Vitamin D Metabolites and Calcium Metabolism in Patients with Nephrotic Syndrome and Normal Renal Function*

Abstract

Patients with nephrotic syndrome (NS) lose 25-hydroxyvitamin D3 (250HD3) in the urine and have low blood levels of this metabolite. This abnormality may be responsible for the hypocalcemia, i.e., low ionized Ca. The mechanism of the hypocalcemia is not evident. The low value of 250HD may result in low blood levels of other vitamin D metabolites, such as 1,25-dihydroxyvitamin D [1,25-(OH)2D] and 24,25-(OH)2D3; a deficiency of these compounds may cause defective intestinal absorption of Ca (.alpha.) and resistance to the calcemic action of parathyroid hormone (PTH), causing hypocalcemia. Studies were performed in 12 patients with NS and normal renal function to evaluate these questions. Blood levels of 250HD, 1,25-(OH)2D, and 24,25-(OH)2D were all significantly (P < 0.01) lower in NS (4.0 .+-. 0.8 ng/ml, 7.0 .+-. 2.3 pg/ml, 1.8 .+-. 0.2 ng/ml, respectively) compared to normal subjects (37.0 .+-. 1.5 ng/ml, 37.0 .+-. 1.2 pg/ml, and 3.4 .+-. 0.2 ng/ml). Both .alpha. (0.21 .+-. 0.2 vs. 0.27 .+-. 0.1; P < 0.05) and the calcemic response to PTH (0.50 .+-. 0.1 vs. 1.35 .+-. 0.16 mg/dl; P < 0.01) in NS subjects were significantly lower than normal. Apparently a deficient state of all of these vitamin D metabolites exists in patients with NS and normal renal function, this abnormality underlies the defect in .alpha. and the resistance to the calcemic response to PTH, and all participate in the genesis of the hypocalcemia, secondary hyperparathyroidism develops and both vitamin D deficiency and elevated blood levels of PTH are responsible for the bone lesions in these patients.