Nephrotic syndrome (NS) is a common paediatric kidney disease characterised by leakage of protein from the blood into the urine through damaged glomeruli. It is classically defined by nephrotic-range proteinuria (≥40 mg/m²/hour or urine protein/creatinine ratio ≥ 200 mg/mL or 3 + protein on urine dipstick), hypoalbuminaemia (<25 g/L) and edema. During NS, vitamin D-binding globulin (DBG), which binds up to 98% of the 25(OH)D and has a molecular weight less than that of albumin may be lost in the urine causing a low 25(OH)D.

Low levels of 25-hydroxycholecalciferol [25(OH)D] have been documented in NS patients during relapse due to the loss of both 25(OH)D and its binding protein in urine at this time. However, since most NS relapses are short lasting, these low levels do not reflect the steady state of body stores. Intracellular, vitamin D acts through the vitamin D receptor (VDR), a nuclear transcription factor to which vitamin D binds through the carboxyl-terminal ligand binding domain. Genetic sequence encoding VDR may differ producing polymorphic forms similar to the variants formed on digestion with restriction enzymes like ApaI and TaqI. A subset of VDR polymorphic variants are linked with decreased vitamin D activity and may result in increasing risk and tendency to several bone and endocrinal disorders.