The Recognition and Management of Acute High Output Renal Failure

Vol. 108, July Printed in U.S.A.

THE JOURNAL OF UROLOGY

Copyright © 1972 by The Williams & Wilkins Co.

THE RECOGNITION AND MANAGEMENT OF ACUTE HIGH OUTPUT RENAL FAILURE GERALD W. IRELAND

AND

ALEXANDER S. CASS

From the Department of Urology, St. Paul-Ramsey Hospital and Medical Center, St. Paul, and the Division of Urology, Department of Surgery, University of Minnesota Medical School, Minneapolis, Minnesota

Acute renal failure denotes loss of renal function with increasing azotemia. It is an ominous development and characteristically has followed many clinical situations associated with surgical, traumatic and toxic conditions with or without hypotension.1-7 Generally multiple factors are present. Acute renal failure is usually considered in association with oliguria or anuria with urinary volumes less than 400 to 600 ml. per day. N on-oliguric or high output renal failure is azotemia with normal or excessive urine output and has been reported previously in association with burns,8• 9 trauma10 • 11 and surgical procedures. 2· 12 · 13 Herein we review diagnostic measures and emphasize established therapeutic principles based on 8 cases of acute renal failure seen in 1969 and 1970, with normal or high urine outputs.

renal failure. Measurements of the blood level or urine level or urine/plasma ratio of waste products have been advocated. 14-17 Renal failure has been suspected with oliguria and the diagnosis based on assessment of the ability of the tubules to concentrate waste products or the ability of the kidney to conserve ions. Measurement of the urine volume is no clue to the detection of high output renal failure. We relied on serial determinations of serum creatinine, blood urea nitrogen (BUN), and serum and urine osmolality for the diagnosis. We considered a rising BUN and serum creatinine with loss of tubular concentration of the urine, indicated by a urine to serum osmolality ratio of close to 1 : 1, with urine volumes more than 600 ml. per day, to be diagnostic of high output renal failure. With these criteria 8 cases of non-oliguric acute renal failure have been recognized.

RECOGNITION OF CLINICAL PROBLEM

Several clinical studies have been reported, involving laboratory data to diagnose early acute

EXPERIENCE

The 8 patients included 6 men and 2 women, ranging in age from 28 to 68 years. Four cases were associated with major trauma, 2 cases with elective operations, 1 case with an emergency operation and 1 case with sepsis. There was a recognizable hypotensive period in 5 cases. No patient had penthrane anesthesia. The lowest daily urinary volume was 785 ml. The largest daily urinary volume was less than 4,000 ml. in 7 cases. One patient had an extreme diuresis with a 24-hour urinary volume of 34,600 ml. The maximum BUN ranged from 74 to 252 mg. per cent. The maximum serum creatinine ranged from 4.2 to 15.3 mg. per cent. The ratio of the urine osmolality to serum osmolality was close to 1: 1 in all cases. The serum osmolality is high because of retained waste products. The urinary level of sodium was 20 mEq. per L or less in 2 patients and 20 to 40 mEq. per L in 5. This urinary sodium loss is not as high as generally seen with oliguric renal failure. In addition, all patients had a marked reduction

Accepted for publication September 15, 1971. Read at annual meeting of American Urological Association, Chicago, Illinois, May 16-20, 1971. 1 Calodney, L. C.: Diagnosis and management of acute renal failure. Rocky Mt. Med. J., 67: 37, 1970. 2 Baxter, C. R. and Maynard, D. R.: Prevention and recognition of surgical renal complications. Olin. Anesth., 3: 322, 1968. 3 Kiley, J.E., Powers, S. R., Jr. and Beebe, R. T.: Acute renal failure: eighty cases of renal tubular necrosis. New Engl. J. Med., 262: 481, 1960. 4 Gillenwater, J. Y. and Westervelt, F. B., Jr.: Current concepts in the pathogenesis and management of acute renal failure. J. Ural., 101: 433, 1969. 6 Hollenberg, N. K., Adams, D. F., Oken, D. E., Abrams, H. L. and Merrill, J.P.: Acute renal failure due to nephrotoxins. Renal hemodynamic and angiographic studies in man. New Engl. J. Med., 282: 1329, 1970. 6 Stokes, J. M.: Diagnostic indices and postoperative renal failure. Arch. Surg., 97: 291, 1968. 7 Bull, G. M., Joekes, A. M. and Love, K. G.: Renal function studies in acute tubular necrosis. Olin. Sci., 9: 379, 1950. 8 Sevitt, S.: Distal tubular necrosis with little or no oliguria. J. Olin. Path., 9: 12, 1956. 9 Vertel, R. M. and Knochel, J. P.: Nonoliguric acute renal failure. J.A.M.A., 200: 598, 1967. 10 Baxter, C.R., Zedlitz, W. H. and Shires, G. T.: High output acute renal failure complicating traumatic injury. J. Trauma, 4: 567, 1964. 11 Snyder, R. D., McCall, D. M. and Hayes, M. A.: Functional defect in postoperative polyuric renal failure. Surg. Forum, 17: 19, 1966. 12 Gant, N. F., Jr., Whalley, P. J. and Baxter, C. R.: N onoliguric renal failure. Report of a case. Obst. Gynec., 34: 675, 1969. 13 Sullivan, M. B., Jr., Morgan, J.M. and Johnson, I. M.: Tubular necrosis with sustained urine output. J. Trauma, 4: 373, 1964.

14 Perlmutter, M., Grossman, S. L., Rothenberg, S. and Dobkin, G.: Urine-serum urea nitrogen ratio. Simple test of renal function in acute azotemia and oliguria. J .A.M.A., 170: 1533, 1959. 16 Malloy, P. J.: The early diagnosis of impaired postoperative renal function. Med. Bull. U. S. Army Europe, 20: 74, 1963. 16 Lindsay, R. M., Linton, A. L. and Langland, C. J.: Assessment of postoperative renal function. Lancet, 1: 978, 1965. 17 Bates, C. P., Pigott, H. W. and Stableforth, P. G.: Changes in blood-urea concentration after operation and their relation to the early diagnosis of acute renal failure. Brit. J. Surg., 67: 360, 1970.

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ACUTE HIGH OUTPUT RENAL FAILURE

in their endogenous creatinine clearance, range 14 to 44 L per 24 hours per 1.73 m2• This measurement returned towards normal with recovery. Only 3 patients had hyaline or granular casts in their urine but proteinuria and hematuria were common. Six patients were managed medically without dialysis. Two were managed with dialysis. One patient who would be subjected to dialysis with present management was managed medically. Seven patients recovered. Renal tissue was obtained from 3 patients for histological examination. Two cases are presented to illustrate management. One patient underwent dialysis and the other was managed medically. CASE REPORTS

Case 1. M. G., a 28-year-old man, had a compound fracture of the left distal humerus and a comminuted fracture of the left tibia and fibula. He had had a hypotensive period for 2 hours that responded to blood replacement. Initial treatment consisted of debridement and closure of the compound wound and simple fracture immobilization. The BUN was 10 mg. per cent and serum creatinine was 0.7 mg. per cent. On day 3 the BUN was 28 mg. per cent and serum creatinine was 1.3 mg. per cent. The patient seemed to be doing well. The urine output was more than 900 ml. daily. An autoanalyzer

laboratory screen on day 6 revealed a BUN of more than 100 mg. per cent and a serum uric acid of 19 mg. per cent. On day 8 the patient became acutely ill with dyspnea and bradycardia. A chest x-ray revealed pulmonary edema. Laboratory studies revealed BUN 180 mg. per cent, serum potassium 8.8 mEq. per L, serum creatinine 9.9 mg. per cent and weight 215 pounds. His usual weight was 180 pounds. He was started on hemodialysis within 1 hour to reduce the serum potassium and to remove fluid and correct the pulmonary edema. He underwent hemodialysis on days 8 and 9. After hemodialysis the BUN rapidly increased and the patient underwent peritoneal dialysis from days 14 to 17 without an increase in weight. Following this an extreme diuresis developed with a maximum urine output of 34,600 ml. on day 22. During diuresis careful and frequent monitoring of the serum electrolytes, central venous pressure, urine volume and electrolytes, and patient's weight was necessary. There was no response to pitressin therapy. The fluid replacement was slowed on day 23 and within 15 minutes the central venous pressure fell from 4 to 0, the blood pressure fell and tachycardia developed. This response was indicative of a reduced vascular volume and proved that treatment was not simply chasing the urine output. Subsequent to this the urine fell in a stepwise fashion (fig. 1). The creatinine clearance at 6 months was 134 L per 24 hours per 1.73 m 2 •

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Fm. 2. Case 2. Clinical course Case 2. E. P., a 32-year-old man, was admitted to the hospital after an automobile accident with blood pressure 85 systolic over O diastolic and pulse of 105 per minute. He had a positive peritoneal lavage. There were dullness and absent breath sounds over the right chest. He was given a right tube thoracostomy for treatment of a right hemopneumothorax. Abdominal exploration revealed multiple liver lacerations and a shattered right kidney. The liver lacerations were sutured and a T-tube was placed in the common bile duct. The right kidney was removed. The BUN was 15 mg. per cent and the serum creatinine was 2.2 mg. per cent. During the next several days he had a urine output never less than 900 ml. per 24 hours with a rising BUN to 127 mg. per cent and serum creatinine of 7.4 mg. per cent. The serum creatinine reached a peak on day 8 and the BUN reached a peak on day 11, then both resolved steadily to normal. At no time did the patient's weight increase. The serum creatinine and BUN were normal by day 30 and the creatinine clearance was 88 L per 24 hours per 1.73 m2 from the remaining kidney (fig. 2). This case demonstrates the progressive rise of the creatinine and BUN with a high urine output and poor tubular function. Typically the serum creatinine reaches a peak before the BUN. PATHOLOGY

The exact mechanisms of acute renal failure are controversial. Experimental and pathological evidence supports the mechanism of 1) tubular obstruc-

tion by casts of necrotic cells and blood or from interstitial edema, 18 2) excessive backflow of filtrate out of damaged tubules19 and 3) reduction of glomerular filtration secondary to reduced or absent renal cortical blood flow. 5 It is probable that the same mechanisms are involved in non-oliguric renal failure. In an organ like the kidney with numerous and complex functions, such as filtration, acid base balance, electrolyte balance and humoral function, it would not seem unreasonable to obtain a decrease or loss in some functional capacities while maintaining other functions relatively intact. Histologically the renal tubules show degeneration, regeneration, dilation and scattered crystals in the tubular lumens. The glomeruli look quite normal. In 1 specimen associated with sepsis, there were scattered areas of lymphocytic infiltration. The histology is similar to that seen in oliguric renal failure, although renal pathology in this situation is extremely variable (fig. 3). DISCUSSION

In cases of renal failure with oliguria or anuria there is reduction of renal blood flow and glomerular filtration, loss of tubular function and reduction or 18 Oliver, J., MacDowell, M. and Tracy, A.: The pathogenesis of acute renal failure associated with traumatic and toxic injury. Renal ischemia, nephrotoxic damage and the ischemuric episode. J. Clin. Invest., 30: 1307, 1951. 19 Bank, N., Muntz, B. F. and Aynedjian, H. S.: The role of "leakage" of tubular fluid in anuria due to mercury poisoning. J. Clin. Invest., 46: 695, 1967.

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ACUTE HIGH OUTPUT RENAL FAILURE

Fm. 3. Renal histology, high output renal failure. Tubular casts, crystals and dilation, tubular degeneration and regeneration, glomeruli normal. loss of urine output. With recovery there is first an increase in the renal blood flow and glomerular filtration rate, then an increase in the urine volume (even to diuresis) and lastly, a return of tubular function. For non-oliguric renal failure the same clinical pattern exists. The damage is not as severe and there is never such a great reduction in renal blood flow, glomerular filtration rate or tubular function and a non-concentrated urine continues to be produced. With recovery, the last to return towards normal are the tubular functions of water and electrolyte regulation. N on-oliguric renal failure is often clinically mild and requires only medical management. The dangers of management are gross overhydration and pulmonary edema, the unpredictable manner in which potassium is handled by these patients with danger of sudden hyperkalemia and the unwise use of nephrotoxic agents-such as mercurial diuretics and particularly renal toxic antibiotics. 1 • 10 For the less severely ill, high output renal failure, careful fluid and electrolyte balance, administration of glucose infusion to minimize protein breakdown, oral or rectal sodium polystyrene sulfonate (kayexalate) to control hyperkalemia and the use of oral or rectal sorbitol to remove excessive body fluids will often be sufficient.1· 4 • 20 Most important is the avoidance of overhydration and hyperkalemia. For the severely ill patient with a rapidly rising BUN and serum creatinine, dialysis should be considered and implemented early. There is no absolute chemical level of the BUN or serum creatinine at 20 Merrill, J. P.: Acute renal failure. J.A.M.A., 211: 289, 1970.

which dialysis is indicated. Dialysis is indicated when there is patient deterioration-particularly cerebral dysfunction-as manifested by confusion and disorientation. Other strong indications are pulmonary edema, pericardia! effusion, pericarditis or uncontrolled hyperkalemia. With early diagnosis the latter situations are avoidable by careful fluid balance and use of ion exchange resins. Uremia should not be allowed to develop. For the more severe case, the institution of dialysis makes management easier. A reasonable homeostasis is maintained and the complications of pulmonary edema, pericarditis, intestinal bleeding, consumptive coagulopathy, seizures, hyperkalemia and cardiac arrest are avoided. The protein in the diet can also be liberalized to 1 to 1.5 gm. per kg. body weight, and thus obtain a positive nitrogen balance early. SUMMARY

Eight cases of high output renal failure have been discussed. This condition is probably the most frequent form of renal failure. Diagnosis was based on increasing azotemia and decreasing tubular function. Pathologic tubular degeneration, regeneration, dilation and crystals have been demonstrated. Clinical awareness, the measurement of metabolic waste products and tubular function will establish diagnosis. With early diagnosis and management complications can be avoided. Dialysis should be instituted early in the severely ill patients. High output renal failure is similar to oliguric renal failure in its clinical associations, renal pathology and management.