Plasma 1,25‐dihydroxyvitamin D levels in primary hyperparathyroidism depend on sex, body mass index, plasma phosphate and renal function

Moosgaard, Bjarke; Vestergaard, Peter; Heickendorff, Lene; Mosekilde, Leif

doi:10.1111/j.1365-2265.2006.02680.x

Cited by 28 publications

(42 citation statements)

References 47 publications

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“…In accordance with a previous study (29), we found no difference between groups in p-25OHD, although low vitamin D status may be associated with higher PTH levels in PHPT and a more severe clinical presentation (13,29,36).…”

Section: Discussionsupporting

confidence: 80%

Renal stones and calcifications in patients with primary hyperparathyroidism: associations with biochemical variables

Starup-Linde

Waldhauer

Rolighed

et al. 2012

European Journal of Endocrinology

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Objective: To study the prevalence of renal stones and nephrocalcinosis in patients with primary hyperparathyroidism (PHPT) and to appraise biochemical variables as risk factors for developing renal calcifications. Design: Cross-sectional. Materials and methods: All patients (nZ177) undergoing diagnostic evaluation and surgery for PHPT at Aarhus University Hospital between 2007 and 2009. All patients underwent routine spiral CT scans of the abdomen to determine the presence or absence of renal calcifications. Results: A total of 45 patients (25.4%, 95% confidence intervals: 19.0-31.4%) had renal stones (15.3%) and/or renal calcifications (10.2%) on the CT scans. Compared with those without calcification (nZ132), the group with calcification had a significantly lower plasma creatinine level (67.0G25.1 vs 74.6G17.5 mmol/l, 2PZ0.03). Moreover, CaE was higher in PHPT patients with renal calcification than in PHPT patients without (0.91G0.28 vs 0.74G0.40 mmol/mmol, 2PZ0.02). The other measured or derived biochemical variables were similar in the two groups. No biochemical variable was predictive for renal calcifications in a multiple regression analysis. Conclusion: We found a high prevalence of renal calcifications among PHPT patients but no deterioration of renal function. The occurrence of calcifications was related to low plasma creatinine and a high urine calcium/creatinine ratio. However, biochemical markers in general were poor predictors for the risk of renal stones or nephrocalcinosis indicating that routine image diagnostics may be needed for the identification of these complications in order to establish indication for surgery and ensure proper treatment.

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Section: Discussionsupporting

confidence: 80%

Renal stones and calcifications in patients with primary hyperparathyroidism: associations with biochemical variables

Starup-Linde

Waldhauer

Rolighed

et al. 2012

European Journal of Endocrinology

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“…In short, plasma 25-hydroxyvitamin D (25OHD) is characteristically reduced independently of season, sex, or age (6). The excess PTH and the hypophosphatemia increase the renal production of 1,25-dihydroxyvitamin D (1,25(OH) 2 D) (7). This effect appears to be mitigated by the hypercalcemia (9,10) and possibly by increased plasma levels of fibroblast growth factor-23 (FGF23) (11,12).…”

Section: Introductionmentioning

confidence: 99%

“…The complexity of vitamin D metabolism in PHPT has previously been described in detail (6)(7)(8). In short, plasma 25-hydroxyvitamin D (25OHD) is characteristically reduced independently of season, sex, or age (6).…”

Section: Introductionmentioning

confidence: 99%

Plasma 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone in familial hypocalciuric hypercalcemia and primary hyperparathyroidism

Christensen¹,

Nissen

Vestergaard³

et al. 2008

European Journal of Endocrinology

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Introduction: Familial hypocalciuric hypercalcemia (FHH) is a lifelong, benign, inherited condition caused by inactivating mutations in the calcium-sensing receptor (CASR) gene. Both FHH and primary hyperparathyroidism (PHPT) are characterized by elevated P-calcium, normal or elevated plasmaparathyroid hormone (P-PTH), and typically normal renal function. In PHPT, vitamin D metabolism is typically characterized by low plasma levels of 25-hydroxyvitamin D (25OHD), and high plasma levels of 1,25-dihydroxyvitamin D (1,25(OH) 2 D). In FHH, the vitamin D metabolism is not very well known. Objective: To compare and evaluate plasma 25OHD, 1,25(OH) 2 D, and PTH in FHH and PHPT. Design: Cross-sectional study. Materials: About 66 FHH patients with mutations in the CASR gene, 147 patients with surgically verified PHPT, and 46 controls matched to FHH patients according to age (G5 years), sex, and season. All patients had a P-creatinine !140 mmol/l. Methods: We measured P-calcium, P-Ca 2C , P-albumin, P-creatinine, P-phosphate, P-magnesium, and P-PTH by standard laboratory methods. P-25OHD and P-1,25(OH) 2 D were measured by RIA or enzyme immunoassay. In FHH, all protein-coding exons in the CASR gene were sequenced and aligned to GenBank reference sequence NM_000388.2. Results: PHPT patients had higher body mass index (2p!0.01), together with higher P-PTH (2p! 0.01) and P-1,25(OH) 2 D (2p!0.01) compared with FHH patients. The groups had similar levels of P-Ca 2C and of P-25OHD. The phenotypic expression of the CASR mutations (as determined by the degree of hypercalcemia) did not influence the levels of P-1,25(OH) 2 D. Conclusion: Even though P-calcium and P-25OHD were comparable, P-1,25(OH) 2 D and P-PTH differed between FHH and PHPT.

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“…1-␣ hydroxylase to produce 1,25 dihydroxy vitamin D 3 (1,31,36,45,46), stimulation of ammoniagenesis (15,47), and stimulation of gluconeogenesis (42,47). The study of the effects of PTH on proximal tubule function is complicated by the fact that PTH receptors are expressed on both apical [brush-border membranes (BBM)] and basolateral membranes (BLM) (32).…”

mentioning

confidence: 98%

“…Specifically, PTH causes inhibition of sodium-dependent phosphate (NaPi) uptake (3,4,39,48,53) and sodium-hydrogen exchange (NHE) at the apical membrane (2, 7, 30, 53), inhibition of Na ϩ -K ϩ -ATPase ion transport (Na-K) at the basolateral membrane (17, 34), stimulation of 1-␣ hydroxylase to produce 1,25 dihydroxy vitamin D 3 (1,31,36,45,46), stimulation of ammoniagenesis (15, 47), and stimulation of gluconeogenesis (42, 47). The study of the effects of PTH on proximal tubule function is complicated by the fact that PTH receptors are expressed on both apical [brush-border membranes (BBM)] and basolateral membranes (BLM) (32).…”

mentioning

confidence: 99%

Parathyroid hormone (PTH) decreases sodium-phosphate cotransporter type IIa (NpT2a) mRNA stability

Murray

Holthouser

Clark

et al. 2013

American Journal of Physiology-Renal Physiology

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The acute inhibitory effects of parathyroid hormone (PTH) on proximal tubule Na(+)-K(+)-ATPase (Na-K) and sodium-dependent phosphate (NaPi) transport have been extensively studied, while little is known about the chronic effects of PTH. Patients with primary hyperparathyroidism, a condition characterized by chronic elevations in PTH, exhibit persistent hypophosphatemia but not significant evidence of salt wasting. We postulate that chronic PTH stimulation results in differential desensitization of PTH responses. To address this hypothesis, we compared the effects of chronic PTH stimulation on Na-P(i) cotransporter (Npt2a) expression and Na-K activity and expression in Sprague Dawley rats, transgenic mice featuring parathyroid-specific cyclin D1 overexpression (PTH-D1), and proximal tubule cell culture models. We demonstrated a progressive decrease in brush-border membrane (BBM) expression of Npt2a from rats treated with PTH for 6 h or 4 days, while Na-K expression and activity in the basolateral membranes (BLM) exhibited an initial decrease followed by recovery to control levels by 4 days. Npt2a protein expression in PTH-D1 mice was decreased relative to control animals, whereas levels of Na-K, NHERF-1, and PTH receptor remained unchanged. In PTH-D1 mice, NpT2a mRNA expression was reduced by 50% relative to control mice. In opossum kidney proximal tubule cells, PTH decreased Npt2a mRNA levels. Both actinomycin D and cycloheximide treatment prevented the PTH-mediated decrease in Npt2a mRNA, suggesting that the PTH response requires transcription and translation. These findings suggest that responses to chronic PTH exposure are selectively regulated at a posttranscriptional level. The persistence of the phosphaturic response to PTH occurs through posttranscriptional mechanisms.

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Plasma 1,25‐dihydroxyvitamin D levels in primary hyperparathyroidism depend on sex, body mass index, plasma phosphate and renal function

Cited by 28 publications

References 47 publications

Renal stones and calcifications in patients with primary hyperparathyroidism: associations with biochemical variables

Renal stones and calcifications in patients with primary hyperparathyroidism: associations with biochemical variables

Plasma 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone in familial hypocalciuric hypercalcemia and primary hyperparathyroidism

Parathyroid hormone (PTH) decreases sodium-phosphate cotransporter type IIa (NpT2a) mRNA stability

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