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昆士兰州慢性铅肾病的病理学及发病机制

The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.

作者信息

Inglis J A, Henderson D A, Emmerson B T

出版信息

J Pathol. 1978 Feb;124(2):65-76. doi: 10.1002/path.1711240202.

Abstract

Many children who suffered acute lead poisoning in Queensland eventually died with contracted kidneys. In most cases the kidneys were granular and showed microscopically fibrosis, hypertensive vascular changes and "alterative glomerulitis". Clinically in these patients, hypertension and chronic renal insufficiency had always preceded death which was usually due to uraemia. In a minority of cases the kidneys showed the changes of benign hypertension but were unusually small; fibrosis and "alterative glomerulitis" were not present. Clinically these patients had had hypertension but minimal renal insufficiency and death was usually due to cerebral haemorrhage. The evidence indicates that lead caused severe damage to the kidney at the time of the lead intoxication by some mechanism other than hypertension. The sequence of events postulated comprises severe renal damage with destruction of glomeruli during childhood lead poisoning, disappearance of the destroyed tissue during childhood and adolescence, onset of hypertension in adolescence or early adult life, gradual onset and progress of chronic uraemia during which fibrosis and granularity developed. In milder cases the sequence is not complete because renal function has remained adequate.

摘要

昆士兰州许多遭受急性铅中毒的儿童最终死于肾萎缩。在大多数情况下,肾脏呈颗粒状,显微镜下可见纤维化、高血压性血管改变和“交替性肾小球肾炎”。临床上,这些患者在死亡前总是先出现高血压和慢性肾功能不全,死亡通常是由于尿毒症。在少数情况下,肾脏显示出良性高血压的变化,但体积异常小;不存在纤维化和“交替性肾小球肾炎”。临床上,这些患者有高血压,但肾功能不全较轻,死亡通常是由于脑出血。证据表明,铅中毒时,铅通过高血压以外的某种机制对肾脏造成了严重损害。推测的事件顺序包括儿童铅中毒期间肾小球破坏导致严重肾损伤,儿童期和青春期受损组织消失,青春期或成年早期出现高血压,慢性尿毒症逐渐发生并进展,在此期间出现纤维化和颗粒状。在较轻的病例中,由于肾功能一直保持正常,所以这个顺序并不完整。

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