Reubi F C
Contrib Nephrol. 1978;10:1-14. doi: 10.1159/000401518.
Acute toxic nephropathy may be produced by a variety of poisons and drugs. Cellular poisons, such as mercuric bichloride, produce tubular necrosis. Many drugs induce an immunologically mediated response presenting as interstitial nephritis, glomerulonephritis or angiitis. Substances, which are not primarily nephrotoxic but induce dehydration, shock, hemolysis, rhabdomyolysis and/or electrolyte disturbances may also lead to secondary acute renal failure. Reduced renal blood flow, suppressed glomerular filtration, increased tubular pressure due to obstruction, and tubular leakage are responsible for the functional breakdown. In addition, specific tubular functions may be impaired. Complete or incomplete recovery is the rule.
急性中毒性肾病可由多种毒物和药物引起。细胞毒物，如二氯化汞，可导致肾小管坏死。许多药物会引发免疫介导反应，表现为间质性肾炎、肾小球肾炎或血管炎。并非主要具有肾毒性但可导致脱水、休克、溶血、横纹肌溶解和/或电解质紊乱的物质，也可能导致继发性急性肾衰竭。肾血流量减少、肾小球滤过受抑制、梗阻导致肾小管压力升高以及肾小管渗漏是功能衰竭的原因。此外，特定的肾小管功能可能受损。完全或不完全恢复是常见情况。
