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 < 0.001 between groups). A K+ 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.
Fundación Jiménez Díaz, Hospital Clinico and Hospital 12 de Octubre, Universidad Autónoma, Madrid, Spain. ccaramelo@fjd.es
C
C
Caramelo
E
E
Bello
E
E
Ruiz
A
A
Rovira
R M
RM
Gazapo
J M
JM
Alcazar
N
N
Martell
L M
LM
Ruilope
S
S
Casado
M
M
Fernández Guerrero
D000328:Adult; D000450:Aldosterone / Q000097:blood; D001120:Arginine / Q000494:pharmacology; D005260:Female; D015658:HIV Infections / Q000097:blood*; D006801:Humans; D006947:Hyperkalemia / Q000150:complications*; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D011446:Prospective Studies; D012083:Renin / Q000097:blood
D000450:Aldosterone; D001120:Arginine; D012083:Renin; D011188:Potassium