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 language | English (US) |
|---|---|
| Pages (from-to) | 1159-1163 |
| Number of pages | 5 |
| Journal | Kidney International |
| Volume | 38 |
| Issue number | 6 |
| State | Published - Dec 1990 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Nephrology
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Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism. / Don, Burl R; Schambelan, Morris.
In: Kidney International, Vol. 38, No. 6, 12.1990, p. 1159-1163.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism
AU - Don, Burl R
AU - Schambelan, Morris
PY - 1990/12
Y1 - 1990/12
N2 - 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.
AB - 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.
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M3 - Article
C2 - 2074657
AN - SCOPUS:0025251151
VL - 38
SP - 1159
EP - 1163
JO - Kidney International
JF - Kidney International
SN - 0085-2538
IS - 6
ER -