Rastogi S, Bayliss J M, Nascimento L, Arruda J A
Kidney Int. 1985 Nov;28(5):801-7. doi: 10.1038/ki.1985.201.
Furosemide increases urinary acidification in control subjects and in certain patients with normokalemic or hypokalemic distal renal tubular acidosis (RTA). We studied the effect of furosemide in 14 patients with hyperkalemic distal RTA. In a group of patients with pure selective aldosterone deficiency, furosemide increased net acid and K excretion in a fashion indistinguishable from controls. This effect of furosemide was observed both in the presence and in the absence of acute mineralocorticoid administration. In another group of patients with hyperkalemic distal RTA, furosemide failed to decrease urine pH and to increase net acid excretion despite acute mineralocorticoid administration. Plasma aldosterone was variable in this group in that some patients had appropriate levels of aldosterone for the degree of hyperkalemia, whereas in the other patients the levels were low. The failure of these patients to respond to furosemide, despite pharmacologic doses of mineralocorticoid, suggests that these patients had a defect in H+ secretion other than that attributable to aldosterone deficiency alone. To gain insight into the mechanism whereby furosemide increases urinary acidification, we studied control and amiloride-treated rats pretreated with mineralocorticoid. In response to furosemide, control rats had a significantly lower urine pH and higher net acid and K excretion than that observed in amiloride-treated rats. These data suggest that furosemide increases H+ and K excretion, at least in part, by creating a favorable electric gradient for secretion of these ions since these effects were blunted in presence of inhibition of distal Na transport by amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)
速尿可增加正常受试者以及某些患有正常血钾或低钾血症性远端肾小管酸中毒（RTA）患者的尿液酸化。我们研究了速尿对14例高血钾性远端RTA患者的影响。在一组单纯选择性醛固酮缺乏的患者中，速尿增加净酸和钾排泄的方式与对照组无明显差异。无论是否给予急性盐皮质激素，速尿均有此作用。在另一组高血钾性远端RTA患者中，尽管给予急性盐皮质激素，速尿仍未能降低尿液pH值和增加净酸排泄。该组患者血浆醛固酮水平各异，部分患者的醛固酮水平与高钾血症程度相符，而其他患者的醛固酮水平较低。尽管给予药理剂量的盐皮质激素，这些患者对速尿无反应，提示这些患者除醛固酮缺乏外，还存在H⁺分泌缺陷。为深入了解速尿增加尿液酸化的机制，我们研究了用盐皮质激素预处理的对照大鼠和用氨氯吡咪处理的大鼠。对速尿的反应中，对照大鼠的尿液pH值明显低于氨氯吡咪处理的大鼠，净酸和钾排泄更高。这些数据表明，速尿至少部分通过为这些离子的分泌创造有利的电化学梯度来增加H⁺和K排泄，因为在氨氯吡咪抑制远端钠转运时这些作用减弱。（摘要截选至250字）
