- Email: [email protected]
Postoperative nephropathy
POSTOPERATIVE C. SERVADIO,
M.D.
I. NISSENKORN, L. GOTLOIB,
NEPHROPATHY
M.D.
M.D.
From the Department of Urology and Renal Unit, Central Emek Hospital, Afula, Israel
ABSTRACT - Two unusual cases are described in which postoperative sodium-losing nephropathy developed. In 1 patient transient bicarbonate-losing and renal glucosuria deueloped. The mechanism of the marked diuresis involved is discussed, as well as the importance of early recognition of the condition and prompt and adequate treatment with accurate replacement offluids and electrolytes. Zf treated promptly and correctly, the condition is totally reversible; howeuer, incorrect treatment may result in death.
The transient excretion of large amounts of urine following release of mechanical obstruction of the urinary tract is fairly common in urologic practice, but true cases of postoperative salt-losing nephropathy rarely appear to be clinical problems. The phenomenon was first noted by Cushmey’ and has been described and investigated by others.2a A normal kidney protects the patient from gross diuresis appearing after relief of obstruction on the other side. Therefore, the condition appears only after relief of bilateral obstruction with a common pathologic condition (usually in the lower urinary tract), or in cases in which there is an obstructed solitary kidney. It occurs in cases of relatively acute and severe obstruction and with advanced but reversible renal failure. Although the phenomenon is considered uncommon, it should be routinely considered by the urologist since it may be fatal if not promptly recognized and properly treated; if treated correctly, however, it is completely reversible. Recently we have seen 2 cases of this condition, both with an interesting clinical history. Case Reports Case 1 A boy, aged fourteen years, was referred for incontinence and growth retardation. His mother had noted that he consumed large amounts of
UROLOGY
/ MARCH 1975 / VOLUME
V, NUMBER
3
liquids and passed large amounts of urine. She had been told years before that her son’s kidneys were severely affected, and there was nothing that could be done for them. The patient had the appearance of an eightyear-old child and was fairly intelligent. His blood pressure and pulse were normal. He was found to have a grossly distended bladder, with a residual urine of 1,800 ml. Urine was infected, with a specific gravity of 1.008. Blood hemoglobin was 12 Gm. per 100 ml. ; urea 79 mg. and creatinine 2 mg. per 100 ml. Creatinine clearance was 14.2 cc. per minute (corrected to 1.73 square millimeters of body surface). Intravenous pyelogram revealed a poor kidney visualization and excretion, with gross distention of bladder, ureters, and collecting system on both sides (Fig. 1A). Cystography revealed gross vesicoureteric reflux bilaterally (Fig. 1B). The urethra appeared to be normal. Cystoscopy confirmed the diagnosis of megacystis-megaureter syndrome. A corrective surgical procedure was planned which would not resort to external deviation of urine. At surgery both ureters were refashioned and reimplanted, with partial excision of the bladder. A T tube was left in each ureter proximal to the lower segment, which had been tailored to guarantee good drainage of the urine in the immediate postoperative period. The patient soon began to pass large amounts of urine on both
347
FIGURE 1. Case 1. (A) Dripinfusion pyelogram showing poorly functioning kidneys with severe dilatation of collecting system and enormously distended bladder. (B) C ystogram showing gross bilateral rejlux.
sides (Fig. 2). Diuresis reaci ccl 16.5 L. per twenty-four hours. The natriurc
FIGURE
dium.
348
2.
Case 1. Daily output 01’urine and so-
postoperatively it was found to be higher, up to 164 mg. per 100 ml. Gradually the amounts of urine decreased and by the tenth postoperative day dropped to the average preoperative level. Renal function had gradually improved. One year later the boy is still under medical care. Creatinine clearance rose rapidly to 26.6 cc. per minute (corrected to 1.73 square millimeter surface). Case 2
This sixty-eight-year-old man had an attack of acute renal colic on the left side. Findings on intravenous pyelography showed signs of acute obstruction of the left ureter, with a late nephrographic effect but no visualization of the ureter. There was no clear evidence of stone. The right side appeared to be completely normal. Apart from tenderness in the left loin, he was found to be in good general condition. Blood pressure was normal. Urine and blood analyses were within normal limits, including urea, creatinine, and electrolytes. He was given symptomatic medical treatment and kept under observation. The pain subsided within the first twenty-four hours. Repeated intravenous pyelography two days later revealed signs of recovery, with good excretion on the left side and no evidence of obstruction. However, there appeared to be a definite mass in the lower pole of the left kidney for which arteriography was subsequently performed. This examination clearly demonstrated a solitary cyst in the left kidney; no residual signs of obstruction of the left ureter were noted (Fig. 3A). Findings on renal angiography revealed a mass in the lower pole of the right kidney which appeared to be malignant and was not evident on the intravenous pyelogram (Fig. 3B). At surgery an abdominal incision was made, and the left kidney was explored. The cyst was
UROLOGY
/ MARCH1975
I VOLUMEV.
NUMBER3
FIGURE 3. Case 2. (‘4,) Left selective renal angiograin clearly demonstrating solitary cyst and patent ureter. (B) Right selectioe renal angiogram showing vascular mass in lower pole diagnosed a.s malignant tumor.
tlr(x di; identifit~d ;mtl txci?.c~l, al: solitary benign condition 1 3s c mf right sicle was then c,xplore(i and :hc kidney was found to be m;t igna rt. was removed. Histologic e\. mm; tio the diagnosis of carcinoma. The en procedrrre was unremarkab t’, w* th or variations in blood press1 I-e. soon after the operatiorr the 1Iat. practically anuric. A bladder c; thr serted; 80 mg. of firrosemide (La;ix‘
!Io
ilrtlav~,llollrl~.. with no change in urinary output. the patient had Fifteen I hours postoperatively passed onl!. 100 ml. of urine. His general physical condition, pulse, and blood pressure remained excellent . Isotope renogram showed definite signs of acute obstruction as the cause of anuria. An attempt was made to pass a catheter up into the left ureter; but it was found to be completely blocked approximately 7 cm. from the orifice. It became obvious that a small nonopaque calculus, which had caused the renal colic and complete obstruction on admission, had not passed spontaneously as assumed but had apparently remained in the ureter causing repeated obstruction and anuria. Less than twenty-four hours after the right nephrectomy the patient had a second surgical procedure. The left ureter was explored, and a small stone was found and removed from its lower third. As soon as the obstruction was relieved, while the patient was still on the operating table, he began to pass large amounts of urine. By the following day he had passed more than 20 L. and 65.7 Cm. of sodium chloride (Fig. 4). This continued for several days. Hourly measurements of excreted urine were made, and the loss of fluids and electrolytes was estimated by careful monitoring of blood and urine. This loss was replaced intravenously and. later on, orally. Diuresis gradually diminished and returned to normal by the eleventh day. The patient’s general physical condition and renal function were good. Blood urea was 59 mg. and blood creatinine 1.8 mg. per 100 ml. Creatinine clearance was 36.5 cc. per minute. Control renogram showed good function and renal excretion on the left side (Fig. 5). The patient was discharged and referred for radiotherapy. He has remained well. Comment
FIGURE
4.
Case 2. (A) Daily outpul of urine
sodium.
UROLOCY
/ MARCH1975
/
VOLUhIE’
NUMBER3
and
The number of reported and well-documented cases ofpostobstructive diuresis is not large which
:349
a
*
.
.
FIGURE 5. Zsotope renogram before hospital discharge showing normal pattern on left and absent kidney on right.
confirms that this is rarely a clinical problem. For the condition to develop, severe obstruction with advanced but potentially reversible renal failure is required. Our 2 cases exhibited the complete nephrologic picture. The first patient, whose body weight was only 20 Kg., reached a maximum daily urinary output of 16.5 L., with a natriuresis of 28 Gm. In Case 2 a daily urinary output of up to 20 L. with 15.7 Gm. of sodium chloride developed. In this patient a fourth factor probably played a major role in the massive diuresis, namely, the removal of the normally functioning contralateral kidney less than twenty-four hours before the release of the obstruction. As is well known from animal experiments and observations in human beings, the removal of one kidney is followed by a very rapid hypertrophy of the remaining kidney, with almost immediate and considerable increase in perfusion and glomerular filtration rate. This phenomenon has probably accentuated the diuretic and natriuretic effect of the normal mechanism of postobstructive diuresis described previously.
350
The mechanism of this massive natriuresis is not clear. Osmotic load (matter) has been claimed to be the driving force, but it does not explain the natriuretic pattern of postobstructive polyuria. Usually electrolytes represent a much higher percentage of urinary solute in patients with postobstructive nephropathy than in those with osmotic diuresis. Conversely, the massive natriuresis indicates that a decreased responsiveness to antidiuretic hormone cannot be the main factor. Sudden increase of glomerular filtration rate after release of urinary obstruction can lead to overload of the proximal tubule and to a marked decrease of the fractional reabsorption of sodium. Thus, the enormous increase of distal delivery (washout) overwhelms the distal reabsorption mechanism by means of rapid distal tubule flow rates, reduced medullary, and decreased responsiveness to antidiuretic hormone, leading to the exaggerated natriuresis. Nevertheless our findings in Case 1 in which transient proximal renal tubular acidosis developed because of bicarbonate-losing and a transient decrease of the renal threshold of glucose suggest that the proximal tubule active transport mechanisms may be affected because of the obstruction. It is interesting to speculate that possibly both the sudden increase of glomerular filtration rate and intrinsic alterations of the proximal tubule cells are at the origin of the postobstructive natriuretic nephropathy. Afula, Israel (DR. SERVADIO)
References 1. CUSHMEY, A. R.: The Secretion of Urine, New York, Longmans, Green and Co., 1917. 2. BRICKER,N. S., et al. : An abnormality in renal function resulting from urinary tract obstruction, Am. J. Med. 23: 554 (1957). 3. WITTE, M. H., SHORT, F. A., and HOLLANDER, Massive polyuria and natriuresis following relief of w.: urinary tract obstruction, Am. J. Med. 37: 329 (1964). 4. MASSRY, S. G., SCHAINUCK,L. J., GOLDSMITH, C., and SCHREINER, G. E.: Studies on the mechanism of diuresis after relief of urinary tract obstruction, Ann. Int. Med. 66: 149 (1967). 5. VAUGHN, E. D., and GILLENWATER, J. Y.: Diagnosis, characterization and management of postobstructive diuresis, J. Urol. 109: 286 (1973). 6. HOWARDS, S. S.: Postobstructive diuresis: a misunderstood phenomenon, ibid. 110: 537 (1973).
UROLOGY /
MARCH 1975 I VOLUME V, NUMBER 3
M.D.
I. NISSENKORN, L. GOTLOIB,
NEPHROPATHY
M.D.
M.D.
From the Department of Urology and Renal Unit, Central Emek Hospital, Afula, Israel
ABSTRACT - Two unusual cases are described in which postoperative sodium-losing nephropathy developed. In 1 patient transient bicarbonate-losing and renal glucosuria deueloped. The mechanism of the marked diuresis involved is discussed, as well as the importance of early recognition of the condition and prompt and adequate treatment with accurate replacement offluids and electrolytes. Zf treated promptly and correctly, the condition is totally reversible; howeuer, incorrect treatment may result in death.
The transient excretion of large amounts of urine following release of mechanical obstruction of the urinary tract is fairly common in urologic practice, but true cases of postoperative salt-losing nephropathy rarely appear to be clinical problems. The phenomenon was first noted by Cushmey’ and has been described and investigated by others.2a A normal kidney protects the patient from gross diuresis appearing after relief of obstruction on the other side. Therefore, the condition appears only after relief of bilateral obstruction with a common pathologic condition (usually in the lower urinary tract), or in cases in which there is an obstructed solitary kidney. It occurs in cases of relatively acute and severe obstruction and with advanced but reversible renal failure. Although the phenomenon is considered uncommon, it should be routinely considered by the urologist since it may be fatal if not promptly recognized and properly treated; if treated correctly, however, it is completely reversible. Recently we have seen 2 cases of this condition, both with an interesting clinical history. Case Reports Case 1 A boy, aged fourteen years, was referred for incontinence and growth retardation. His mother had noted that he consumed large amounts of
UROLOGY
/ MARCH 1975 / VOLUME
V, NUMBER
3
liquids and passed large amounts of urine. She had been told years before that her son’s kidneys were severely affected, and there was nothing that could be done for them. The patient had the appearance of an eightyear-old child and was fairly intelligent. His blood pressure and pulse were normal. He was found to have a grossly distended bladder, with a residual urine of 1,800 ml. Urine was infected, with a specific gravity of 1.008. Blood hemoglobin was 12 Gm. per 100 ml. ; urea 79 mg. and creatinine 2 mg. per 100 ml. Creatinine clearance was 14.2 cc. per minute (corrected to 1.73 square millimeters of body surface). Intravenous pyelogram revealed a poor kidney visualization and excretion, with gross distention of bladder, ureters, and collecting system on both sides (Fig. 1A). Cystography revealed gross vesicoureteric reflux bilaterally (Fig. 1B). The urethra appeared to be normal. Cystoscopy confirmed the diagnosis of megacystis-megaureter syndrome. A corrective surgical procedure was planned which would not resort to external deviation of urine. At surgery both ureters were refashioned and reimplanted, with partial excision of the bladder. A T tube was left in each ureter proximal to the lower segment, which had been tailored to guarantee good drainage of the urine in the immediate postoperative period. The patient soon began to pass large amounts of urine on both
347
FIGURE 1. Case 1. (A) Dripinfusion pyelogram showing poorly functioning kidneys with severe dilatation of collecting system and enormously distended bladder. (B) C ystogram showing gross bilateral rejlux.
sides (Fig. 2). Diuresis reaci ccl 16.5 L. per twenty-four hours. The natriurc
FIGURE
dium.
348
2.
Case 1. Daily output 01’urine and so-
postoperatively it was found to be higher, up to 164 mg. per 100 ml. Gradually the amounts of urine decreased and by the tenth postoperative day dropped to the average preoperative level. Renal function had gradually improved. One year later the boy is still under medical care. Creatinine clearance rose rapidly to 26.6 cc. per minute (corrected to 1.73 square millimeter surface). Case 2
This sixty-eight-year-old man had an attack of acute renal colic on the left side. Findings on intravenous pyelography showed signs of acute obstruction of the left ureter, with a late nephrographic effect but no visualization of the ureter. There was no clear evidence of stone. The right side appeared to be completely normal. Apart from tenderness in the left loin, he was found to be in good general condition. Blood pressure was normal. Urine and blood analyses were within normal limits, including urea, creatinine, and electrolytes. He was given symptomatic medical treatment and kept under observation. The pain subsided within the first twenty-four hours. Repeated intravenous pyelography two days later revealed signs of recovery, with good excretion on the left side and no evidence of obstruction. However, there appeared to be a definite mass in the lower pole of the left kidney for which arteriography was subsequently performed. This examination clearly demonstrated a solitary cyst in the left kidney; no residual signs of obstruction of the left ureter were noted (Fig. 3A). Findings on renal angiography revealed a mass in the lower pole of the right kidney which appeared to be malignant and was not evident on the intravenous pyelogram (Fig. 3B). At surgery an abdominal incision was made, and the left kidney was explored. The cyst was
UROLOGY
/ MARCH1975
I VOLUMEV.
NUMBER3
FIGURE 3. Case 2. (‘4,) Left selective renal angiograin clearly demonstrating solitary cyst and patent ureter. (B) Right selectioe renal angiogram showing vascular mass in lower pole diagnosed a.s malignant tumor.
tlr(x di; identifit~d ;mtl txci?.c~l, al: solitary benign condition 1 3s c mf right sicle was then c,xplore(i and :hc kidney was found to be m;t igna rt. was removed. Histologic e\. mm; tio the diagnosis of carcinoma. The en procedrrre was unremarkab t’, w* th or variations in blood press1 I-e. soon after the operatiorr the 1Iat. practically anuric. A bladder c; thr serted; 80 mg. of firrosemide (La;ix‘
!Io
ilrtlav~,llollrl~.. with no change in urinary output. the patient had Fifteen I hours postoperatively passed onl!. 100 ml. of urine. His general physical condition, pulse, and blood pressure remained excellent . Isotope renogram showed definite signs of acute obstruction as the cause of anuria. An attempt was made to pass a catheter up into the left ureter; but it was found to be completely blocked approximately 7 cm. from the orifice. It became obvious that a small nonopaque calculus, which had caused the renal colic and complete obstruction on admission, had not passed spontaneously as assumed but had apparently remained in the ureter causing repeated obstruction and anuria. Less than twenty-four hours after the right nephrectomy the patient had a second surgical procedure. The left ureter was explored, and a small stone was found and removed from its lower third. As soon as the obstruction was relieved, while the patient was still on the operating table, he began to pass large amounts of urine. By the following day he had passed more than 20 L. and 65.7 Cm. of sodium chloride (Fig. 4). This continued for several days. Hourly measurements of excreted urine were made, and the loss of fluids and electrolytes was estimated by careful monitoring of blood and urine. This loss was replaced intravenously and. later on, orally. Diuresis gradually diminished and returned to normal by the eleventh day. The patient’s general physical condition and renal function were good. Blood urea was 59 mg. and blood creatinine 1.8 mg. per 100 ml. Creatinine clearance was 36.5 cc. per minute. Control renogram showed good function and renal excretion on the left side (Fig. 5). The patient was discharged and referred for radiotherapy. He has remained well. Comment
FIGURE
4.
Case 2. (A) Daily outpul of urine
sodium.
UROLOCY
/ MARCH1975
/
VOLUhIE’
NUMBER3
and
The number of reported and well-documented cases ofpostobstructive diuresis is not large which
:349
a
*
.
.
FIGURE 5. Zsotope renogram before hospital discharge showing normal pattern on left and absent kidney on right.
confirms that this is rarely a clinical problem. For the condition to develop, severe obstruction with advanced but potentially reversible renal failure is required. Our 2 cases exhibited the complete nephrologic picture. The first patient, whose body weight was only 20 Kg., reached a maximum daily urinary output of 16.5 L., with a natriuresis of 28 Gm. In Case 2 a daily urinary output of up to 20 L. with 15.7 Gm. of sodium chloride developed. In this patient a fourth factor probably played a major role in the massive diuresis, namely, the removal of the normally functioning contralateral kidney less than twenty-four hours before the release of the obstruction. As is well known from animal experiments and observations in human beings, the removal of one kidney is followed by a very rapid hypertrophy of the remaining kidney, with almost immediate and considerable increase in perfusion and glomerular filtration rate. This phenomenon has probably accentuated the diuretic and natriuretic effect of the normal mechanism of postobstructive diuresis described previously.
350
The mechanism of this massive natriuresis is not clear. Osmotic load (matter) has been claimed to be the driving force, but it does not explain the natriuretic pattern of postobstructive polyuria. Usually electrolytes represent a much higher percentage of urinary solute in patients with postobstructive nephropathy than in those with osmotic diuresis. Conversely, the massive natriuresis indicates that a decreased responsiveness to antidiuretic hormone cannot be the main factor. Sudden increase of glomerular filtration rate after release of urinary obstruction can lead to overload of the proximal tubule and to a marked decrease of the fractional reabsorption of sodium. Thus, the enormous increase of distal delivery (washout) overwhelms the distal reabsorption mechanism by means of rapid distal tubule flow rates, reduced medullary, and decreased responsiveness to antidiuretic hormone, leading to the exaggerated natriuresis. Nevertheless our findings in Case 1 in which transient proximal renal tubular acidosis developed because of bicarbonate-losing and a transient decrease of the renal threshold of glucose suggest that the proximal tubule active transport mechanisms may be affected because of the obstruction. It is interesting to speculate that possibly both the sudden increase of glomerular filtration rate and intrinsic alterations of the proximal tubule cells are at the origin of the postobstructive natriuretic nephropathy. Afula, Israel (DR. SERVADIO)
References 1. CUSHMEY, A. R.: The Secretion of Urine, New York, Longmans, Green and Co., 1917. 2. BRICKER,N. S., et al. : An abnormality in renal function resulting from urinary tract obstruction, Am. J. Med. 23: 554 (1957). 3. WITTE, M. H., SHORT, F. A., and HOLLANDER, Massive polyuria and natriuresis following relief of w.: urinary tract obstruction, Am. J. Med. 37: 329 (1964). 4. MASSRY, S. G., SCHAINUCK,L. J., GOLDSMITH, C., and SCHREINER, G. E.: Studies on the mechanism of diuresis after relief of urinary tract obstruction, Ann. Int. Med. 66: 149 (1967). 5. VAUGHN, E. D., and GILLENWATER, J. Y.: Diagnosis, characterization and management of postobstructive diuresis, J. Urol. 109: 286 (1973). 6. HOWARDS, S. S.: Postobstructive diuresis: a misunderstood phenomenon, ibid. 110: 537 (1973).
UROLOGY /
MARCH 1975 I VOLUME V, NUMBER 3