Vitamin lead nephropathy

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Several adulterants added to nonherbal supplements, vitamins, and herbal medicine preparations can cause renal dysfunction and renal failure. Aristolochic acid is used as a herbal remedy for weight loss and has been reported to cause Chinese herb nephropathy characterized by extensive interstitial fibrosis with tubular atrophy and loss. Herbal medicine preparations produced in South Asia contain potentially harmful levels of lead, mercury, and/or arsenic which can lead to renal toxicity. 

Oral phosphate administration leading to renal calcium phosphate precipitation has been described in children with X-linked hypophosphatemic rickets. Children with this condition are treated with oral phosphate and vitamin D and frequently developed ultrasonographic evidence of nephrocalcinosis, and the grade of nephrocalcinosis correlates with cumulative phosphate intake [46]. Renal biopsy findings are similar to those seen in acute phosphate nephropathy, with calcifications confined to tubules and the peritubular interstitium [47]. 

While strong evidence exists implicating cadmium as a major causative factor in itai-itai disease, other factors, such dietary deficiencies in minerals and vitamins, may have contributed to the disease (Tsuchiya 1978 Kjellstrom 1986). Serum la,25(OH)2-vitamin D concentrations were depressed in cadmium-exposed cohorts presenting with clinical nephropathy (Nogawa et al. 1987), which suggests that cadmium-induced bone effects may result from disruption of vitamin D and parathyroid hormone metabolism. Because kidney injury results from chronic cadmium exposure, a cadmium-related inhibition of the renal conversion of 25(OH)-vitamin D to la,25(OH)2 Vitamin D may lead to decreased calcium reabsorption, demineralization of bone, and eventually osteomalacia (Friberg et al. 1986). 

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