ABSTRACT
Aminoglycoside nephrotoxicity in experimental animals can be reduced by calcium loading, inducing diabetes, and giving thyroid hormone, while a potassium deficient diet enhances aminoglycoside nephrotoxicity. This study investigated whether potassium loading protects against gentamicin nephrotoxicity in the rat. In part I, group GK ate a diet containing 3.5% potassium and drank 0.2 mol/L KCl. Pair-fed rats eating a standard diet, group G, ate a 1% potassium diet and drank water. After 10 days, each group received gentamicin subcutaneously, 60 mg/kg twice daily for 8 days. The control groups, K and C, received the high or normal potassium diet, respectively. To control for a protective effect from a high solute load, the effect of equimolar NaCl loading was studied in group GNa and Na. At the end of the 8 days of gentamicin, inulin clearance was significantly higher in GK compared with G(0.6 +/- 0.1 v 0.3 +/- 0.1 mL/min per 100 g body weight [BW], P less than 0.05), but group GNa (0.4 +/- 0.1 mL/min per 100 g BW) was not different from group G. Morphological studies demonstrated that potassium-loaded rats (group GK) had significantly less proximal tubular necrosis compared with rats on a standard potassium diet, group G. Sodium loading did not protect against cellular necrosis. Part II studied renal function, cortical Na,K-adenosine triphosphatase (ATPase) and gentamicin accumulation after 2 days of gentamicin to determine the early functional and biochemical effects of potassium loading before overt renal functional impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Gentamicins/toxicity , Kidney/drug effects , Potassium Chloride/pharmacology , Animals , Gentamicins/antagonists & inhibitors , Kidney Function Tests , Kidney Tubules, Proximal/pathology , Necrosis , Potassium Chloride/administration & dosage , Rats , Rats, Inbred Strains , Sodium Chloride/pharmacology , Sodium-Potassium-Exchanging ATPase/analysisABSTRACT
Infection with Herpesvirus hominis, often associated with oral ulceration, was found to be more frequent in patients with myeloproliferative and lymphoproliferative disorders than in normal populations or patients with other diseases. This increased frequency was not associated with any deficiency of the humoral antibody response, suggesting a possible impairment of cell-mediated immunity. The otherwise untreatable oral lesions appeared to respond effectively to local irradiation.
