Diabetic nephropathy and Vitamin D: A narrative review

Diabetic nephropathy is a major complication of diabetes and a leading cause of chronic kidney disease and end-stage renal disease. This review explains that the disease develops through multiple interacting mechanisms, including hyperglycemia, intrarenal RAAS activation, inflammation, oxidative stress, podocyte injury, endothelial dysfunction, and progressive fibrosis, which together cause albuminuria and a decline in eGFR. Vitamin D deficiency is common in diabetic nephropathy and may worsen as kidney function declines. It describes how reduced sunlight exposure, poor dietary intake, obesity, proteinuria, tubular damage, and decreased renal activation of vitamin D all contribute to low vitamin D status in these patients. Vitamin D may have renoprotective effects by suppressing RAAS activity, reducing inflammatory cytokines, inhibiting fibrosis, preserving podocyte structure, and improving endothelial function. These mechanisms make vitamin D a biologically plausible adjunct in diabetic kidney disease, but the strongest evidence remains experimental rather than definitive clinical proof. Vitamin D or vitamin D receptor activators may reduce albuminuria or proteinuria in some patients, especially when added to standard RAAS blockade. However, the evidence is inconsistent, and there is insufficient evidence that vitamin D therapy alone can reliably slow long-term eGFR decline, prevent kidney failure, or improve survival. Correcting vitamin D deficiency is reasonable in selected patients, especially those with CKD-MBD or clear deficiency, but vitamin D should remain an adjunct to established treatments for diabetic kidney disease rather than a replacement for proven therapies.