Batlle D C, Arruda J A, Kurtzman N A
N Engl J Med. 1981 Feb 12;304(7):373-80. doi: 10.1056/NEJM198102123040701.
We studied renal function in 13 patients with obstructive uropathy and hyperkalemic metabolic acidosis to characterize the pathogenesis of this disorder. Base-line fractional potassium excretion was lower in all patients than in controls with similar glomerular filtration rates. Acetazolamide was given to 11 patients but failed to increase fractional potassium excretion to normal. In five patients, impaired potassium excretion was associated with decreased ammonium excretion, a urinary pH below 5.5 (5.18 +/- 0.07, mean +/- S.E.M.), and aldosterone deficiency. In the remaining eight patients, the urinary pH did not fall below 5.5 (6.4 +/- 0.2) with acidosis, and we failed to lower the urinary pH and increase fractional potassium excretion to normal by administering a mineralocorticoid and sodium sulfate. A syndrome of hyperkalemic distal renal tubular acidosis may occur in patients with obstructive uropathy. In some patients, this syndrome results from a defect in hydrogen and potassium secretion in the distal nephron rather than from aldosterone deficiency. Obstructive uropathy should be included in the differential diagnosis of hyperkalemic acidosis and renal insufficiency.
我们对13例梗阻性尿路病合并高钾血症性代谢性酸中毒患者的肾功能进行了研究，以明确该疾病的发病机制。所有患者的基础钾排泄分数均低于肾小球滤过率相似的对照组。11例患者给予乙酰唑胺，但未能使钾排泄分数增加至正常水平。5例患者钾排泄受损与铵排泄减少、尿pH值低于5.5（5.18±0.07，均值±标准误）以及醛固酮缺乏有关。其余8例患者酸中毒时尿pH值未降至5.5以下（6.4±0.2），给予盐皮质激素和硫酸钠后，我们未能使尿pH值降低并使钾排泄分数增加至正常水平。梗阻性尿路病患者可能会发生高钾血症性远端肾小管酸中毒综合征。在一些患者中，该综合征是由远端肾单位氢和钾分泌缺陷引起，而非醛固酮缺乏所致。梗阻性尿路病应列入高钾血症性酸中毒和肾功能不全的鉴别诊断中。
