Vitamin-D Metabolism in Nephrotic Syndrome

Barragry, John; Carter, N.D.; Beer, M.; Cohen, R. D.; France, Michael; Auton, Jennifer; Boucher, Barbara J

doi:10.1016/s0140-6736(77)92498-9

Cited by 101 publications

(40 citation statements)

References 14 publications

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“…In fact, serum ion ized calcium, urinary excretion and intestinal absorption of calcium are frequently reduced in the nephrotic syn drome [8][9][10][11][12], In addition, several studies have docu mented the occurrence of osteomalacia and hyperpara thyroidism in this population [8,13], These abnormalities strongly point to the central role of altered vitamin D metabolism as a cause of these abnormalities. In fact, plasma concentrations of various vitamin D metabolites including 25(OH)D,, l,25(OH)2D3 and 24,25(OH)2D3 are all reduced in the nephrotic syndrome [8][9][10][11][12][13][14][15][16][17][18], Re duced plasma concentration of 25(OH)D3 is associated with, and largely due to, massive urinary/renal losses of this prohormone along with its binding protein (vitamin D binding protein) [9,[19][20][21]. This observation is further supported by rapid urinary excretion of injected radiolabelled vitamin D [22], In addition, normal intestinal absorption of vitamin D demonstrated by in vivo perfu sion experiments in nephrotic rats has excluded the possi ble role of malabsorption as a culprit [21], While the mechanism of reduced plasma 25(OH)D3 concentration 363 is reasonably clear, the reason for demonstrated reduction in 1,25(OH)2Dj (calcitriol), the active hormonal form of vitamin D, is less evident.…”

Section: Vitamin D Metabolismmentioning

confidence: 99%

Endocrinological Consequences of the Nephrotic Syndrome

Nd¹

1993

Am J Nephrol

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The nephrotic syndrome can profoundly affect metabolism and regulation of protein or protein-bound hormones or prohormones. The present paper provides an overview of the published studies on erythropoietin, vitamin D and thyroid metabolism as well as hypothalamic-pituitary-gonadal axis in nephrotic syndrome. On each occasion the clinical significance and practical implications of the reported abnormalities are emphasized. In addition, attention is drawn to the areas needing further investigations.

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Section: Vitamin D Metabolismmentioning

confidence: 99%

Endocrinological Consequences of the Nephrotic Syndrome

Nd¹

1993

Am J Nephrol

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“…Patients with liver disease (16-18) and the nephrotic syndrome (19,20) have DBP levels that are lower than normal. Low 1,25(OH)2D concentrations have been reported in these conditions by some investigators (21,22) but not by others (23,24).…”

Section: Introductionmentioning

confidence: 99%

Free 1,25-dihydroxyvitamin D levels in serum from normal subjects, pregnant subjects, and subjects with liver disease.

Bikle¹,

Gee²,

Halloran³

et al. 1984

J. Clin. Invest.

302

162

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Abstract. We measured the free concentration of 1,25-dihydroxyvitamin D (1,25[OHJ2D) using centrifugal ultrafiltration, and the level of vitamin D-binding protein (DBP) in 24 normal subjects, 17 pregnant subjects, and 25 alcoholic subjects with liver disease. Our objective was to determine whether the increase in total 1,25(OH)2D levels in pregnant women and the reduction in total 1,25(OH)2D levels in subjects with liver disease reflected a true difference in free 1,25(OH)2D levels or whether such differences were due solely to the variations in DBP levels (and thus, the amount of 1,25[OH]2D bound) in these groups. In subjects with liver disease the mean total 1,25(OH)2tD concentration (22.6±12.5 pg/ml) and the mean DBP concentration (188±105 fsg/ dl) were nearly half the normal values (41.5±11.5 pg/ ml and 404±124 ,g/dl, respectively, P < 0.001), whereas the mean free 1,25(OH)2D level was similar to normal values (209±91 fg/ml and 174±46 fg/ml, respectively). In contrast, in pregnant subjects the mean total 1,25(OH)2D level (82±21 pg/ml) and mean DBP level (576±128 Ag/dl) were significantly higher than normal (P < 0.001). Although the mean percent free 1,25-(OH)2D level in pregnant subjects was below normal (0.359±0.07% vs. 0.424±0.07%, P < 0.001), the mean free 1,25(OH)2D level was 69% higher than normal (294±98 fg/ml vs. 174±46 fg/ml, P < 0.001). When data from all three groups were combined, there was a linear correlation between total 1,25(OH)2D and DBP levels but not between DBP and percent free 1,25(OH)2D levels; the increased DBP levels in the pregnant subjects were associated with less of an effect on percent free 1,25(OH)2D than were the reduced DBP levels in the subjects with liver disease.Our data suggest that (a) free 1,25(OH)2D levels appear to be well maintained even in subjects with liver disease and reduced DBP levels, (b) free 1,25(OH)2D levels are increased during pregnancy despite the increase in DBP levels, and (c) free 1,25(OH)2D levels cannot be inferred accurately from measurements of total 1,25(OH)2D and DBP levels alone in subjects with various physiologic and pathophysiologic conditions.

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“…Recently, Goldstein et al (5), Schmidt-Gayk et al (6), and Barragry et al (7) reported that patients with nephrotic syndrome have very low levels of 25-hydroxyvitamin D (25-OH-D)l most probably because of losses of this metabolite in urine. Goldstein et al (5) found that patients with nephrotic syndrome and normal renal function have low blood concentrations of ionized calcium and modest elevations in the blood level of parathyroid hormone (PTH).…”

mentioning

confidence: 99%

Osteomalacia and Hyperparathyroid Bone Disease in Patients with Nephrotic Syndrome

Malluche¹,

Goldstein²,

Massry³

1979

J. Clin. Invest.

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A B S T R A C T Patients with nglml).Blood levels of both total (8.1±0.12 mgldl) and ionized (3.8±0.21 mg/dl) calcium were lower than normal and three patients had true hypocalcemia. Blood immunoreactive parathyroid hormone levels were elevated in all. Volumetric density of osteoid was significantly increased in three out of six patients and the fraction of mineralizing osteoid seams was decreased in all. Evidence for an increase in active lacunae (bone-osteoclast interface) occurred in three out of six patients and in inactive (Howship's lacunae) bone resorption in six out of six. The data indicate that the loss of 25-OH-D in urine of patients with nephrotic syndrome and normal renal function may result in a decrease of blood levels of ionized calcium, secondary hyperparathyroidism and enhanced bone resorption. In addition, the vitamin D-deficient state causes osteomalacia as evidenced by defective mineralization and increased osteoid volume.

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Vitamin-D Metabolism in Nephrotic Syndrome

Cited by 101 publications

References 14 publications

Endocrinological Consequences of the Nephrotic Syndrome

Endocrinological Consequences of the Nephrotic Syndrome

Free 1,25-dihydroxyvitamin D levels in serum from normal subjects, pregnant subjects, and subjects with liver disease.

Osteomalacia and Hyperparathyroid Bone Disease in Patients with Nephrotic Syndrome

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