Reflex Anuria from Unilateral Ureteral Obstruction

0022-5347 /80/1232-0265$02.00/0 Vol. 123, February Printed in U.S.A..

THE JOURNAL OF UROLOGY

Copyright© 1980 by The Williams & Wilkins Co.

REFLEX ANDRIA FROM UNILATERAL URETERAL OBSTRUCTION JOE D. HULL,* SUBHASH KUMAR

AND

PETER G. PLETKA

From the Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts

ABSTRACT

A 20-year-old woman had 18 hours of pain and anuria associated with a calcium oxalate stone impacted in the distal left ureter. The stone passed spontaneously and the urine output returned. There was no abnormality of the right kidney on excretory urography. We believe that this is a cause of reflex anuria not previously described. Severe pain may be the initiating event in this unusual but interesting syndrome and mechanisms proposed by previous authors are reviewed. DISCUSSION

Reflex anuria is cessation of urine output from both kidneys in response to irritation or trauma to 1 kidney or its ureter, or severely painful stimuli to other organs. I Mechanical obstruction of the ureters, acute intrinsic renal diseases and hypotensi.on as causes of anuria are not included in this definition. The mechanism of the reflex is poorly understood and 2 general theories have been advanced. The first is diffuse spasm of the intrarenal arterioles sufficient to abolish glomerular filtration. 2 The second postulates spasms of both ureters producing functional obstruction.I Both are considered to occur from severe pain. This syndrome is unusual and it is not known why an occasional patient, such as the one described herein, becomes anuric after calculous obstruction of only 1 ureter. CASE REPORT

A 20-year-old woman presented to the emergency room with a 16-hour history of anuria accompanied by dull pain in the left lower abdomen. The pain was constant and did not radiate. There were no other urinary complaints and she had had no desire to void. She was perfectly well before this episode and medical history was unremarkable. There was no history of psychiatric disease and the patient was not taking any medications. Her mother had had renal stones during childhood. The patient and her mother gave consistent histories. Physical examination revealed a mildly obese woman who was alert and cooperative. Pulse was 78 per minute, blood pressure was 120/80 mm. Hg and oral temperature was 37C. Examination of the abdomen revealed tenderness in the left lower quadrant only. It was soft and no organs or masses were palpable. Physical examination was otherwise normal and mental status and affect were appropriate. Complete blood count, electrolytes and serum calcium were normal. Blood urea nitrogen was 10 mg./dl. and serum creatinine was 1.0 mg./dl. A Foley catheter was inserted and only 2 ml. of urine were obtained. The specific gravity was 1.027 and there was no protein, sugar or acetone. Microscopic examination of the urine sediment showed 30 to 40 red and 1 to 2 white blood cells per high power field. A plain x-ray of the abdomen showed a 2 mm. radiopaque stone in the area of the left ureterovesical junction. The pain subsided during the next 2 hours and the patient began to void. An excretory urogram the next morning showed prompt excretion of the radio-contrast agent bilaterally from normal-sized kidneys. There was mild hydronephrosis and hydroureter on the left side. The density was indeed a stone at the left ureterovesical junction. Shortly thereafter she passed the stone and the pain disappeared. Analysis revealed calcium oxalate. Accepted for publication April 27, 1979. * Requests for reprints: Division of Renal Medicine, Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts 01605.

The mechanism of anuria following irritation or obstruction of 1 ureter has not been studied extensively or completely reproduced in animals. One proposed mechanism is reflex spasm of the renal vasculature. Hix has shown decreases in ipsilateral renal blood flow of 20 per cent following ureteral catheterization in conscious dogs. 2 When stressful stimuli were added ipsilateral renal blood flow decreased another 58 per cent and contralateral renal blood flow decreased 85 per cent. These effects were blocked with anesthetization, denervation of the ureter or transplantation of the kidney. This ureterorenal reflex was thought to involve sensory fibers from the ureter that communicate with renal efferent vasoconstrictor fibers. However, anuria was not produced. A study casting doubt on intense reflex spasm of the renal arterioles as the mechanism of anuria was that of Block and associates. 3 Electric stimulation of the renal nerves caused sufficient renal vasoconstriction to produce anuria or oliguria for only 70 minutes and renal blood flow returned to base line values in 1 to 2 hours despite continued stimulation. Shearlock and Howards described a young woman with a solitary kidney who had acute renal failure with anuria for 6 days without obvious cause. 4 Ureteral catheterization failed to induce urine flow, although the radio-contrast agent drained freely from the renal pelvis down to the bladder. They concluded that the anuria was produced by reflex spasm of the renal arterioles on angiography, which was supported by repeated demonstration of ureteral patency. Parker and associates reported on a 62-year-old man with unilateral anuria, which they considered to be caused by ureteral irritation from a passed calculus. 5 The evidence was ureteral patency on retrograde pyelography and decreased caliber of the cortical arterioles on renal angiography suggesting cortical ischemia. A second mechanism postulated for reflex anuria is paininduced spasm of the ureters causing functional ureteral obstruction. The only previously well documented case of bilateral reflex anuria thought to be caused by this mechanism was reported by Suzuki and associates. I A 10-year-old boy had unexpected anuric renal failure 11 days after resection of the right lobe of the liver for anaplastic sarcoma. Bilateral ureteral catheters were advanced to about 10 cm. from the ureteral orifices. Oliguria recurred 1 week later and was relieved promptly by antispasmodics. They concluded that bilateral upper ureteral spasm was induced by severe pain from leaking bile, blood or the abdominal drain. Catheterization-induced obstruction of the ureteral orifices producing anuria is not really included in the aforementioned definition of reflex anuria. Sirota and Narins reported on 3 patients who had anuric renal failure after bilateral ureteral catheterizations at retrograde pyelography during the investigation of renal calculi. 6 On repeat cystoscopy the cause of the anuria was found to be bullous edema of the ureteral orifices

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secondary to trauma, formaldehyde for catheter sterilization or the radio-contrast agent used for retrograde pyelography. These authors concluded that the anuria was caused by mechanical obstruction of the ureters and doubted the existence of reflex anuria as a real entity. A similar patient described by Wolf probably had mechanical ureteral obstruction, since anuric renal failure developed after bilateral ureteral catheterization and autopsy showed diffuse bilateral pyelonephritis and multiple small abscesses. 7 Unfortunately, no comment was made on ureteral patency. We believe that these 4 cases do not qualify as true cases ofreflex anuria since mechanical ureteral obstruction was documented in 3 and was probable in 1. The diagnosis of reflex anuria in our case depends heavily on the history. There was no overt evidence of psychiatric disease or motive for secondary gain. The patient did not request narcotics, hospitalization, insurance or compensation benefits, or permission for time off from work. Like many disorders in internal medicine, our diagnosis is based on a seemingly reliable history. The mechanism of prolonged anuria in our case could have been either intense constriction of the renal vasculature or bilateral ureteral spasm from the pain caused by impaction of the stone in the distal left ureter. Because of the short duration of anuria and normal renal function after presenting to us neither renal angiography nor ureteral catheterization was indicated to differentiate further between the 2 possibilities. Although reflex anuria is an unusual clinical event it is sometimes associated with acute renal failure and uremia. It may be diagnosed more often with increased awareness of the entity. It also is potentially treatable if owing to bilateral ureteral spasm since ureteral catheterization or antispasmodics may reverse the anuria. REFERENCES 1. Suzuki, T., Komuta, H. and Tsuchiya, R.: Postrenal reflex anuria.

Arch. Jap. Chir., 35: 421, 1966. 2. Hix, E. L.: Uretero-renal reflex facilitating renal vasoconstrictor responses to emotional stress. Amer. J. Physiol., 192: 191, 1958. 3. Block, M.A., Wakim, K. G. and Mann, F. C.: Renal function during

stimulation ofrenal nerves. Amer. J. Physiol., 169: 670, 1952. 4. Shearlock, K. T. and Howards, S. S.: Post-obstructive anuria: a documented entity. J. Urol., 115: 212, 1976. 5. Parker, R. M., Basch, R. I. and Harrison, J. H.: Unilateral vasoconstrictive anuria. Surg., Gynec. & Obst., 127: 66, 1968. 6. Sirota, J. H. and Narins, L.: Acute urinary suppression after ureteral catheterization: the pathogenesis of "reflex anuria'-'. New Engl. J. Med., 257: 1111, 1957. 7. Wolf, G. A., Jr.: Mechanism ofreflex anuria. Ann. Intern. Med., 23: 99, 1945.

EDITORIAL COMMENT Reflex anuria from irritation to 1 side of the upper urinary tract, which causes oliguria or anuria on the other side, is a fascinating topic that has never been "nailed down" on an experimental basis. It does exist, although it must be a rare occurrence. In this interesting article on reflex anuria owing to unilateral ureteral obstruction the authors have given us a clear, clinical account of an event that does not otherwise seem easily explained. It is, indeed, a tantalizing and interesting description. In 1950 in the experimental laboratories at the Brady Urological Institute we described decreased renal function after ice water or a tourniquet was applied to 1 hind leg in dogs and monkeys. 1 The curious thing about those experiments was that they were not always consistent and yet usually with that type of stimulus the kidney on the same side as the stimulus to the extremity became oliguric. This was followed subsequently by oliguria or anuria in the opposite kidney. Decreases in glomerular and tubular function usually were parallel and we thought that these changes were probably owing to a neurovascular mechanism. If that is so, it is reasonable to think that 1 injured kidney can signal its distress to the opposite side, which then temporarily goes into neurovascular anuria.

Willard E. Goodwin Division of Urology UCLA School of Medicine Los Angeles, California 1. Goodwin, W. E., Harris, A. P. and Scott, W.W.: Effects of peripheral

stimuli on divided renal function. Amer. J. Physiol., vol. 163, No. 3, December 1950.