REFLEX ANURIA

Authors


Miles Nakaska, Department of Vascular Surgery, Staten Island University Hospital, 977 father capodanno bvld, Staten Island, NY 10306, USA. e-mail: milo_eyeworx@hotmail.com

INTRODUCTION

Anuria and acute renal failure (ARF) due to reflex anuria (RA) is a rare condition that occurs almost always after surgical procedures and manipulation of the ureter or bladder [1]. This rare condition has only been reported in the form of case presentations during pelvic surgery and colorectal procedures. However uncommon it may be, this article is devoted to describing RA as one of the causes of anuria that should be considered in the differential diagnosis of ARF.

PROBLEM

RA is defined as ‘cessation of urine output from both kidneys in response to irritation or trauma to one kidney or its ureter or severely painful stimuli to other organs’[1–4] The condition has been described in situations when there is unilateral ureteric obstruction, where the contralateral kidney was expected to retain its normal functions [5]. RA with ARF can also occur in instances where there was no organic obstruction, but ureteric manipulation was present during pelvic surgery [6]. In all instances, the anuria was accompanied by ARF as evidenced by a rise of serum creatinine. This rare condition must be differentiated from ARF secondary to pre-renal, renal or post-renal obstruction because ARF due to RA is related to a reflex mechanism leading to arteriolar vasoconstriction and ureteral spasm [5].

FREQUENCY

Exact data on the prevalence of RA is difficult to obtain. This is because this entity is very rare in the general population and very few reports exist [1,5,7]. Sirota and Narins [8] in 1954 were among the first to use the term ‘reflex anuria’ to describe the occurrence of anuria after urethral catheterization. Shearlock and Howards in 1976 described RA in a 32-year-old nurse who underwent a right nephrectomy because of xanthogranulomatous pyelonephritis. Retrograde pyelography and arteriography were normal, suggesting a reflex mechanism of renal arteriolar vasoconstriction for the cause of the anuria [9]. In 1979, Hull et al. defined RA in describing a case of anuria due to unilateral distal ureteric stone that resolved after removal of the stone. Since 1979, a handful of case reports have supported RA as a cause for ARF [1,3,5–7].

AETIOLOGY AND PATHOPHYSIOLOGY

Varying mechanisms have been proposed to explain RA. Those that support the concept of RA have proposed two mechanisms: neurovascular reflex resulting in profound arteriolar vasoconstriction, and bilateral ureteric spasm secondary to unilateral ureteric or renal parenchymal damage. The uretero-renal or reno-renal reflexes are examples of the neurovascular mechanism. The latter is supported by the case of RA resulting from unilateral chemoembolization of a renal tumour [7]. The uretero-renal reflex suggests that injury to one ureter can cause bilateral or contralateral renal arteriolar vasoconstriction. Several experimental studies have supported this neurovascular hypothesis. Di Salvo and Fell [10] demonstrated cessation of renal blood flow using pulsatile renal nerve stimulation. Francisco et al. [11] conducted the most analytical investigation using a canine model to show a 20% decrease in contralateral renal blood flow with unilateral ureteric obstruction.

The other neurovascular mechanism to explain RA is ureteric spasm or arteriolar intrarenal spasm, both associated with pain [2]. Suzuki et al. [12] reported a case where the patient had anuria after partial hepatectomy, which resolved with heavy diuresis after bilateral ureteric catheterization. In another case of RA reported by Maletz et al. [3], the positioning of a ureteric stent was followed by the disappearance of pain and the start of diuresis. These cases showed the possibility that anuria could be resolved with stopping ureteric spasm.

While there are many proponents of the neurovascular hypothesis, others have cited mechanical obstruction as the primary cause behind the anuria. In 1954, Sirota mentioned that vesico-ureteric obstruction due to oedema was the cause of the anuria after urethral catheterisation [8]. Stamey in 1974 described occurrence of anuria after urethral catheterization and suggested vesico-ureteric obstruction attributed to oedema [13]. Sheikh et al. [14] implicated ureteric obstruction as an important factor in anuria after the removal of prophylactic ureteric catheters in colon surgery. They demonstrated oedema of the uretero-vesicular orifices on cystoscopy, suggesting that anuria was due to an obstructive phenomenon. Leff et al. [15] cited oedema at the uretero-vesical junction as the cause of post-stent anuria.

PRESENTATION

Patients who present with RA usually have had a history of irritation or trauma to one kidney or its ureter or severe painful stimuli to other organs. History includes anuria (urine volume <20 mL daily) or oliguria that may occur after a surgical or pelvic procedure. It is also essential to ascertain whether the patient had any nephrotoxic agents, infection or dehydration. The diagnosis of RA is based on three criteria:

  • 1A normal contralateral kidney, which retains normal function soon after the disease causing non-functional kidney has been treated.
  • 2Subsequent investigation of the normal contralateral kidney shows that a pathological process is unlikely to have caused its loss of function.
  • 3Surgical intervention to the contralateral ‘shutdown’ kidney does not result in the return of function in either of the kidneys.

EVALUATION

LABORATORY STUDIES

Part of the preoperative clearance before any surgical procedures usually includes a full chemistry panel. The routine preoperative test should show normal serum creatinine (0.5–1.4 mg/dL). RA should be suspected with ARF post-procedure or a single ureteric obstruction accompanied by rise of serum creatinine levels. In addition, urine sediment and cytological studies should reveal no evidence of malignancy, acute tubular necrosis, glomerulonephritis or interstitial nephritis. Urine electrolytes should be sent for calculation of a fractional excretion of sodium. FENa may be found to be consistent with a post-renal pathology.

IMAGING STUDIES

The standard primary imaging study for RA is renal ultrasonography (US), which allows the provider to perform a real-time, 360° evaluation of both kidneys, ureters and bladder. Detailed evaluation should be done to detect any organic obstruction. US may show normal sized kidneys without evidence of hydronephrosis or hydroureter. US of the kidneys may also show bilateral moderate hydronephrosis, but cortical thickness and corticomedullary differentiation should be normal.

A 99mTc-DTPA can be performed to assess flow to the kidneys and drainage of the collecting system. The scan may show severely decreased flow to the kidneys in the perfusion phase and decreased parenchymal uptake. In late images, good parenchymal transit of activity can be seen with delayed drainage and increased background uptake. These findings are consistent with delayed drainage of the kidneys with relatively good glomerular filtration and early parenchymal uptake, suggesting post-renal pathology.

Voiding cystourethrography and retrograde pyelography can be used to show any mechanical obstruction to the ureters.

DIAGNOSTIC PROCEDURES

Cystoscopy and ureteroscopy should show no obvious signs of injury at the ureteric orifices. This procedure helps evaluate for any mechanical obstruction or inflammation to the ureters.

TREATMENT

MEDICAL THERAPY

Medical management for RA includes haemodialysis, control of hypertension and correction of fluid and electrolyte imbalance.

SURGICAL THERAPY

Several reports have described successful treatment of RA by insertion of bilateral ureteric stents. In the case report of Suzuki et al. [12] bilateral ureteric stent placement was shown to be effective, where the patient had anuria after partial hepatectomy, in whom bilateral ureteric catheterisation was followed by heavy diuresis.

FOLLOW-UP

Patients have had successful outcomes with RA after medical and surgical interventions. Diuresis was established with insertion of ureteric stents, and there was notable decrease in creatinine within days of treatment or intervention. For those who had stents, they were gradually removed in a graded fashion and at time of discharge had normal kidney function (serum creatinine, 1.4 mg/dL) and relatively good general condition.

CONFLICT OF INTEREST

None declared.

Ancillary