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