Renal osteodystrophy is described by anomalies in bone turnover, mineralization, and bone volume. The impacts of treatment modalities for renal osteodystrophy on bone ought to be broken down as for these variations from the norm. The significant treatment modalities for renal osteodystrophy incorporate phosphate covers, nutrient D mixes, and calcimimetics. Aluminum-containing phosphate fasteners have been demonstrated to be poisonous to bone auxiliary to their impacts on bone turnover, mineralization, and bone volume. The utilization of calcium-based phosphate folios has been related with the advancement of adynamic bone ailment (low bone turnover), bone misfortune, and exacerbating of vascular calcifications. New nonaluminum, noncalcium phosphate folios have been created (sevelamer hydrochloride and lanthanum carbonate). These operators show a potential for development in bone turnover and bone volume. Patients with renal osteodystrophy are lacking in calcitriol and regularly in calcidiol. Calcidiol insufficiency has been undervalued and has the right to be tended to in the treatment of patients with renal osteodystrophy. Three significant remedial gatherings are accessible for the administration of ROD: phosphate folios (P-fasteners), nutrient D or nutrient D analogs, and calcimimetics.