Acute renal response to large doses of intravenous prednisolone in kidney homograft recipients and in normal subjects.
Year: 1971
Type: article
Abstract: The immediate renal response to large intravenous doses of prednisolone was studied in 18 kidney homograft recipients and in 6 normal subjects. Clearance rates of inulin (CIN), creatinine (CCR), p-aminohippurate (CPAH), and electrolytes were measured over 3 one-hour periods following intravenous infusion of prednisolone (1 Gm.) and compared with corresponding clearance rates after a placebo infusion. CIN, CCR, and CPAH rates and ( CCR CIN) ratios exhibited a substantial decrease during all collection periods following the infusion of prednisolone, both in the normal subjects and in the patients. Fractional excretion of potassium ( CK CIN) increased in a progressive fashion reaching peak values after 3 hours. Biphasic variations were observed in the fractional excretion of sodium ( CNA CIN); an increase during the first hour was followed by a decrease during the third hour. The changes in the fractional excretions of ultrafiltrable calcium ( CCa CIN), ultrafiltrable magnesium ( CMg CIN), and phosphorus ( CP CIN) were minimal. Normal subjects exhibited significant decreases in ( CCa CIN) and ( CMg CIN) following the infusion of prednisolone; there was no significant change in the patients. ( CP CIN) increased significantly both in the normal subjects and in the patients. These results indicate that acute suppression of kidney function is a general renal response to large doses of glucocorticoids. The marked decrease in the creatinine clearance ratio ( CCR CIN) observed after the administration of prednisolone is consistent with a depressed tubular secretion of creatinine and emphasizes the inadequacy of cCR as an indication of glomerular filtration rate (GFR) under conditions in which large doses of glucocorticoids are employed. © 1971.
Source: PubMed
Language: English
Subfield: Transplantation
Field: Medicine
Domain: Health Sciences
Open Access status: green
Funder: Max Kade Foundation
OpenAlex ID: W58644586