Hyperkalemia in patients infected with the human immunodeficiency virus: Involvement of a systemic mechanism

Hyperkalemia in patients infected with the human immunodeficiency virus: Involvement of a systemic mechanism. Background The appearance of hyperkalemia has been described in human immunodeficiency virus (HIV)-positive patients treated with drugs with amiloride-like properties. Recent in vitro data suggest that individuals infected with HIV have alterations in transcellular K + transport. Methods With the objective of examining the presence of alterations in transmembrane K + equilibrium in HIV-positive patients, we designed a prospective, interventional study involving 10 HIV-positive individuals and 10 healthy controls, all with normal renal function. An infusion of L-arginine (6%, intravenously, in four 30-min periods at 50, 100, 200, and 300 ml/hr) was administered, and plasma and urine electrolytes, creatinine, pH and osmolality, total and fractional sodium and potassium excretion, transtubular potassium gradient, plasma insulin, renin, aldosterone, and cortisol were measured. Results A primary disturbance consisting of a significant rise in plasma [K + ] induced by L-arginine was detected in only the HIV patients but not in the controls ( P + redistribution origin of the hyperkalemia was supported by its rapid development (within 60 min) and the lack of significant differences between HIV-positive individuals and controls in the amount of K + excreted in the urine. The fact that the HIV-positive individuals had an inhibited aldosterone response to the increase in plasma K + suggested a putative mechanism for the deranged K + response. Conclusions These results reveal that HIV-infected individuals have a significant abnormality in systemic K + equilibrium. This abnormality, which leads to the development of hyperkalemia after the L-arginine challenge, may be related, in part, to a failure in the aldosterone response to hyperkalemia. These results provide a new basis for understanding the pathogenesis of hyperkalemia in HIV individuals, and demonstrate that the risk of HIV-associated hyperkalemia exists even in the absence of amiloride-mimicking drugs or overt hyporeninemic hypoaldosteronism.