Renal Disease

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Acute Renal Failure Due to Urinary Tract Obstruction Manuel Marlinez-Maldonado, MD, * and Dana A. Kumjian, MDt

Obstruction of the urinary tract is a frequent cause of renal dysfunction, particularly in view of the increasing number of elderly male patients who develop prostatic disease and associated problems. 16.44 The development of chronic obstructive disease is insidious and usually long lasting, so that its clinical consequences and form of presentation are almost always related to chronic renal insufficiency. Although less common, acute obstruction to the flow of urine as a result of complete obstruction of the urinary conduits of both or, when such is the case, of a singly functioning kidney, may present as acute renal failure. Complete obstruction of a few days' duration may be accompanied by severe acidosis and hyperkalemia. This may pose a diagnostic dilemma as to the cause of the acute renal failure, which, because the disorder is potentially life threatening but reversible, must be solved. It is the purpose of this article to provide some of the necessary tools to permit an analysis of the patient with obstructive uropathy based on the pathophysiologic underpinnings of the clinical manifestations of this condition. CAUSES OF RENAL OBSTRUCTION Obstruction of urine flow can occur at several levels in the kidney. Table 1 and Figure 1 demonstrate the level at which various diseases and conditions can obstruct the flow of urine. Systemic and Metabolic Diseases In general, systemic or metabolic diseases may lead to intrarenal obstruction either because some product of the body cells is precipitated *Professor and Vice Chairman, Department of Medicine, Emory University School of Medicine; and Chief, Medical Service, Department of Veterans Affairs Medical Center, Atlanta, Georgia tFellow, Division of Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee

Medical Clinics of North Arnerica-Vo!. 74, No. 4, July 1990

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Table 1. Causes of Obstruction to Urine Flow Intrinsic Renal Uric acid Myeloma protein Oxalic acid Tumor lysis syndrome Renal Infundibulum Strictures Aberrant vessels Calculus Neoplasm, renal or perirenal Cyst, renal or peripelvic Primary urothelial tumor Renal Pelvis Calculus Neoplasm, renal and extrarenal Bilateral papillary necrosis Fungus ball Aberrant vessels Ureteropelvic fibrous bands Ureteropelvic stricture Ureter: Extrinsic Retroperitoneal fibrosis Retroperitoneal abscess Retroperitoneal hematoma Aneurysm, aortic or renal Urinoma Lymphocele Pregnancy Bowel impaction Neoplasm, metastatic or primary Endometriosis

Ureter: Intrinsic Calculus Infiltrative tumors Necrosis Surgical Inflammatory bowel disease Sloughed papillae Post-radiation therapy Bladder and Bladder Neck Bladder neoplasm Functional (neurogenic) Hematoma Fungus ball Benign prostatic hypertrophy Surgical Prostatitis Prostatic abscess Prostatic neoplasm Urethral Stricture Calculus Valves (posterior or perivesicular) Polyp or diverticulum Foreign body Phimosis Meatal stenosis or inflammation Paraurethral abscess Condyloma acuminata

in the lumina of renal tubules 33• 36 or because cellular infiltration of the kidney parenchyma may increase the pressure in the renal interstitium or subcapsular space. 35 Increased parenchymal pressure can lead to collapse of the tubules and the generation of sufficient intratubular pressure to oppose filtration pressure at the glomerulus. As a consequence, glomerular filtration does not occur. Examples of these conditions include precipitation of intratubular urate to form uric acid concretions, as may be seen after chemotherapy (and occasionally spontaneously) in malignant disorders characterized by a large cellular mass of high turnover,20 and the intratubular deposition of oxalic acid, which may result from ethylene glycol poisoning. 21 In the former example, renal cellular infiltration may also contribute to renal parenchymal expansion, enlargement of the kidneys, and high intrarenal pressures resulting from the resistance offered by the relatively rigid renal capsule. Diseases of the Pelvis, Ureters, and Bladder

Pelvis. Tumor or stone disease is the most common cause of renal pelvis obstruction. 54 Clearly, the disease would have to be bilateral to produce renal failure and of sudden unilateral worsening in order to lead

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ACUTE RENAL FAILURE DUE TO URINARY TRACT OBSTRUCTION INTRINSIC RENAL

RENAL PELVIS

DISTAL CONVOLUTED

TUBULE COLLECTING DUCT LOOP OF

HENLE

URETER-INTRINSIC

~ URETER-EXTRINSIC

BLADDER

~

BLADDER NECK URETHRA

Figure 1. Causes of renal failure due to urinary tract obstruction.

to acute reductions in filtration rate and urine flow. This may occur in patients with bilateral staghorn calculi in whom infection, hypercalcemia from underlying illness (e.g., hyperparathyroidism), or breakage of calcareous particles may lead to either renal hemodynamic alterations, further obstruction, or both, with overall worsening of renal function. In cases of bilateral papillary necrosis, acute bilateral obstruction may supervene. The most propitious setting for this syndrome is the patient with sickle cell hemoglobinopathy or diabetes mellitus with urinary tract infection, but it has also been observed in abusers of analgesics, particularly phenacetin.17 There may also be an increased incidence in patients with liver cirrhosis, ankylosing spondylitis, and other conditions, who, in addition to phenacetin, have been taking cyclooxygenase inhibitors. 46 Patients with nephrostomy tubes or immunocompromised, debilitated individuals receiving chemotherapy or steroid treatment may develop renal pelvis or bladder fungus balls that will lead to functional renal failure. 3, 31 Ureters. Bilateral urolithiasis can cause obstruction and acute renal failure. Stone disease is more likely to cause acute renal failure if the patient has undergone unilateral nephrectomy for complications related to the calcareous disease. Infiltrative tumors or those that invade lymph nodes (e.g., lymphomas and lymphosarcomas) of the retroperitoneal area may cause obstruction of the ureters. Retroperitoneal fibrosis or physical displacement of the urine conduits by peritoneal or retroperitoneal masses

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may result in renal failure. Although this process is a slowly developing one, we have seen patients in whom the diminution or cessation of urine flow, with its attendant changes in blood chemistries (vide infra), was relatively sudden and the cause of diagnostic uncertainty and confusion. A special consideration must be given to obstructive problems arising in uninephric individuals. In addition to congenital lesions, such as unilateral hypoplasia of the kidney, patients may have lost a kidney because of disease (nephrolithiasis, tuberculosis, tumor), accidents (fractured or ruptured kidneys), or kidney donation. Moreover, the special circumstance of a kidney transplant recipient must be recognized as one particularly vulnerable to obstruction, principally in the early post-transplant period. 26 In this setting, necrosis of the ureter, hematoma, urinoma, lymphocele, or dihiscence at the site of the urinary bladder anastomosis may be responsible for interruption of urine excretion and acute renal failure; this condition must be distinguished from acute tubular necrosis and rejection. 43 In the other circumstances mentioned earlier, it is not difficult to realize that extrinsic or intrinsic obstruction of any part of the urine collecting system or the lower conduits may lead to acute renal insufficiency. Bladder and Urethra. Blood clots, stones or tumors of the bladder, or their presence in the urethra may acutely cause cessation (If urine flow. These anomalous conditions may have been preceded by the ability to produce urine until shortly before the patient seeks medical help and can account for the rare, but real, syndrome of episodic polyuria and anuria, which may be pathognomonic of lower tract obstruction. This, of course, is the result of a movable object that may intermittently cause obstruction by inserting or removing itself from the channels that allow urine to find its way out of the body. An important cause of acute failure to excrete urine is bladder atony or frank paralysis as a consequence of neuropathy.41 Diabetics are particularly prone, but elderly and debilitated patients may also have a propensity for atonv. Pe;haps the most common cause of partial or complete loss of the ability to excrete urine is alteration in the size of the prostate. The elderly man is the principal victim of what may be a disconcerting and most uncomfortable condition. Massive prostatic hypertrophy, but milder degrees of enlargement as well, can lead to urine retention. Also, carcinoma of this retrovesicular organ may distort the course and caliber of the urethra and suspend the normal flow of urine. Not infrequently, because of prostatic disease, elderly patients with phimosis or with uncircumcised and redundant prepuce may develop swelling of this tissue and of the external meatus as a result of catheterization attempts. This may go undetected for a time and urine retention may ensue. It should be remembered that occasionally, accidental ureteralligation or severance may occur during surgery in women (gynecologic and obstetric surgery) and men (extensive urologic or abdominal surgery). A high degree of suspicion of this occurrence must be kept in mind in patients in whom anuria or oliguria occurs after surgery, particularly if no major event points to hemodynamic or toxic causes of acute renal failure.

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CLINICAL MANIFESTATIONS History

Intra renal Obstruction. It is beyond the scope of this article to go into a detailed analysis of the etiology, history, and physical and laboratory findings of the systemic diseases that lead to intrarenal obstruction and acute renal failure. Nevertheless, it is essential to review, no matter how briefly, some of the fundamental aspects of these conditions. Multiple Myeloma. The proliferation of plasma cells in this disease is responsible for the production of enormous quantities of abnormal gamma globulins. In addition, there is bone invasion by the cells, and their presence diminishes the marrow's capacity to produce erythrocytes. Because it is a disease that is commonest in the sixth and seventh decades, the usual presentation is that of an elderly patient (males predominate over females 2:1) with bone pain (usually low vertebral) and anemia. The diagnosis is established by identification of excessive number of plasma cells in bone marrow examination, demonstration of a monoclonal gammopathy in plasma electrophoresis, and the presence oflytic bone lesions. Very frequently, mild to moderate chronic renal failure is present, and acute renal failure is seen in approximately 1 in every 50 patients. l5 . 37 Hypercalcemia of modest (12 to 15 mg/dl) or severe nature (> 15 mg/dl) may be present and contribute to the diminution in renal function because of its induction of dehydration, depletion of the volume of extracellular fluid, and reduced renal blood flow and filtration rate as a consequence of the constrictive effects of calcium on vascular smooth muscle, including the mesangium of the glomerulus. 7 Uric Acid Nephropathy. Deposition of uric acid stones in the pelvis may be seen in patients in whom metabolism of purines is accelerated and, as a result, so is urate excretion. This could lead to bilateral, constantly growing stones (more so if the urine is maximally acid) and obstruction. [9 Such patients, however, are usually individuals with congenital gout, and knowledge of their chronic urate nephropathy is most likely available. This, of course, increases physician suspicion and helps to establish the diagnosis. The situation may be different in a patient with lymphoproliferative or myeloproliferative disorders or in a patient with lymphomatous diseases receiving chemotherapy. The presence of large tumor masses may lead to spontaneous cell death and extrusion of nuclear material into the circulation that leads to marked production of uric acid. The high filtered loads of uric acid will precipitate in the distal convoluted and collecting tubules, particularly if the tubular fluid is maxim ally acid. Because many of these patients are susceptible to the development of systemic acidosis as a result of lactic acid accumulation, the setting is most propitious for the development of intratubular urate cast obstructive disease. 12 Physicians today are fully aware that chemotherapy should be preceded in individuals susceptible to the development of acute uric acid nephropathy (large lymphoid or myeloid cell masses, particularly if immature) by prevention of conversion of purines to uric acid (inhibition of xanthine oxidase by allopurinol before chemotherapy is commenced), adequate hydration, and maneuvers that lead to urine alkalinization. 32

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Tumor Lysis Syndrome. In some patients with large abdominal tumoral masses or leukocyte counts exceeding 100,000 per cubic millimeter, high levels of serum or plasma lactic dehydrogenase, and mildly elevated serum phosphorus, chemotherapy can result in marked rises in plasma phosphate and the precipitation of calcium phosphate in the renal tubules. Acute renal failure may supervene. 11 Ethylene Glycol Poisoning. Although the main clinical manifestation of this condition is severe, frequently lethal, metabolic acidosis, the increased metabolism of glycol to oxalate leads to the intratubular precipitation of calcium oxalate and acute renal failure. 8 Avoidance of oxalate production and correction of the acidosis is of primary importance. Postrenal Obstruction. The history of postrenal obstruction may be entirely related to the underlying cause. In the case of stone disease, longstanding complaints of colic may be prominent. Episodes of gross or microscopic hematuria may have occurred. It is important, for reasons already discussed, to elicit a history of analgesic or anti-inflammatory drug use in those patients suspected of suffering from frank papillary necrosis. Ill-defined lower abdominal pain with difficulty in beginning urination or actual diminution in the production of urine may be prominent. Those patients in whom the obstruction has been modest before major falls in renal function have taken place may give a history of nocturia or polyuria, which results from the defective capacity to concentrate the urine that may be caused by chronic obstruction. Symptoms of prostatic disease such as dribbling, hesitancy, straining, diminution in the caliber of the stream, and so forth may be important clues to the development of acute urine retention in men. One should keep in mind that detrusor muscle abnormalities in women, although rare, may lead to urine retention. A history of systemic anticoagulation or recent instrumentation of the lower tract or obstetric or gynecologic surgery may lead to the formation of clots and obstruction of the lower tract. Signs and Symptoms It is outside the scope of this review to consider the signs and symptoms of systemic illnesses that may lead to intrarenal obstruction. In the previous section on systemic diseases, we gave the most salient features of the conditions most likely to lead to this problem. The degree and types of symptoms and signs caused by urinary tract obstruction depend on the cause and the site as well as the rapidity with which the obstruction has developed. Renal colic is the result of the rich innervation of the entire urinary tract. The pelvis and the upper ureters are rich in sensory innervation. Thus, patients with unilateral or bilateral foreign material (stones, clots, sloughed papillae) will complain bitterly of flank (bi- or unilateral, as the case may be) pain. On occasions, renal colic may lead to intestinal paralytic ileus; thus, severe flank pain with a history of diminution in urine output and diminished intestinal peristalsis may point the diagnostic work-up in the proper direction. 23 It is not uncommon to feel a mass-like effect or fullness in the flanks of acutely obstructed individuals. This is more likely to be the case in

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children under circumstances in which the level of flow interruption is high (close to the renal pelvis). 24 In addition, bladder neck or urethral obstruction may present as a lower abdominal mass, which mayor may not be tender (globus vescicalis). - Urinary tract obstruction may lead to acute hypertension in some patients. I, 28 Patients with solitary kidneys and those with severe acute bilateral obstruction appear to be more prone to rises in blood pressure. Elevated blood pressure in a previously normotensive individual with acute renal failure should make one aware of the possibility of urinary tract obstruction. Laboratory Findings We will emphasize in this section the laboratory findings for acute urinary tract obstruction rather that those of systemic diseases that may cause intrarenal obstruction. Urinalysis. There are no specific findings in examination of the urine other than those predictable from the underlying disease. 57 Thus gross or microscopic hematuria can be found in cases of nephrolithiasis. Pyuria and bacteriuria can be found when infection has complicated urine stasis, and mild «1 g/24 hr) proteinuria may be present. All forms of cellular and hyaline casts may occur, but they are rare. This occasionally includes the presence of red cell casts if intrarenal bleeding has occurred. Some patients exhibit histiocyte-like cells in the urine, the origin and significance of which are obscure. 57 It is of interest that recent experimental studies in the rabbit have uncovered macrophages and monocytes in the renal parenchyma infiltrates of fibroblast-like cells. 47 The possibility that the histiocyte-like cells seen in the urinalysis of some patients are transformed inflammatory cells or resident macrophages present as a direct result of obstruction may be inferred from these observations. Blood Analysis. Complete blood cell counts may reveal normal, low, or elevated hemoglobin. Rare cases have been described in which hemoglobin and red cell counts are above normal. Conceivably, this is the result of increased erythropoietin production by obstructed kidneys,25 because the polycythemia disappeared upon release of the obstruction. Yet, when measured in some patients, albeit with possibly insensitive methodology, it was undetectable. 22 A relationship between ureteral obstruction and polycythemia is clearer in experimental animals. Leukocytosis may accompany infection, particularly if bacteriuria and pyuria are also present. It may also be a manifestation of papillary necrosis. The most important findings, however, are those relating to blood urea nitrogen (BUN) and serum creatinine. Postrenal obstruction is characterized by a disproportionate rise in BUN because of enhanced tubular urea reabsorption from fluid stasis and inability to excrete this end product of protein metabolism. Although serum creatinine also rises, it does so at a slower pace, so that the BUN/creatinine ratio is abnormally high (> 15); in contrast to contraction of extracellular fluid volume, however, in which the ratio is also high, serum creatinine in obstruction is clearly abnormal and usually above 2.5 mg/dl. In the presence of high urine osmolality (>750 mOsm/kg), low urine flow, and rising serum creatinine, the high BUN/

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creatinine ratio is even more valuable, because acute obstruction to urine flow is one of the conditions in which urine concentration may be initially preserved. As the rate of urine flow falls, there is increased distal sodium reabsorption and increased medullary solute concentration, which will propitiate tubular reabsorption of water in the descending limb of Henle and the collecting duct. 18. 51 As a consequence of increased reabsorption of distal delivered solute (including sodium chloride), the fractional excretion of sodium, in contrast to that in acute tubular necrosis, will be low. The longer the duration of the acute obstruction, the more likely one is to observe hyperphosphatemia and low plasma calcium; this will not be seen in obstruction of lesser duration. Needless to say, in conditions such as tumor lysis syndrome or chemotherapy-induced cell death, hyperuricemia may also be present. In this context, it should be recalled that a fractional urate excretion exceeding one (urine urate concentration/plasma urate over urine creatinine/plasma creatinine) in a spot urine is diagnostic of acute urate nephropathy.29 The ratio is less than one in other types of acute renal failure.

Radiologic Procedures Plain films of the abdomen may be valuable in assessing the size of the renal shadows (a bilateral, small, contracted kidney eliminates the presence of an acute process) and the presence of radiopaque stones. In addition, it may permit identification of paralytic ileus and thus help in the diagnosis of colic. Also, pelvic, retroperitoneal, or abdominal masses that may be the cause of the obstruction may be identified. 42 Intravenous and retrograde pyelograms are useful in certain circumstances, but they have given way to ultrasound techniques as first-line diagnostic procedures. If the clinical manifestation is dominated by colic or flank pain, these procedures may be necessary. In contrast, if obstruction leading to calyceal dilatation or hydronephrosis is present, ultrasound is clearly superior. 45, 50 The sensitivity of this test for detection of hydronephrosis exceeds 90%; in most series, specificity is close to 100%.45 Computerized Tomography and Magnetic Resonance lmaging. These procedures may be needed for special circumstances, such as evaluation of tumor presence or recurrence that causes obstruction, but they play a secondary role to ultrasonography in the diagnosis of obstructive disease. 27. 30

Radionuclide Studies Radiohippuran and DMSA-scintigraphy are useful, particularly in children, to assess upper urinary tract obstruction. 52 PATHOPHYSIOLOGY

Effects on Renal Blood Flow Most experimental studies have evolved around models of acute unilateral ureteral obstruction. However, those that have examined bilateral obstruction have revealed that the hemodynamic and glomerular filtration

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changes in acute bilateral obstruction are similar to those observed when the phenomenon is unilateral.:38 Bilateral obstruction leads to an acute transient rise in renal blood flow, the consequence of a reduction in renal vascular resistance. The increase in blood flow may last for as long as 3 hours and may result from intrarenal release of vasoactive hormones. It has been repeatedly described that bilateral and unilateral ureteral obstruction lead to rises in renin release. 2 It has also been described that the increase in renal blood flow and in renin secretion is partially abolished by the administration of cyclooxygenase inhibitors. This suggests that prostaglandins may mediate both the increase in renal blood flow and the enhanced renin secretion.'9 In this context, it is important to note that the vasodilatation is independent of neuroadrenergic tone, because renal denervation and alpha- and betaadrenergic blockade do not alter the increased blood flow. 55, 56 Increases in blood and plasma flow per glomerulus have been shown to occur when these have been measured in Munich-Wistar rats, whose superficial glomeruli permit micropuncture of the vascular and tubular structures of individual nephrons. Glomerular plasma flow per nephron (QJ rises during ureteral obstruction primarily because of a decrease in afferent arteriolar resistance. 13 Although the observation of partial and, in some studies, complete abolition of the vasodilation and increased renal blood flow by indomethacin points toward prostaglandins as mediators of the hyperemia, other vasodilators have been implicated. Histamine in renal tissue increases following acute ureteral obstruction, and the use of HI receptor antagonists (chlorpheniramine) but not H2 antagonists (cimetidine) nearly abolishes the renal vasodilatation in response to acute ureteral obstruction. 4 Moreover, H2 antagonists diminish the renal vasodilatory response to exogenous prostaglandin 12 and E2 in the dog. Recent studies have shown that after 4 hours or longer, ureteral obstruction is associated with increased synthesis of thromboxane A2 and that this may be responsible for renal vasoconstriction. 39 In experimental models of hydronephrosis, the enhanced arachidonic acid metabolism, which may mediate intrarenal vasoconstriction, is associated with an inflammatory cell influx into the kidney parenchyma. The influx of infiltrating cells can be blocked, and the enhanced production of eicosanoids can be reduced by inhibition of the lipoxygenase, but not the cyclooxygenase pathway, which suggests a role for leukotriene B4 but not thromboxane A2 in mediating infla~mation in hydronephrosis. 48 Also, some of the paren~ chymal swelling and inflammation may be due to enhanced production of prostaglandins by the infiltrative interstitial cells of the obstructed kidney in response to bradykinin. 53 It has also been proposed that atrial natriuretic peptide (ANF) may participate in the hemodynamic alterations of the hydronephrotic kidney. This hormone causes vasodilatation of the afferent arterioles and vasoconstriction of the efferent arterioles of the glomerulus in hydronephrotic rats. Patients who undergo massive volume expansion might conceivably suppress release of ANF. Its absence from the circulation would reduce GFR by facilitating vasoconstriction of the afferent arterioles and vasodilation of the efferent arterioles.:3:3 Release of the obstruction by restoring extracellular

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volume would reestablish secretion of ANF. The peptide will revert afferent arteriolar vasoconstriction and increase efferent tone. This would help recuperation of glomerular filtration rates (GFR) and may contribute to postobstructive diuresis (vide infra). Glomerular Filtration Rate Glomerular filtration rate is a complex process that depends on a number of factors. An important determinant of how much filtration occurs across the glomerular basement membrane is the plasma flow received by each glomerulus (QA)' This in turn is controlled by the resistances of the afferent and efferent arterioles, which are under neural and hormonal control. What percentage of the plasma flow will be filtered is determined by the setting of arteriolar resistances across the glomerulus, the permeability characteristics of the basement membrane (a product of their intrinsic permeability to water and the surface area: Kr or ultrafiltration coefficient), and the net ultrafiltration pressure (the difference between intraglomerular capillary hydraulic and oncotic pressures, and the intratubular pressure). Any circumstance in which intratubular pressure approaches the net glomerular filtration pressure will lead to reductions in glomerular filtration. 10 Micropuncture studies have shown that in the obstructed kidney, the vasodilatation of the afferent arteriole that leads to increased blood flow is not translated into increased filtration because the ultrafiltration coefficient falls and the intratubular pressure rises. 9 Although even in complete obstruction there is a finite value for single nephron GFR, this is the result of "replacement filtration"; in other words, reabsorbed tubular fluid causes the intratubular pressure to fall and some filtration to be reestablished. The mechanism by which the Kr falls may be related to the enhanced renal production of renin and increased intrarenal angiotensin II production, which will cause Kr to fall. Although it also leads to afferent arteriolar constriction, the enhanced prostaglandin production already mentioned will maintain the afferent arteriolar vasodilatation, at least temporarily. In conclusion, experimental studies have not been able to clarify completely the changes in total versus single-nephron GFR. In essence, there is a modest but definite fall in GFR upon acute obstruction of the ureter. Also, the changes in hemodynamics and glomerular filtration in acute bilateral obstruction are similar to those observed when the phenomenon is unilateral. TREATMENT It is not possible to discuss the numerous surgical and urologic approaches that may be available to relieve urinary tract obstruction. It should be emphasized that, in contrast to the situation 5 or 10 years ago, the development of lithotripsy and urologic endoscopic techniques has simplified resolution of obstructive problems secondary to stone disease. One important consequence of lower tract catheterization in patients with a massively distended bladder is gross hematuria from ruptured engorged bladder vessels during rapid decompression. To avoid this, fluid

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evacuation must bc slow, with removal of no more than 100 to 300 mllhr. Also, rapid decompression can lead to a vasovagal reflex, which often precipitates sudden bradycardia and hypotension. General mcdical measures are needed for those individuals affected bv systemic illness presenting as acute intrarenal obstruction. In the case ~f multiple myeloma, plasmapheresis with or without dialysis has proved highly beneficial for some patients and may result in reversal of acute renal failure. Maintenance of a brisk and adequate urine flow (>50 ml/hr) and alkalinization of the urine is essential in the treatment of uric acid nephropathy. In this condition, the use of allopurinol to block the production of uric acid is of major therapeutic importance. Blockade of glycolate metabolism by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, may help reduce the metabolism of glycolate and the production of oxalate in ethylene glycol poisoning,6 although, as already mentioned, patients may require hemodialysis. The other complication of sudden relief of bilateral urinary tract obstruction is the syndrome of postobstructive diuresis. In its commonest form, excess extracellular volume retained during the obstructive episode is lost into the urine. Perhaps because tubular dilatation and some of the solute and water reabsorption functions are not quite normal, the rate of urine flow may be high. A clinical assessment that the patient may be wasting extracellular volume is made, and the patient's urine losses are meticulously replaced. This leads to a state of permanent and copious polyuria that frequently varies with the rate of intravenous fluid infusion (we have seen patients with 24-hour urine outputs exceeding 15 L). The cure for this impressive, if tiresome, phenomenon is not to exceed more than 50 ml/hr of fluid replacement after relief of urinary tract obstruction. Occasionally, approximately 1 or 2 out of every 15 patients will lose fluid in excess of their baseline extracellular fluid and develop postural hypotension and even shock. 40 The setting for this may be patients with massive postrelief saline diuresis, those with enormous elevations of BUN (>75 mg/dl), or those who have received inappropriate amounts of intravenous glucose in water, in hopes that this erroneous treatment may restore urine flow. It is important to recognize that prominent natriuresis may occur but is frequently absent in patients exhibiting osmotic diuresis (retained urea, or previously administered glucose or mannitol). Patients presenting large volumes of saline diuresis after relief of obstruction may harbor tubular defects in sodium and water reabsorption as a result of tubular dilatation or intrarenal humoral changes (vide supra). It is important to keep in mind that even after release of obstruction, patients exhibit defects in urine acidification and potassium excretion that may lead to clinically important systemic acidosis or hyperkalemia. 5 Magnesium losses leading to hypomagnesemia have also been described. 14 SUMMARY Urinary tract obstruction is a frequent cause of acute renal failure that is potentially life threatening but reversible, if it is promptly recognized

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and corrected. The level of urinary tract obstruction is variable, dependent on the underlying disease, and may range from the loop of Henle to the urethral meatus. Clinical manifestations are most commonly due to renal failure, but the history and physical examination can aid in d~termining the localization and cause of the obstruction. Laboratory findings may suggest urinary tract obstruction as the etiology for acute renal failure. Radiologic procedures, most prominently ultrasonography, can establish the diagnosis. Treatment is variable, but patient management may need to be altered during the postobstructive phase of urinary tract obstruction owing to physiologic response to reestablishment of urine flow.

REFERENCES 1. Abramson M, Jackson B: Hypertension and unilateral hydronephrosis. J Urol 132(4):746, 1984 2. Astoin M: Response dn flux sanguin renal a r elevation de la pression ureterale. J Physiol (Paris) 58:201, 1966 3. Baetz-Greenwalt B, Debaz B, Kumar ML: Bladder fungus ball: A reversible cause of neonatal obstructive uropathy. Pediatrics 81(6):826, 1988 4. Banks RO, Jacobson EO: Renal vasodilation with ureteral occlusion and prostaglandins: Attenuation by histamine HI antagonists. Am J PhysioI149:F851, 1985 5. Battle DC, Arruda JAL, Kurtzman NA: Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy. N Engl J Med 304:373, 1981 6. Baud FJ, Galliot M, Astier A, et al: Treatment of ethylene glycol poisoning with intravenous 4-methylpyrazole. N Engl J Med 319(2):97, 1988 7. Benabe J, Martinez-Maldonado M: Hypercalcemia nephropathy. Arch Intern Med 138:777, 1978 8. Bennan LB, Schreiner GE, Feys J: The nephrotoxic lesion of ethylene glycol. Ann Intern Med 46:611, 1957 9. Blantz RC, Konnen KS, Tucker BJ: Glomerular filtration response to elevated ureteral pressure in both the hydropenic and the plasma-expanded rat. Circ Res 37:819, 1975 10. Brenner BM, Ichikawa I, Deen WM: Glomerular filtration. In The Kidney, vol 1. Philadelphia, WB Saunders, 1981, p 289 11. Cohen LF, Balow JE, Magrath IT, et al: Acute tumor lysis syudrome. Am J Med 68:486, 1980 12. Crittenden DR, Ackermann GL: Hyperuricemic acute renal failure in disseminated carcinoma. Arch Intern Med 137:97, 1977 13. Dal Canton A, Stanziale R, Corradi A, et al: Effects of acute ureteral obstruction on glomerular hemodynamics in rat kidney. Kidney Int 12:403, 1977 14. Davis BD, Preuss HG, Murdaugh HV: Hypomagnesemia following the diuresis of postrenal obstruction and renal transplant. Nephron 14:275, 1975 15. DeFronzo RA, Humphrey RL, Weight JR, et al: Acute renal failure in multiple myeloma. Medicine 54:209, 1975 16. Denton T, Cochlin DL, Evans C: The value of ultrasound in previously undiagnosed renal failure. Br J Radiol 57(680):673, 1984 17. Eknoyan G, Qunibi WY, Grisson RT, et al: Renal papillary necrosis: An update. Medicine 61:55, 1982 18. Eknoyan G, Suki WN, Martinez-Maldonado M, et al: A chronic hydronephrosis: Observations on the mechanism of the defect in urine concentration. Proc Soc Exp BioI Med 134:634, 1970 19. Emmerson B, Gout T: Uric acid and renal disease. Med J Aust 1:403, 1976 20. Fer MF, McKinney TO, Richardson RL, et al: Cancer and the kidney: Renal complications of neoplasms. Am J Med 71:704, 1981 21. Gabow PA, Clay K, Sullivan JB, et al: Organic acids in ethylene glycol intoxication. Ann Intern Med 105:16, 1986

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