Transplant renal artery stenosis (TRAS) is a reversible cause of severe hypertension and graft dysfunction. Posterior reversible encephalopathy syndrome (PRES) in kidney transplant recipients is commonly attributed to calcineurin inhibitor (CNI) toxicity; however, the biochemical signatures of CNI toxicity and TRAS differ markedly. We report a 32-year-old woman, five months post-transplant, presenting with seizures, severe hypertension, and MRI-confirmed PRES. She exhibited hypokalaemia (2.6 mmol/L) and metabolic alkalosis (pH 7.50, bicarbonate 34 mmol/L)— findings less typical of tacrolimus toxicity, which more typically produces a Gordon-like physiology with hyperkalaemia and metabolic acidosis due to excess activity of the NCC (Na-Cl cotransporter). Doppler ultrasound and digital subtraction angiography confirmed TRAS. Percutaneous angioplasty resulted in rapid renal recovery. PRES with hypokalaemia should prompt evaluation for renovascular hypertension rather than tacrolimus toxicity.
Thanigasalan et al. (Tue,) studied this question.