The effects of angiotensin converting enzyme inhibitors on potassium homeostasis in dialysis patients with and without residual renal function.

Hyperkalemia is exacerbated by angiotensin converting enzyme inhibitors (ACE-I). Distal potassium (K(+)) secretion is negligible in anuric patients. ACE-I therapy may reduce renal, peritoneal, and colonic K(+) losses. We examined the effect of ACE-I therapy on serum, urinary, and dialysate K(+) in a cross-section of peritoneal and hemodialysis patients. Serum, 24-h urine K(+), and peritoneal dialysate excretion K(+) levels were measured and the results were compared in the various dialysis and treatment groups. Eighty-one hemodialysis (HD) and 32 peritoneal dialysis (PD) patients were included. Serum K(+) in HD patients with no residual renal function (RRF) was higher in those receiving ACE-I therapy (P = 0.02). Serum K(+) levels in HD patients receiving ACE-I treatments with RRF was similar to that in oligoanuric HD patients not receiving an ACE-I. Urinary K(+) excretion was significantly reduced in those on ACE-I therapy versus those not on an ACE-I (P < 0.05). Mean serum K(+) was lower in PD versus HD patients (P < 0.05). PD patients with no RRF on ACE-I therapy had higher serum K(+) concentrations (P = 0.002) and dialysate K(+) excretion was lower (P = 0.05), in comparison with PD patients not on an ACE-I. PD patients with RRF on ACE-I therapy had higher serum K(+) concentrations compared with those not on ACE-I therapy (P = 0.03). Both urinary and dialysate K(+) excretion were reduced (P = 0.001 and P = 0.002, respectively). ACE-I therapy increases serum K(+) concentration in dialysis patients. PD patients have relatively lower serum K(+) levels compared with HD patients. In PD patients, ACE-I therapy reduces dialysate K(+). These changes may result from reduced peritoneal movement of K(+).