Bilateral Renal Shutdown: A Rare Case of Reflex Anuria Causing Acute Kidney Injury

Introduction

Reflex anuria is classically defined as “cessation of urine output from both kidneys in response to irritation or trauma to 1 kidney or its ureter, or severely painful stimuli to the other pelvic organs” [1]. More recently, it has been characterized by 3 criteria: (1) a normal contralateral kidney that retains function after treatment of the affected kidney; (2) no underlying disease is found on further evaluation of the contralateral kidney; and (3) surgical intervention on the “shutdown” kidney does not restore function in either kidney.[2]

It is an exceedingly rare cause of acute kidney injury, most often reported in the context of urologic or gynecologic procedures. Due to its rarity and frequent misdiagnosis, its epidemiology is not well described. It is considered a functional, rather than a parenchymal, disorder and should be recognized and distinguished from other causes of AKI to ensure appropriate management [3]. Here, we present a case of reflex anuria causing AKI after pelvic surgery, serving as an important reminder of this underrecognized complication of urogynecologic procedures.

Case Report

A 68-year-old woman with a history of hypertension presented with decreased urine output less than 24 hours after undergoing total laparoscopic hysterectomy with bilateral salpingo-oophorectomy, laparoscopic sacrocolpopexy, and cystoscopy for uterovaginal prolapse at an outside facility. During a follow-up telephone visit conducted within 24 hours postoperatively, she reported minimal urine output from her catheter bag since discharge despite adequate oral fluid intake, along with abdominal distension and discomfort. She was advised to come to the clinic, where a bladder scan showed 91 mL of retained urine. A renal ultrasound was unremarkable. She was referred for hospital admission for further evaluation and management.

On presentation, her vital signs were normal: blood pressure 108/70 mmHg, heart rate 71 beats per minute, respiratory rate 16 breaths per minute, oxygen saturation 95%, and temperature 98.8°F (37.1°C). She weighed 87.1 kg with a BMI of 34.1 kg/m2. Physical examination showed moist mucous membranes, no pedal edema, mild abdominal distension with generalized tenderness, and clean surgical incision sites without erythema or purulence. Initial laboratory studies showed hyponatremia, azotemia, and an elevated serum creatinine of 3.6 mg/dL (baseline 0.92 mg/dL), along with leukocytosis. Urinalysis demonstrated proteinuria and microscopic hematuria (5 red blood cells/HPF) without casts. Nitrites, trace leukocyte esterase, and pyuria were also present, although without symptoms or signs of infection. Urine culture was negative at 48 hours. The urine protein-to-creatinine ratio was 3348 mg/g, corresponding to an estimated 3.4 g/day of proteinuria (Table 1). A non-contrast CT scan of the abdomen and pelvis demonstrated only expected postoperative changes without evidence of hydronephrosis (Figure 1).

She was started on isotonic intravenous fluids for suspected pre-renal AKI. Her Foley catheter was replaced, but it drained no urine. Her home antihypertensives (lisinopril and hydrochlorothiazide) were held, and empiric ceftriaxone was initiated due to concern for urinary tract infection. Cystoscopy with bilateral retrograde pyelogram was performed, revealing a normal-appearing bladder and unobstructed bilateral ureters, without evidence of extravasation or injury (Figure 2).

Despite continued intravenous hydration and empiric antibiotics, her serum creatinine levels continued to rise (Table 2). She passed only small amounts of dark urine initially, but her abdominal symptoms, leukocytosis, and hyponatremia gradually improved. Urine culture returned negative. One anaerobic blood culture bottle was positive but was deemed a contaminant.

Given the abrupt onset of anuria and rising creatinine in the absence of intraoperative hypotension, rapidly progressive glomerulonephritis was considered. A renal biopsy was subsequently performed and corticosteroids were initiated. Unfortunately, the biopsy was non-diagnostic due to a sampling error, as only the medulla was obtained, without cortical tissue (Figure 3). The medullary interstitium showed no significant hemorrhage, fibrosis, or necrosis (Figure 4), and tubular lumens contained scattered pigmented casts that stained strongly positive for hemoglobin and weakly positive for myoglobin. Congo red staining was negative for amyloid. Concurrent serologic studies, including C3, C4, ANA, and ANCA, were all negative. Corticosteroids were discontinued when no significant clinical improvement was observed. The patient was monitored closely and soon demonstrated increasing urine output. As urine output improved and creatinine levels declined, a repeat kidney biopsy was no longer considered.

Based on the clinical presentation and exclusion of other potential etiologies of AKI, reflex anuria was deemed the most likely diagnosis. Acute tubular necrosis (ATN) was initially suspected; however, the abrupt transition from a non-oliguric state to anuria within 24 hours, in the absence of perioperative hypotension or sepsis, made ATN less likely. Acute interstitial nephritis (AIN) was also considered due to postoperative ketorolac use; however, it is usually a non-oliguric disease occurring 1 to 2 weeks after exposure that presents with a stepwise increase in creatinine. She subsequently entered the polyuric phase of AKI, likely because of solute diuresis from severe azotemia, during which she developed hypomagnesemia, which was appropriately corrected. She was eventually discharged in stable condition with improved renal function. Follow-up 2 weeks later in the clinic showed her serum creatinine had normalized to 0.77 mg/dL, which was marginally below her documented baseline level (Table 2).

Discussion

Reflex anuria has been associated with unilateral ureteral obstruction [1,4,5] and most often occurs following procedures that directly or indirectly involve manipulation of the urinary tract. Reported triggers include prophylactic ureteral catheterization [6,7], retrograde pyelography [8,9], renal tumor embolization [10], and gynecological surgeries such as hysterectomy and myomectomy [11–13].

Although its pathogenesis is unclear, reflex anuria is generally believed to result from reflex spasm involving either the ureters or the intrarenal arterioles of both kidneys [1,3]. Vasospasm within the renal circulation leads to a marked reduction or complete cessation of glomerular filtration, whereas ureteral spasm causes urinary tract obstruction, resulting in hydronephrosis and an empty bladder. This phenomenon has been further classified based on the origin of the triggering stimulus, whether renal, ureteral, or from adjacent organs. The associated reflex pathways include neurovascular, ureterorenal, and radiated renovascular reflexes for renal arteriolar spasm, and the reno-ureteral, uretero-ureteral, and radiated ureteral reflexes for ureteral spasm [3].

Our patient demonstrated unobstructed ureters on cystoscopy and retrograde pyelography, making ureteral spasm from uretero-ureteral reflex unlikely. Instead, her presentation was most consistent with a ureterorenal reflex, in which direct stimulation of the pelvi-ureteral system during gynecologic surgery triggers reflex spasm of the intrarenal arterioles. This mechanism is rarely described in the literature, where most reported cases of reflex anuria involve ureteral spasm rather than renal vasoconstriction. The pigmented casts identified on biopsy further support a vasoconstrictive process, likely reflecting cellular debris from tubular injury secondary to prolonged intrarenal arteriolar spasm. Rhabdomyolysis and hemolysis were excluded given her normal total creatine kinase and bilirubin levels. Renal vein thrombosis was also considered less likely due to the absence of characteristic findings such as gross hematuria, flank pain, thrombocytopenia, or predisposing hypercoagulable conditions like nephrotic syndrome.

Although perioperative anesthesia and antibiotic records were unavailable, drug-induced nephrotoxicity was initially considered. A single exposure to certain medications can rarely cause abrupt and severe renal impairment as a hypersensitivity or idiosyncratic reaction. However, AIN typically presents days to weeks after exposure and is usually non-oliguric. More broadly, even when drug exposure results in dense AKI, a rapid transition from an anuric to a non-oliguric state within 24 hours would be unexpected. Extensive parenchymal or tubular injury would be anticipated to follow a prolonged clinical course and would not be expected to immediately produce urine, given that urine output is the first sign of renal recovery. In contrast, our patient exhibited abrupt postoperative anuria followed by rapid restoration of urine output despite a continued rise in serum creatinine, a pattern consistent with a functional renal process. On this basis, reflex anuria was deemed the most likely diagnosis.

Initial treatment of anuria typically involves diuretics such as furosemide and, in some cases, corticosteroids [3]. Further management should be guided by the suspected underlying mechanism. When ureteral spasm is implicated, bilateral ureteral stent placement may relieve obstruction and restore urine flow, while renal arterial vasospasm may benefit from vasoactive agents such as dopamine or phentolamine [3]. In all cases, medical management includes blood pressure control, fluid and electrolyte management, and renal replacement therapy when indicated. In our patient, intravenous methylprednisolone was administered on hospital days 3 and 4 due to concern of rapidly progressive glomerulonephritis. Because urine output failed to improve and serum creatinine continued to rise, steroids were discontinued and management shifted to supportive care. She subsequently developed spontaneous diuresis on hospital day 5. Hou et al [3] reviewed several cases of reflex anuria that resolved without invasive interventions, with the duration of anuria ranging from 13 hours to 8 days, and concluded that conservative treatment is a reasonable option in selected patients.

Following the post-oliguric phase of AKI, polyuria can occur. During this phase, close monitoring of volume status and correction of electrolyte abnormalities is essential. Our patient had 3 days of polyuria with associated electrolyte abnormalities that were subsequently corrected. This case highlights the importance of careful monitoring not only of renal function but also of fluid and electrolyte status during both the acute and recovery phases of reflex anuria.

Conclusions

This case highlights a rarely described mechanism of reflex anuria in which ureterorenal reflex–mediated renal arteriolar vasospasm appears to drive postoperative anuria. This variant is important to recognize because normal ureteral imaging results can obscure the diagnosis. Considering this functional etiology is essential when obstructive, parenchymal, and interstitial causes have been excluded. Increased awareness can enhance diagnostic accuracy, guide appropriate management, and optimize patient outcomes in similar clinical scenarios. Establishing a baseline preoperative creatinine and closely monitoring renal function and electrolyte disturbances are paramount during the perioperative period.