Pharmacological blockade of the renin-angiotensin-aldosterone system (RAAS) is the cornerstone of renoprotective therapy, and the reduction of persistent RAAS activation is considered to be an important target in the treatment of chronic kidney disease (CKD). Vitamin D is a steroid hormone that controls a broad range of metabolic and cell regulatory functions. It acts as a transcription factor and can suppress the renin gene, thereby acting as a negative endocrine regulator of RAAS. RAAS activation can reduce renal Klotho expression, and the Klotho-fibroblast growth factor 23 interaction may further reduce the production of active vitamin D. Results from both clinical and experimental studies suggest that vitamin D therapy is associated with a reduction in blood pressure and left ventricular hypertrophy and improves cardiovascular outcomes. In addition, a reduction in angiotensin II through RAAS blockade may have anti-proteinuric and anti-fibrotic effects. Vitamin D has also been shown to modulate the immune system, regulate inflammatory responses, improve insulin sensitivity and reduce high-density lipoprotein cholesterol. Taken together, these pleiotropic effects of vitamin D may slow down the progression of CKD. In this review, we discuss the experimental and early clinical findings that suggest a renoprotective effect of vitamin D, thereby providing an additional rationale beyond mineral metabolism for the close monitoring of, and supplementation with vitamin D from the earliest stages of CKD.