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Diabetes mellitus accelerates vascular calcification (VC) and increases the risk of end-stage renal disease (ESRD). Nevertheless, the impact of VC in renal disease progression in type 2 diabetes mellitus (T2DM) is poorly understood. We addressed the effect of VC and mechanisms involved in renal dysfunction in a murine model of insulin resistance and obesity  (ob/ob) , comparing with their healthy littermates (C57BL/6). We analyzed VC and renal function in both mouse strains after challenging them with Vitamin D 3  (VitD 3 ). Although VitD 3  similarly increased serum calcium and induced bone disease in both strains, 24-hour urine volume and creatinine pronouncedly decreased only in  ob/ob  mice. Moreover,  ob/ob  increased urinary albumin/creatinine ratio (ACR), indicating kidney dysfunction. In parallel,  ob/ob  developed extensive intrarenal VC after VitD 3 . Coincidently with increased intrarenal vascular mineralization, our results demonstrated that Bone Morphogenetic Protein-2 (BMP-2) was highly expressed in these arteries exclusively in  ob/ob . These data depict a greater susceptibility of  ob/ob  mice to develop renal disease after VitD 3  in comparison to paired C57BL/6. In conclusion, this study unfolds novel mechanisms of progressive renal dysfunction in diabetes mellitus (DM) after VitD 3   in vivo  associated with increased intrarenal VC and highlights possible harmful effects of long-term supplementation of VitD 3  in this population.

Excessive cholecalciferol supplementation increases kidney dysfunction associated with intrarenal artery calcification in obese insulin-resistant mice