Calcium lead nephropathy

Emmerson BT. Chronic lead nephropathy. The diagnostic use of calcium EDTA and the association with gout. Aust Med J 1963 12 310-324. 

Scinchez-Fructuoso Al, Blanco J, Montserrat C, Ortega L, Arroyo M, Fernandez C, Prats D, Barrientos A. Experimental lead nephropathy treatment with calcium disodium ethylenediaminetetraacetate. Am J Kidney Dis 2002 40 59-67. Scinchez-Fructuoso Al, Toralbo A, Arroyo M, Lunque M, Ruilope LM, Santos JL, Cruceyra A, Barrientos A. Occult lead intoxication as a cause of hypertension and renal failure. Nephrol Dial Transplant 1996 11 1775-1780. 

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]. 

III. Contraindications. Since calcium EDTA increases renal excretion of lead, anuria is a reiative contraindication. Accumuiation of EDTA increases the risk of nephropathy, espedaliy in voiume-depieted patients, in patients with moderate renal insufficienr, reduce the dose in reiative proportion to the deficit in creatinine clearance. The use of EDTA in conjunction with hemodialysis or hemofiltration has been reported in patients with renai faiiure. 

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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