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硝苯地平诱发的肾功能障碍。肾血流动力学改变。

Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics.

作者信息

Diamond J R, Cheung J Y, Fang L S

出版信息

Am J Med. 1984 Nov;77(5):905-9. doi: 10.1016/0002-9343(84)90540-0.

Abstract

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.

摘要

硝苯地平导致4例慢性肾功能不全患者的肾功能出现急性、可逆性恶化。无低血压、临床病程、良性尿沉渣以及肾脏超声检查结果正常排除了急性肾小管坏死、肾盂肾炎、间质性肾炎、梗阻性尿路病和急性肾小球肾炎。据推测,这种慢钙通道阻滞剂在中度至重度肾功能损害的情况下产生了有害的肾内血流动力学改变。硝苯地平可能通过阻止钙进入肾血管平滑肌来改变肾功能,从而降低血管收缩激素在调节肾血流量和肾小球滤过率方面的功效。另一种解释是,硝苯地平可能抑制血管舒张性前列腺素E2的代偿性合成,这类似于在已有肾功能不全的患者中使用非甾体抗炎药导致肾功能急性恶化的临床观察结果。这些观察结果表明,临床医生在给有潜在肾功能不全的患者使用硝苯地平时应密切监测肾功能并谨慎用药。

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