcal glomerulonephritis (APSGN). Renal Pathophysiology (7) .ProSono copyright 2008 a. although several years of proteinuria and hematuria may have preceded the diagnosis. altering membrane permeability and leading to proteinuria. Activated complement attacks epithelial cells. but there is no specific treatment for the glomerulonephritis. Occasionally. There may be no history of renal disease before the diagnosis. Symptoms usually occur 10 to 21 days after infection and include hematuria. commonly in children. which alters IgG with binding of anti-IgG to the glomerulus. 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). c. decreased GFR. Insulin-dependent diabetes mellitus and lupus erythematosus are secondary causes of chronic glomerular injury. Most individuals. or after viral diseases such as varicella and hepatitis B. Sporadic occurrences have been observed after bacterial endocarditis. proteinuria. oliguria. Proliferation of mesangial cells (cells in connective tissue supporting the glomerular capillaries) may be focal or diffuse with segmental fibrosis and glomerular deterioration. More severe renal disease is observed after a prolonged infection before antibiotic therapy. and hypertension. Hypercholesterolemia also has been associated with progressive glomerular injury. Formation of antibodies specific against the glomerular basement membrane iii. b. Serum complement levels are usually low because they are consumed by the initial infection. Pathophysiology: Three types of immune mechanisms contribute to glomerular injury: i. The thickening of the glomerular membrane contributes to the decreased GFR. edema. Chronic glomerulonephritis: Chronic glomerulonephritis encompasses several glomerular diseases with a progressive course leading to chronic renal failure. with diffuse mesangial cell and capillary endothelial cell proliferation of the entire glomeruli. The edema of acute glomerulonephritis tends to be around the eyes but may involve dependent areas such as the feet and ankles. The primary cause may be difficult to establish because advanced pathologic changes may obscure specific disease characteristics. Immunofluorescent findings from renal biopsy indicate the presence of immune complex deposits in the glomerulus and neutrophil and macrophage recruitment and activation. red blood cell casts. Various pathologic changes are evident in the glomerulus. recover without significant loss of renal function or recurrence of disease. ascites or pleural effusions develop. which may be associated with streptococcal or staphylococcal organisms.

which damage glomerular cell walls.ProSono copyright 2008 The severity of glomerular damage and renal insufficiency is related to the size. vi. and renal epithelial cells in urine. mild hypertension. Complement is deposited with the antibodies. anorexia. location (focal or diffuse). other infection. History of preceding streptococcal or. Concurrent systemic vasculitis or hypersensitivity reaction. red blood cell casts. Gross hematuria. protein. These processes alter membrane permeability and may cause loss of the negative electrical charge across the glomerular filtration membrane. These substances then increase glomerular permeability. contributing to fluid volume expansion and hypertension. Glomerular damage generally occurs from activation of biochemical mediators of inflammation (complement. and type of antigen-antibody complexes. causing proteinuria or hematuria or both. deposits in the membrane. The characteristics of hematuria from red blood cells escaping through the glomerular membrane include a smoky brown-tinged urine. rarely. mesangial proliferation. low-grade fever. ii. Glomerular bleeding provides prolonged contact with the acidic urine and transforms hemoglobin to methemoglobin. and swelling reduce renal blood flow and depress glomerular filtration. number. The coagulation system also may be activated and lead to fibrin deposition in Bowman space. Urine changes: Several disorders may produce hematuria because bleeding can occur anywhere along the urinary tract. which leads to fluid retention. fibrin). The immune-mediated inflammatory response with cellular infiltration decreases GFR. whereby platelets release vasoactive amines such as serotonin or histamine. Salt and water are reabsorbed. Changes in membrane permeability and electrical charge permit the passage of protein molecules or red blood cells into the urine. especially nitrogen retention. d. 1. Membrane damage can lead to platelet aggregation and degranulation. headache. iv. which begins after the antibody or antigen-antibody complexes have localized in the glomerular capillary wall. Malaise. duration of exposure. Bleeding from sites lower in the urinary tract may produce a pinkor red-colored urine. white cells. Mild generalized edema. followed by a sequence of metabolic events that initiate an attack on the glomerular membrane. Clinical manifestations: i. which has a brownish color and no blood clots. and an accompanying proteinuria. Complement activation can serve as a chemotactic stimulus for attraction of neutrophils and monocytes. The neutrophils and monocytes further the inflammatory reaction by releasing lysosomal enzymes. Evidence of impaired renal function. The history and physical examination may disclose Renal Pathophysiology (8) . red cell casts. granular and hyaline casts. leukocytes. iii. contributing to crescent formation (deposition of substances in Bowman space). v. Membrane proliferation. retinal hemorrhages.

white blood cells. Nephrotic Syndrome: Nephrotic syndrome is the excretion of 3. and Henoch-Schönlein purpura. and lipiduria. membranous glomerulonephritis. hyperkalemia. and focal glomerulosclerosis are directly related to nephrotic syndrome. Microscopic evaluation from renal biopsy provides a specific determination of renal injury and type of pathology. amyloidosis. The large amount of urine protein is characteristic of glomerular injury. and casts . malignancies. Hypoalbuminemia results from urinary loss of albumin combined with a diminished synthesis of replacement albumin by the liver. biochemical. 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. infections. particularly albumin and some immunoglobulins. a.5g/day iii. and hyperlipidemia. e. red blood cells. hyperlipidemia. Free fat. Creatinine clearance evaluates the extent of glomerular damage. which may be metabolic. and serum creatinine concentration is elevated. preventing or minimizing immune responses. Specific treatment regimens are necessary for particular types of glomerulonephritis. lead to increased permeability to protein. Management principles for treating glomerulonephritis are related to treating the primary disease. occurs across the injured glomerular filtration membrane. Albumin is lost in the greatest quantity because of its high plasma concentration and low molecular weight. Nephrotic syndrome also is seen in association with certain drugs. edema. Clinical Manifestations: i. Secondary forms of nephrotic syndrome occur as a result of other organic pathologic processes. Massive edema ii. Serum complement is decreased. hypertension. fatty casts in urine Renal Pathophysiology (9) .5g or more of protein in the urine per day. Systemic diseases often implicated in secondary nephrotic syndrome include diabetes mellitus. Pathophysiology: Loss of plasma proteins. and correcting accompanying problems such as edema. Proteinuria > 3. Hypoalbuminemia < 3g/dL iv. When present as a secondary complication with renal diseases. Disturbances in the glomerular basement membrane. b. Hyperlipidemia with cholesterol >300mg/dL v. Lipoid nephrosis (minimal change disease).ProSono copyright 2008 findings that differentiate glomerular disease from another source of urinary tract bleeding. and vascular disorders. systemic lupus erythematosus. oval bodies. c. nephrotic syndrome often signifies a more serious prognosis. although these conditions can occur with other types of glomerular disease. 2. or physiochemical. Other findings include hypoalbuminemia.

although the process may be reversible. and neurologic changes.ProSono copyright 2008 Renal Failure Classification: The terms renal insufficiency. When less than 10% of renal function remains. acute tubular necrosis or cortical necrosis) or many other diseases. Uremia represents the numerous consequences related to renal failure. a common characteristic that explains the overlap in definitions of terms. Acute Renal Failure: Acute renal failure (ARF) is an abrupt reduction in renal function with elevation of BUN and plasma creatinine levels. this is termed end-stage renal failure (ESRF). disseminated intravascular coagulation. including retention of toxic wastes. progressing to ESRF over a period of months or years . hypovolemia. renal insufficiency refers to a decline in renal function to about 25% of normal or a GFR of 25 to 30 ml/min. Generally. Acute pre-renal failure may occur when chronic renal failure exists if a sudden stress is imposed on already marginally functioning kidneys. vomiting. and electrolyte disorders. including acute glomerulonephritis. Renal failure may be acute and rapidly progressive. azotemia. hypotension. 1. malignant hypertension. Uremia is a syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue. Both azotemia and uremia indicate an accumulation of nitrogenous waste products in the blood. The GFR declines because of the decrease in filtration pressure.. commonly it is classified as pre-renal. A combination of ischemic or hepatotoxic factors may produce acute renal failure. Most types of acute renal failure are reversible if diagnosed and treated early. or severe glomerular disease. severe hypotension including vascular obstruction. and renal vasculitis. Levels of serum creatinine and urea are mildly elevated. Poor perfusion can result from renal vasoconstriction. or inadequate cardiac output. pruritus. Failure to restore blood volume or blood pressure may cause acute tubular necrosis or acute cortical necrosis b. anorexia. and uremia are all associated with decreasing renal function. Acute tubular Renal Pathophysiology (10) . hemorrhage. renal failure. intra-renal. deficiency states. Azotemia and uremia are sometimes incorrectly used interchangeably. Acute renal failure is usually associated with oliguria (urine output of less than 30 ml/hr or less than 400 ml/day).g. Often. they are used synonymously. although with some distinctions. Renal insufficiency or renal failure causes azotemia. although urine output may be normal or increased. Renal failure often refers to significant loss of renal function. or post-renal. Pre-renal acute renal failure: Pre-renal acute renal failure is caused by impaired renal blood flow. Acute renal failure can be caused by different clinical conditions. a. Intra-renal acute renal failure: Intra-renal acute renal failure may result from pre-renal acute renal failure (e. Renal failure also can be chronic. nausea. Azotemia means increased serum urea levels and frequently increased creatinine levels as well.

Tissue destruction due to crushing injury. amphotericin B. and diabetes mellitus tend to enhance nephrotoxicity from either aminoglycosides or radiocontrast media..g.. gramnegative bacteremia with shock. e. concurrent renal insufficiency. phenytoin. iii. arsenic). Causes: There are many possible causes of ARF. and mushroom poisoning. obstetric complications. e. Immunologic mechanisms induced by methicillin. d. Complications of pregnancy. iv. or myocardial infarction.g. carbon tetrachloride. mercury bichloride. peritonitis. Clinical Manifestations i. e. Traumatic shock due to severe injury. v. sulfonamides. renal disease. Infectious diseases. Xray contrast materials are hazardous in patients with dehydration. bilateral cortical necrosis. diethylene glycol. but ATN is also associated with sepsis.016. This type of renal failure can occur after diagnostic catheterization of the ureters. or bilateral ureteral obstruction). heavy metals (mercury. Toxic agents. (Oliguria may not occur). leptospirosis. liver failure. Necrosis caused by nephrotoxins is usually uniform and limited to the proximal tubules. hemorrhagic fever. advanced age. tobramycin) are the major culprits. specific gravity of 1. Nephrotoxic ATN can be produced by numerous antibiotics. Radiocontrast media (x-ray media) also may be nephrotoxic. e. rhabdomyolysis. or severe burns.g. aminoglycoside antibiotics. They include: i. ATN caused by ischemia occurs most frequently after surgery (40% to 50% of cases). gentamicin. but the aminoglycosides (neomycin. Dehydration. toxic shock syndrome. ii.. and ischemia associated with surgery on the abdominal aorta (vasomotor nephropathy).. Sudden onset of oliguria.ProSono copyright 2008 necrosis (ATN) is the most common cause of acute renal failure. and other drugs. arsenic. vii. burns. surgical shock. diabetic nephropathy.010 -1. Post-renal acute renal failure: Post-renal acute renal failure usually occurs with urinary tract obstruction that affects the kidneys bilaterally (e. incompatible blood transfusion). Renal Pathophysiology (11) . a procedure that may cause edema of the tubular lumen.g. Ischemic necrosis tends to be patchy and may be distributed along any part of the nephron. bladder outlet obstruction. methoxyflurane. penicillin. Other substances such as excessive myoglobin (oxygentransporting substance in muscles). intravascular hemolysis (transurethral resection of the prostate. A pattern of several hours of anuria with flank pain followed by polyuria is a characteristic finding. c. urine volume 20-200 mL/day. or multiple myeloma. carbon tetrachloride. or methoxyflurane anesthesia may promote renal failure. vi. ii. Disseminated intravascular coagulation. Proteinuria and hematuria. prostatic hypertrophy.

v. and eosinophilia. exhibit remarkable adaptive abilities. by pressure. bicarbonate. Progressive and irreversible loss of renal function (chronic renal failure). and symptomatic changes resulting from increased creatinine. Progressive increase in serum urea nitrogen. however. calcium. v. Recovery may be complete 2. and calcium metabolism. Cysts may be found in the liver and pancreas. and others. b. nonsteroidal anti-inflammatory agents. decrease in sodium. The kidneys. 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. arthralgia. Cystic Disease of the Kidney a. Polycystic Kidneys i. blood pressure. but those present enlarge and. viruses. nausea and vomiting. Etiology: May be due to systemic infections from bacteria. Hematuria ii. and spirochetes and sensitivity to drugs. lethargy. regardless of the cause. Signs of uremia. excretion of waste products. Occasionally.ProSono copyright 2008 iii. diuretics. sulfate. and alterations in salt and water balance usually do not become apparent until the renal function declines to less than 25% of normal. and secretion of hormones that regulate red blood cell production. iv. Enlargement of the kidneys are commonly demonstrable. Chronic Renal Failure: The kidney has many important regulatory functions. The Renal Pathophysiology (12) . Signs and Symptoms: i. potassium. affects these vital processes with changes manifest throughout all organ systems. cause destruction of adjacent tissue. Proteinuna iii. solute concentration and dilution. Some patients will show other signs of hypersensitivity such as rash. Anorexia. acid-base balance. fever. Pathology: Polycystic kidney disease is familial (autosomal dominant) and often involves not only the kidney but the liver and pancreas as well. c. elevation of blood pressure. 2. potassium. Spontaneous recovery in a few days to 6 weeks. including antibiotics. acute renal failure may occur. Pathology: Diffuse inflammation of the interstitial tissue (non-glomerular) tissue of the kidney. including body fluid volume. urea. phosphate. iv. Renal Parenchymal Disease 1. Interstitial Nephritis a. New cysts do not form. creatinine.

although there is often an inability to produce concentrated urine. On physical examination. Medullary Sponge Kidney: Sponge kidney is asymptomatic and is discovered by the characteristic appearance of the urogram.g. any one of these organs may be asymptomatic or symptomatic. and only symptomatic therapy for ureteral impaction of a stone or for infection is required. by diagnostic study in patients presenting with pyelonephritis or hematuria.. the term re-infection implies infection with another organism. 3. Life expectancy is not affected. where bacteria are introduced into the urethra (from fecal flora on the perineum or the vaginal vestibule. Otherwise. ii. or by instrumentation) and travel up the urinary tract to reach Renal Pathophysiology (13) . Far commoner is ascending infection. the symptoms and signs are those commonly seen in hypertension or renal insufficiency. Infection in any part of the urinary tract may spread to any other part of the tract. Anemia is usually the initial manifestation.. but azotemia. The latter occurs during bacteremia (e. the enlarged. with staphylococci) and results in abscess formation in the cortex or the perirenal fat. At any given time. Enlargement of the papillae and calices and small cavities within the pyramids are demonstrated by the contrast media in the excretory urogram. 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. prostatitis.g. pyelonephritis. cystitis. and infection may be troublesome. Hypertension may develop. Symptomatic urinary tract infection may be acute or chronic. or there may be evidence of infection of an organ. Many small calculi often occupy the cysts. acidosis. or by investigating the families of patients with polycystic disease. Pathogenesis: Urine secreted by normal kidneys is sterile until it reaches the distal urethra.ProSono copyright 2008 incidence of cerebral vessel (“berry”) aneurysms is higher than normal. flank pain due to hemorrhage into a cyst will call attention to a kidney disorder. Many small cysts are scattered through the renal medulla. and hyperphosphatemia soon become evident. b. The urine is not remarkable. e. Infections of the Urinary Tract a. At times. i. Medullary Cystic Disease: Medullary cystic disease is a familial disease (either autosomal dominant or recessive) that may become symptomatic during adolescence. The term relapse implies recurrence of infection with the same organism. Microorganisms may be evident only in the urine (bactericidal). irregular kidneys are easily palpable b. Renal transplantation is indicated by the usual criteria for the operation. Bacteria can reach the urinary tract by the ascending route or by hematogenous spread. Signs and Symptoms: Cases of polycystic disease are discovered during the investigation of hypertension. urethritis.

the prognosis for preservation of renal function appears to be good. Lower Urinary Tract (Urethritis. In these patients. Signs and Symptoms Renal Pathophysiology (14) . and abdominal pain. and nephrectomy may be curative. ureter..g. progressive renal failure. Chronic pyelonephritis may lead to widespread fibrosis and scarring of functional cortical and medullary tissue.. Acute Urinary Tract Infection i. Free flow. Occasionally. Cystitis. c.g. chronic infection is due to a unilateral structural abnormality (e. frequency. or dark urine. chills and fever. in the absence of anatomic abnormalities.g. Recurrent urinary tract infection may cause only minimal changes or progressively more severe scarring in any part of the tract. d. and acid pH are important antibacterial defenses. The prominent lesion in the kidney is acute inflammation of the interstitial tissue. scarring. vasculitis. Papillary necrosis (e. rarely. The most important factor in aiding or perpetuating ascending infection is anatomic or functional obstruction to free urine flow. iii. In most patients with these pathologic findings. Some women have chronic bacteremia. vomiting. ii. Pyuria e. use of analgesics). resulting in renal insufficiency: it appears unlikely that repeated urinary tract infection causes renal insufficiency unless there is concomitant obstruction. malaise. Chronic Urinary Tract Infection (Cystitis. i. which is asymptomatic. chronic bacterial pyelonephritis may progress to inflammation of interstitial tissue. costovertebral angle pain and tenderness. hypersensitivity. Upper Urinary Tract: (Pyelonephritis) Manifestations include: headache. and suprapubic or lower abdominal discomfort. Pyelonephritis): Manifestations include burning pain on urination. There are usually no positive physical findings unless the upper tract is involved also. Pyelonephritis): Chronic or recurrent episodes of urinary tract infection usually produce no permanent harm unless obstruction is present. Chronic interstitial nephritis may result from bacterial infection or from other causes (e. or renal pelvis. foul-smelling. ureteral stricture). Bacteriuria 2. however. With bilateral nephritis. complete emptying of the bladder. and. Laboratory Findings: 1. The absence of upper tract signs does not exclude bacterial invasion of the upper tract. in diabetics) may lead to slough of papillae and ureteral obstruction. Pathology: Acute urinary tract infection shows inflammation of any part of the tract and sometimes intense hyperemia or even bleeding of the mucous membranes.. chronic suppression of infection may stabilize renal function. atrophy. often with turbid. “chronic pyelonephritis” is in fact not caused by infection but instead represents interstitial nephritis of immunologic or toxic cause. which may progress to frank suppuration and patchy necrosis.ProSono copyright 2008 the bladder. large urine volume.

but persistent asymptomatic bacteriuria. occasionally in women. Even gentle palpation of the prostate results in expression of copious purulent discharge. True renal stones may be present as well in these patients. sarcoidosis. Recurrent episodes of lower or upper tract involvement. 3. may occur in sponge kidney. Palpation reveals a symmetrically enlarged. mild dysuria and frequency. ii. Anemia 3. Prostatitis is thus commonly associated with urethritis. which appear as minute calcific densities with linear streaks in the region of the renal papillae. In acute prostatitis. the prostate feels enlarged. The diagnosis is usually established by x-ray demonstration of calcium deposits in the kidney. and scanty urethral discharge. Absence of symptoms or signs referable to the urinary tract. and laboratory findings are those of the primary disease. 4. 2. and excess calcium and alkali intake. Pathology: Chronic hypercalciuria and hyperphosphaturia may result in precipitation of calcium salts in the renal parenchyma (nephrocalcinosis). Signs and Symptoms: These include perineal pain.ProSono copyright 2008 1. or with active bacterial infection of the lower urinary tract. Signs and Symptoms: The symptoms. the de Toni-Fanconi syndrome. fluctuation occurs only if an abscess has formed. Renal Pathophysiology (15) . or papillary necrosis. ii. Laboratory Findings: 1. there may be dull lumbo-sacral and perineal pain. and destruction of bone by metastatic carcinoma. frequency. Urinary Stones a. Chronic interstitial nephritis predisposes to nephrocalcinosis. dysuria. hypervitaminosis D (particularly with associated high calcium intake). Elevated serum BUN and creatinine 2. and very tender. Nephrocalcinosis: Urinary stones and calcification in the kidney may be associated with metabolic disease. 4. Bacteriuria may or may not be present f. Prostatitis: Bacteria may reach the prostate from the bloodstream or from the urethra. or may be idiopathic. The incidence of urinary tract calculus is higher in men i. In chronic prostatitis. boggy. signs. Impairment of renal function rare unless obstruction is present. tuberculosis of the kidney. renal tubular acidosis. and urethral discharge. boggy. fever. Obstruction or other anatomic abnormality in the urinary tract is consistently found in men. The commonest causes are hyperparathyroidism. i. and slightly tender prostate. may be secondary to infection in the urinary tract. Other causes include acute osteoporosis following immobilization.

May be asymptomatic. Chills and fever and bladder irritability if infection is present. a. Hematuria. c. a. Physical changes in urine a. Horseshoe kidney. Uricosuria—Crystals of uric acid or sodium hydrogen urate may initiate precipitation of calcium oxalate from solution. neurogenic bladder. Exacerbations of infection when obstruction occurs. Nucleus (nidus) for stone formation a.g. diverticula. i. Signs and Symptoms: 1. 4. Bladder Stone: Vesical stones occur most commonly when there is residual urine infected with urea-splitting. and cystocele. 3. Increased concentration of urine solute as a consequence of low intake of fluid and low urine volume b.organisms (e. Bits of necrotic tissue. bladder stones are associated with urinary stasis due to bladder neck or urethral obstruction. Nausea. vomiting. abdominal distention.ProSono copyright 2008 b. Calcium b. Etiologies: 1. Oxalate c. d. 2. Ulceration and bladder inflammation predispose to stone Renal Pathophysiology (16) . 4. ii. staphylococci). 2. 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. Gastrointestinal symptoms common. Thus. Often asymptomatic. with flank pain and colic. Ureteral Stone: Ureteral stones are formed in the kidney but produce symptoms as they pass down the ureter. blood clots. The pathologic changes may be modified by ischemia due to pressure or by infection. Proteus. Changes in urine pH 3. Symptoms of obstruction of calix or ureteropelvic junction. Signs and Symptoms: 1. 5. particularly in the presence of stasis or infection. b. i. 3. Urine usually contains fresh red cells. and clumps of bacteria. c. may serve as a nucleus for stone formation 4. Congenital or acquired deformities of the kidneys. b. Obstruction of ureter produces severe colic with radiation of pain to regions determined by the position of the stone in the ureter. 5. Excessive excretion of relatively insoluble urinary constituents. Local caliceal obstruction or defect. Sponge kidney. Uric acid 2. Foreign bodies in the bladder act as foci for stone formation.

bands. and the secretion of hydrogen ion. Extrinsic tumors. Renal papillae become flattened. 5. and glomerular filtration is impeded. 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. Functional impairment of tubule function affects the excretion of solute. Renal Pathophysiology (17) . early detection and treatment are required to prevent irreversible function and anatomic damage. or clot that obstructs a ureter or the bladder neck iii. involuntary voiding. Chronic urethral obstruction may result in a distended bladder with “overflow” dribbling. with dysuria. Neuromuscular disorder related to the spinal cord or peripheral nerve lesions c. Uric acid stones are common in the presence of an enlarged prostate and uninfected urine.ProSono copyright 2008 formation. there may be overflow dribbling from a distended bladder. Interruption of urinary stream as stone occludes urethra. and the complication of urinary tract infection determine the presenting manifestations a. ureterovesical. Congenital anatomic abnormalities (eg. Destruction of the kidney results within a few weeks. 4. The site and degree of obstruction. and frequency with incomplete emptying of the bladder. calcium oxalate. Pathology: Complete obstruction to the flow of urine produces increase in pressure in the ureters and in the renal pelvis. Signs and Symptoms: The site of obstruction and rapidity of onset determine the presentation. or stone will produce painful distention of the bladder. which then become dilated. tumor. Partial obstruction produces lesser impairment of renal function. ureteropelvic. Stone. Hematuria and pyuria. or fibrosis iv. Signs and Symptoms: 1. or urethral stricture) ii. Renal blood flow is reduced. or magnesium ammonium phosphate. Benign prostatic hypertrophy is occasionally present in men. 2. Most vesical stones are composed of calcium phosphate. the duration of obstruction. b. Chronic or low-grade obstruction is usually asymptomatic. Bladder irritability. Etiology: Obstructive uropathy is the result of: i. Acute obstruction of the urethra by an enlarged prostate. 3. postoperative bladder dysfunction. urgency. Obstructive Uropathy: Obstruction of the urinary tract can result in serious damage to the kidneys. the reabsorption of sodium. the renal tubules dilate. If a neurologic lesion is the cause of bladder dysfunction. and frequency. i.

Orchitis: Acute orchitis is usually due to mumps and occurs during the years just following adolescence. 2. filariasis. In older men. b. This tumor metastasizes early to the lungs. On microscopic examination. Orchiopexy of the other testis is desirable because of the high incidence of the bilateral anatomic abnormality associated with torsion 7. the cells resemble renal tubule cells arranged in cords and varying patterns. Testicular Disease a. Signs and Symptoms: Sudden pain in the scrotum. An anomaly of the tunica vaginalis or of the relationship of the epididymis to the testis is usually present. liver. Hypernephroma) i. Destruction of the testis usually leaves some hormonal cell function. and schistosomiasis haematobia. painful testicle may occur . It rarely occurs before age 35 and more commonly after age 50. spermatic cord. Elevation of the scrotum provides some relief. Pathology: Acute epididymitis is caused by bacterial infection ascending from the urethra or prostate. which occurs more frequently in men. Epididymitis i. made worse by elevation of the scrotum. The testis is swollen. orchitis. Testicular Torsion: Testicular torsion (torsion of the spermatic cord) is most common in adolescent males and young men under age 25. It invades blood vessels early. Adenocarcinoma of the Kidney (Renal cell carcinoma. rapid unilateral scrotal enlargement. Adenocarcinoma of the kidney apparently arises from renal tubule cells or adenomas. Pathology: The commonest malignant tumor of the kidney is adenocarcinoma. and groin are the characteristic manifestations. c. The characteristic presentation is with a sudden onset of unabating pain in the scrotum. Enlarged kidney may be palpable Renal Pathophysiology (18) . tuberculosis. and retracted. ii. 3. Signs and Symptoms 1. Secondary orchitis with a swollen. or lower abdomen. leprosy. Fever. Treatment consists of immediate surgery to remove the infarcted testis. it usually follows urinary tract obstruction and infection or instrumentation of the lower genitourinary tract ii. Chronic orchitis may be due to syphilis. and marked tenderness of the testes. Testicular torsion must be differentiated from epididymitis. groin. and trauma to the testis. It is most often unilateral but may be bilateral. Mumps may produce acute oophoritis as well. Tumors of the Genitourinary Tract a. tender. and long bones. Gross hematuria with or without flank pain.ProSono copyright 2008 6.

Acute urinary retention. Enlarged prostate. Metastases involve regional lymph nodes. Signs and Symptoms 1. 3. Hard consistency of the prostate. and lungs ii. gross or microscopic. Hematuria. and when cancer has extended beyond the prostate to the periprostatic tissue or to bone. 4. Signs and Symptoms 1. particularly in the low back.ProSono copyright 2008 b. At least 75% of bladder tumors occur in men over age 50. The serum acid phosphatase concentration thus provides a good index of extension and growth of the tumor ii. reduced force and caliber of the urinary stream. Signs and Symptoms 1. ii. 3. The prostatic tissue is rich in acid phosphatase. Uremia follows prolonged obstruction d. Metastases to bone produce pain. Pathology: Cancer of the prostate is rare before age 60. 4. It metastasizes early to the bones of the pelvis and locally may produce urethral obstruction with subsequent renal damage. Tumors of the Bladder i. The growth of the tumor is increased by androgens and inhibited by estrogens. c. epidermoid tumors. Malignant cells by urine cytology. Prostatism: hesitancy and straining to initiate micturition. Tumors usually arise at the base of the bladder and involve ureteral orifices and the bladder neck. 2. which is often of low-grade malignancy. the serum acid phosphatase is increased. 3. and sarcomas are rare. Visualization of tumor at cystoscopy. Suprapubic pain and bladder symptoms associated with infection. Pathology: Bladder tumors are the second most common urinary tract tumors. 2. The common tumor is transitional cell carcinoma. 4. bone. Prostatism. 5. Pathology: Hyperplasia of the prostatic lateral and subcervical lobes that are invaded by periurethral glands results in enlargement of the prostate and urethral obstruction. Elevated PSA (prostate specific antigen) Renal Pathophysiology (19) . Carcinoma of the Prostate i. Elevated serum acid phosphatase in 85% of patients with extension of the cancer beyond the prostatic capsule. 2. nocturia. adenocarcinomas. Benign Prostatic Hyperplasia (BPH) i. liver.

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