Don B R, Schambelan M
Medical Service, San Francisco General Hospital Medical Center, California.
Kidney Int. 1990 Dec;38(6):1159-63. doi: 10.1038/ki.1990.327.
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 less than 0.005) and plasma renin activity (0.3 +/- 0.2 vs. 4.3 +/- 0.6 ng/ml/hr, P less than 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.
据报道，急性肾小球肾炎患者可出现短暂性高钾血症，但发病机制尚未得到系统研究。我们研究了4例感染后肾小球肾炎男性患者高钾血症（5.7至6.7 mmol/升）的机制。所有4例患者的临床表现均符合急性肾小球肾炎（水肿、高血压、蛋白尿、血尿和抗链球菌溶血素O滴度升高），3例患者进行了肾活检，确诊了该病。与正常受试者（N = 18）相比，血浆醛固酮（5.4±1.6对22.8±2.6 ng/dl，P<0.005）和血浆肾素活性（0.3±0.2对4.3±0.6 ng/ml/hr，P<0.005）降低。随着肾炎消退和利尿，2例患者的高钾血症在1至2周内消退，随访时测得的醛固酮和肾素水平正常。另外2例患者尽管使用速尿诱导利尿，但高钾血症仍持续存在，但氟氢可的松治疗后消退。因此，急性肾小球肾炎患者的高钾血症部分是低肾素性低醛固酮血症的表现。通过盐皮质激素治疗可改善，随着肾小球肾炎的消退可自行改善。
