Hypertensive emergency in kidney transplant recipient with autosomal dominant polycystic kidney disease

Abstract

Background: Aldosterone agonist is used for calcineurin inhibitor (CNI)-induced hyperkalemia in kidney transplant recipient; however, it potentially causes uncontrolled blood pressure (BP). We report a hypertensive kidney transplant recipient with hyperkalemia resolved by aldosterone agonist. Case Description: A 65-year-old man with ESRD from type 2 diabetes mellitus underwent uneventful kidney transplantation. Tacrolimus and prophylaxis trimethoprim/sulfamethoxazole (TMP/SMZ) was started. He had persistent hyperkalemia with serum potassium (K) of 5.1-5.7 mmol/L and non-anion gap metabolic acidosis (NAGMA). BP was uncontrolled with average SBP and DBP of 180 and 60 mmHg, respectively (Figure 1). On posttransplant day 11, K increased up to 6.4 mmol/L even good urine output (UOP) of 1.6-2.2 L/day and serum creatinine (SCr) of 2.3 mg/dL from the pretransplant SCr of 10.31 mg/dL. In addition to low K diet, he was treated with sodium polystyrene sulfonate with several bowel movements; however, K still elevated. Therefore, fludrocortisone was started and K was normalized. BP medications were adjusted. Discussion: Tacrolimus causes distal tubular defect mimicking type 4 renal tubular acidosis (T4RTA) by inhibiting basolateral Na-K ATPase at the collecting duct causing impaired transepithelial K secretion from decreased sodium uptake. It also causes hypertension (HTN) from renal afferent arteriolar vasoconstriction and activation of Na-Cl cotransporter (NCC) in the distal collecting tubule (DCT) and subsequently HTN. Hyperkalemia in our patient is from tacrolimus since he had posttransplant hyperkalemia even with improving renal allograft function. TMP/SMX could contribute to hyperkalemia. Aldosterone agonist corrects hyperkalemia but causes uncontrolled BP. Conclusions: Uncontrolled HTN limits the utility of aldosterone agonist for the treatment of CNI-induced hyperkalemia. Since tacrolimus stimulates NCC, thiazide diuretics could potentially be used for BP control once renal allograft function is stable.