Polyuria after Renal Transplantation: A Case Report and Review of Literature

Abstract

Polyuria is defined as a urine output (UOP) of more than 3 litres per day in adults or 2 l/m2/day in children. Polyuria is common following live donor kidney transplantation (LDKT). This case report and review describes a 32-year-old male with chronic kidney disease who underwent LDKT. The donor was his brother. He had polyuria in the postoperative period with the maximum urine flow rate of 3700 ml/hr and the first 24-hour urine output of 42 litres. He was managed with intravenous crystalloid solutions guided by the central venous pressure and the mean arterial pressure. Electrolytes were replaced with potassium chloride, calcium gluconate and magnesium sulfate. He made an uneventful recovery. The Polyuria improved without any pharmacological interventions. Therefore, guided fluid and electrolyte administration is the key to the successful management of post-transplant polyuria.

Conn´s syndrome after kidney transplantation

“…Conn's syndrome, a unilateral aldosterone-producing adenoma, is defined as excessive and relatively autonomous aldosterone production escaping regulation by the renin-angiotensin-aldosterone system. The incidence of Conn's syndrome in the early period after kidney transplantation is low; it is usually an unrecognized cause of arterial hypertension before kidney transplantation (9,18). Diagnosis of Conn's syndrome in patients with end-stage renal failure and in the early period after renal transplantation is problematic because of low glomerular filtration rate in patients with end-stage renal failure and immunosuppression together with loop diuretic, and possibly potassium-restricted dietary habits prior to the transplantation period, may mask the effect of hyperaldosteronemia on potassium, which, together with arterial hypertension, is crucial for the suspicion of Conn's syndrome.…”

“…Protracted cold ischemia may be the cause of acute tubular necrosis. Activation of the renin-angiotensin-aldosterone system (RAAS) leads to decreased glomerular filtration and fluid retention, resulting in com-pensatory suppression of RAAS activity with subsequent polyuria leading to hyponatremia, hypokalaemia, hypomagnesaemia, and hypophosphatemia (9). Renal tubular acidosis (RTA) represents a disorder of transport mechanisms at the tubular level.…”