铅对生化配合基有强烈的亲合力,因此它可以作用于酶,并置换其必需的金属,调节其合成和阻止它与萃取物之间的相互作用。这些生化变化可导致接触动物和人类肾脏线粒体和内浆核网结构的改变。人类肾脏对慢性铅接触的反应可分成很多期;而核内包合体似乎只存在于第一期。 Dingwall-Fordyce和Lane(1963)的研究曾报告在蓄电池工厂严重地接触铅的退休工人很多死于脑血管意外。可惜这个研究没有报导关于肾脏病或高血压的发病情况。而其他研究则指出工人接触铅可引起肾脏病和高血压,但对接触情况未作详细说明。只有在注意监视管理的工厂,工人(虽然比非接触者吸收较多的铅,)可以避免发生肾脏病和血管改变的危险。 Sandstead等(1970)曾报告在9名铅中毒(其中一人患高血压)病人发现血浆高血压朊原酶活性降低和醛甾酮分泌减少。据此,虽然在铅接触者由于高血压或肾脏病可使血浆高血压朊原酶活性 Lead has a strong affinity for biochemical ligands, so it acts on the enzyme and displaces its essential metals, modulates its synthesis and prevents its interaction with the extract. These biochemical changes can lead to changes in the structure of mitochondria and endoplasmic reticulum in contact with animal and human kidneys. The response of human kidneys to chronic lead exposure can be divided into many phases; the inclusion of nucleosomes appears to exist only in the first phase. Research by Dingwall-Fordyce and Lane (1963) reported that many retired workers who had serious exposure to lead in the battery factory died of cerebrovascular accidents. Unfortunately, this study did not report on the incidence of kidney disease or hypertension. Other studies point out that workers exposed to lead can cause kidney disease and high blood pressure, but the details of exposure are not elaborated. Only in factories that monitor surveillance should workers (even though they absorb more lead than non-contact ones) to avoid the risk of kidney disease and vascular changes. Sandstead et al. (1970) reported reduced plasma prostatic enzyme activity and reduced aldosterone secretion in nine patients with lead poisoning, one of whom suffered from hypertension. Accordingly, although in patients with lead exposure because of hypertension or kidney disease can make plasma hypertensive prioninase activity