Acute lead (Pb) exposure increases calcium oxalate crystallization in the inner medullary collecting duct, and is ameliorated by Ca/Mg-ATPase inhibition, as well as Capa receptor and SPoCk C knockdown in a Drosophila melanogaster model of nephrolithiasis.

Calcium oxalate (CaOx) kidney stones accumulate within the renal tubule due to high concentrations of insoluble deposits in the urine. Pb-induced Ca mobilization along with Pb-induced nephrotoxic effects within the proximal tubule have been well established; however, Pb mediated effects within the collecting duct remains insufficiently studied. Thus in vitro and ex vivo model systems were treated with increasing concentrations of lead (II) acetate (PbAc) ± sodium oxalate (NaCO) for 1 h, both individually and in combination.

Lead (Pb)-induced calcium oxalate crystallization ex vivo is ameliorated via inositol 1,4,5-trisphosphate receptor (InsPR) knockdown in a Drosophila melanogaster model of nephrolithiasis.

Nephrolithiasis causes severe pain and is a highly recurrent pathophysiological state. Calcium-containing stones, specifically calcium oxalate (CaOx), is the most common type accounting for approximately 75 % of stone composition. Genetic predisposition, gender, geographic region, diet, and low fluid intake all contribute to disease pathogenesis.