Kaizu K, Uriu K
Kidney Center, University of Occupational and Environmental Health, School of Medicine.
Nihon Rinsho. 1995 Aug;53(8):2052-6.
The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
肾脏是易受重金属中毒影响的器官之一。全身负担和肾组织中的“饱和”水平是肾损伤发生的重要限制因素。急性或慢性接触多种重金属可导致肾小管间质性损伤，包括急性肾小管坏死、慢性肾小管间质性肾炎、范科尼综合征、肾小管酸中毒以及无形态学改变的肾小管功能障碍。慢性镉中毒可导致伴有慢性肾小管间质性肾炎的不可逆范科尼综合征。尿低分子量蛋白排泄和尿镉排泄（大于200 - 400 ppm）都是慢性镉中毒时肾小管间质损伤最可靠的早期标志物。金属硫蛋白的作用对于理解镉诱导的肾病至关重要。儿童急性铅中毒可导致可逆性范科尼综合征。高血压、高尿酸血症和血清肌酐升高（无范科尼综合征）是成人慢性铅暴露的临床表现。近端肾小管细胞中的核内包涵体具有特征性。长期接触无机锗可导致慢性肾衰竭，且无尿液异常，这是由于肾小管变性和间质纤维化所致，主要发生在髓袢升支粗段和远曲小管。
