Oliguria, anuria and urinary obstruction: Case

This male infant presents anuria with a palpable distended bladder and bilateral hydronephrosis, the classic presentation of posterior urethral valves complicated by an acute kidney injury and hyperkalaemia. The absence of any urine for 18 hours meets the anuria threshold of complete absence for 12 hours or more by the KDIGO criteria. The palpable suprapubic mass that does not empty with gentle pressure is a distended bladder, and the ultrasound confirms the lower tract obstruction with the dilated posterior urethra and the thick-walled bladder. The potassium of 6.7 mmol per litre with peaked T waves is immediately life-threatening, and the metabolic acidosis reflects the accumulating acid from the failing, obstructed kidney. [1]

Clinical findings

The pattern is that of a lower urinary tract obstruction from posterior urethral valves, complicated by an acute kidney injury with hyperkalaemia. The palpable distended bladder and the dilated posterior urethra on the ultrasound localise the obstruction to the bladder outlet, and the bilateral hydronephrosis confirms the upper tract effect of the raised pressure. The anuria, the elevated creatinine, and the hyperkalaemia confirm the acute kidney injury, and the peaked T waves on the ECG mark the immediate cardiac risk. The irritability and the tachypnoea reflect the metabolic acidosis and the uraemia. The diagnosis is posterior urethral valves, to be confirmed by a voiding cystourethrogram once the infant is stabilised. [6]

The differential at presentation includes the other causes of anuria in a male infant. A bilateral renal anomaly such as bilateral renal agenesis or severe bilateral renal dysplasia produces anuria but without a distended bladder and with absent or abnormal kidneys on the ultrasound. Acute tubular necrosis from a perinatal insult produces anuria but without the obstruction and with a normal-calibre urinary tract on the ultrasound. The palpable bladder and the dilated posterior urethra settle the differential in favour of posterior urethral valves, and the immediate management is the same regardless: the decompression of the obstruction. [6]

Investigations and diagnosis

The diagnosis is posterior urethral valves with an obstructive acute kidney injury and hyperkalaemia. The renal ultrasound confirms the bilateral hydronephrosis, the thick-walled bladder, and the dilated posterior urethra, and a voiding cystourethrogram, performed once the infant is stabilised and decompressed, confirms the valve by showing the abrupt transition from the dilated posterior urethra to the narrow anterior urethra. The bloods confirm the acute kidney injury and its complications: the creatinine is elevated, the potassium is life-threatening, and the venous gas shows the metabolic acidosis. A urine specimen is sent for culture once the catheter is draining, because the obstructed urinary tract is prone to infection. [6]

Management and outcome

The immediate priority is to relieve the obstruction and to treat the hyperkalaemia in parallel. A paediatric urethral catheter, 6 to 8 French, is passed to drain the retained urine and to relieve the obstruction, and the drainage of a large volume confirms the diagnosis. If the urethral catheter will not pass, the team escalates to a suprapubic catheter or urgent urology. The hyperkalaemia with ECG changes is treated with intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution over 5 to 10 minutes for the myocardial membrane stabilisation, followed by the insulin with glucose, the nebulised salbutamol, and the sodium bicarbonate to shift the potassium into the cells. [6]

After the decompression, the team monitors for the post-obstructive diuresis. Over the first 24 hours the infant's urine output rises to 14 mL per kg per hour, which is above the 3 mL per kg per hour threshold and marks a pathological post-obstructive diuresis. The team replaces approximately 50 to 75 percent of the previous hour's urine output with an isotonic fluid, monitoring the weight, the blood pressure, and the serum sodium and potassium every 6 to 12 hours, and the diuresis settles over three days as the tubules recover their concentrating ability. The full replacement of the urine output is avoided because it perpetuates the diuresis. [7]

The definitive management is the primary valve ablation by a paediatric urologist once the infant is stable, and the voiding cystourethrogram confirms the valve before the ablation. The discharge plan addresses the bladder and the bowel function, the avoidance of the urinary tract infections, and the structured nephrology follow-up. The family is counselled on the prognosis honestly, because the systematic review by Hafizar and colleagues shows that a substantial proportion of boys with posterior urethral valves progress to chronic kidney disease despite early ablation, and this infant is enrolled in life-long nephrology follow-up with serial blood pressure, creatinine, and urinalysis. [4]