Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism

Burl R Don, Morris Schambelan

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Transient hyperkalemia has been reported to occur in patients with acute glomerulonephritis, but the pathogenetic mechanism has not been investigated systematically. We studied the mechanism of hyperkalemia (5.7 to 6.7 mmol/liter) in four men with post-infectious glomerulonephritis. All four patients had clinical findings consistent with acute glomerulonephritis (edema, hypertension, proteinuria, hematuria, and an elevated ASO titer) and a renal biopsy performed in three of the patients confirmed the diagnosis. In comparison to normal subjects (N = 18), plasma aldosterone (5.4 ± 1.6 vs. 22.8 ± 2.6 ng/dl, P < 0.005) and plasma renin activity (0.3 ± 0.2 vs. 4.3 ± 0.6 ng/ml/hr, P < 0.005) were reduced. Hyperkalemia resolved within one to two weeks in two patients as the nephritis resolved and diuresis ensued, and aldosterone and renin levels obtained at follow-up visits were normal. Hyperkalemia persisted despite furosemide-induced diuresis in the other two patients, but resolved with fludrocortisone treatment. Thus, hyperkalemia in patients with acute glomerulonephritis is a manifestation, in part, of hyporeninemic hypoaldosteronism. It is ameliorated by mineralocorticoid therapy and improves spontaneously with resolution of the glomerulonephritis.

Original languageEnglish (US)
Pages (from-to)1159-1163
Number of pages5
JournalKidney International
Volume38
Issue number6
StatePublished - Dec 1990
Externally publishedYes

ASJC Scopus subject areas

  • Nephrology

Fingerprint Dive into the research topics of 'Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism'. Together they form a unique fingerprint.

  • Cite this