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Background: Pediatric nephrotic syndrome is characterized by massive proteinuria, which facilitates the urinary loss of vitamin D-binding protein, leading to significant alterations in mineral metabolism and bone health. Objectives: This study aimed to quantify the prevalence of vitamin D deficiency and its relationship with calcium and phosphorus homeostasis in this specific population. Methods: We conducted a comprehensive cross-sectional evaluation of 75 pediatric patients, analyzing demographic, nutritional, and biochemical markers across various relapse categories. Inclusion criteria were 75 children aged 1 to 12 years admitted with a clinical and laboratory-confirmed diagnosis of nephrotic syndrome. To maintain the validity of the biochemical assessments, exclusion criteria were strictly applied to patients with pre-existing chronic kidney disease, those who had received high-dose vitamin D or calcium therapy within the previous ninety days, and children presenting with secondary causes of nephrotic syndrome or systemic bone disorders. Serum 25-hydroxyvitamin D levels were measured alongside serum calcium and phosphorus to determine the extent of metabolic disruption and the impact of disease activity on mineral status. Results: The analysis revealed a high prevalence of vitamin D deficiency (37.33 percent) and insufficiency (42.67 percent) among the participants. The Frequent Relapse group demonstrated the most severe depletion, with a mean serum level of 12.8 ng/mL (p less than 0.001). Statistical analysis confirmed a significant positive correlation between vitamin D and serum calcium (r=0.58, p less than 0.01), while a significant negative correlation was observed with serum phosphorus (r=-0.45, p less than 0.01). These findings suggest that the severity of vitamin D depletion is closely linked to the frequency of nephrotic episodes and the duration of the disease. Conclusion: The findings indicate that vitamin D depletion is a pervasive complication in pediatric nephrotic syndrome, directly influenced by disease chronicity and relapse frequency. The strong association with mineral imbalances suggests that current management protocols may be insufficient in addressing secondary metabolic bone disease. J Com Med Col Teachers’ Asso July 2026; 30(2): 107-111
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Islam et al. (2026) studied this question.
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