25-hydroxyvitamin-d-2 and Nephrotic-Syndrome

Although abnormalities of calcium and vitamin D metabolism are recognized in children with nephrotic syndrome, longitudinal observations are not available in these patients during periods of relapse and remission. We report observations in 58 children (mean age 10.1 years) with nephrotic syndrome and normal glomerular filtration rate. Hypocalcemia, modest hyperparathyroidism, and strikingly low calcidiol levels were identified during episodes of relapse. Most alterations were transient, and normalized on remission. The plasma concentration of calcitriol, the most active metabolite of vitamin D, was found to be normal in both relapse and remission. In the presence of hypocalcemia and hyperparathyroidism, however, normal plasma calcitriol levels in relapse may be inappropriately low and reflect a state of relative deficiency. Concurrent glucocorticoid therapy did not modify the results. A corollary of our observations is that children with relapsing or protracted nephrotic syndrome are at risk of developing metabolic bone disease, even without impairment of glomerular filtration rate.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Adult; Calcium; Child; Child, Preschool; Ergocalciferols; Glomerular Filtration Rate; Humans; Hyperparathyroidism; Hypocalcemia; Nephrotic Syndrome; Parathyroid Hormone; Recurrence; Vitamin D

Patients with the nephrotic syndrome may exhibit low serum 25-OH-D concentrations. We developed a method for isolation of 25-OH-D from urine, with measurement by competitive binding assay. Daily urinary 25-OH-D excretion in healthy subjects averaged 0.17 +/- 0.15 nmol/day. Among nephrotic patients, urinary 25-OH-D excretion ranged from 0.27 to 10 nmol/day, in direct relation to the severity of proteinuria (r=0.76) and averaged 3.7 +/- 3.5 nmol/day. The 25-OH-D in the urine of nephrotic patients was unconjugated, implying that it was excreted with the serum VDBG, which has been shown to have a molecular weight and isoelectric point similar to that of albumin. We conclude that low serum 25-OH-D concentrations among nephrotic patients are principally the result or urinary losses of steroid. (J Lab Clin Med 99:325, 1982.)

Topics: 25-Hydroxyvitamin D 2; Adult; Aged; Creatinine; Ergocalciferols; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Proteinuria; Serum Albumin

Serum concentrations of 25-hydroxyvitamin D (25OHD) and 24,25-dihydroxyvitamin D (24,25(OH)2D) in patients with various types of renal disease were measured by a competitive protein binding assay. There was a significant (P less than 0.001) inverse correlation between serum levels of either 25OHD or 24,25(OH)2D and the degree of proteinuria in patients with chronic glomerulonephritis or idiopathic nephrotic syndrome. The ratio of 24,25(OH)2D to 25OHD was relatively low in patients with creatinine clearances (CCr) less than 30 ml/min/1.48 m2, while the ratio was higher in those with clearances greater than 85 ml/min/1.48 m2. There was a linear correlation (r = 0.783, P less than 0.001) between the ratio and the CCr in patients whose CCR ranged from 30 to 85 ml/min/1.48 m2. The 24,25(OH)2D/25OHD ratio also appeared to be correlated significantly (P less than 0.001) with the PSP-test. The serum levels of 25OHD and 24,25(OH)2D were lowered in nephrotic patients during treatment with prednisolone. The serum levels of 24,25(OH)2D were increased by 1 alpha-hydroxyvitamin D3 treatment in patients with chronic renal failure.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Adolescent; Adult; Child; Child, Preschool; Chromatography, Gel; Chromatography, High Pressure Liquid; Dihydroxycholecalciferols; Female; Glomerulonephritis; Humans; Hydroxycholecalciferols; Male; Methods; Middle Aged; Nephrotic Syndrome; Protein Binding