AIMS: Primary hyperparathyroidism (PHPT) causes hypercalcemia by increasing tubular calcium reabsorption. Because chronic kidney disease (CKD) is associated with normocalcemia, we inferred that calcium reabsorption is also normal, and hypothesized that normal reabsorption requires excessive parathyroid hormone (PTH) in CKD. METHODS: The following were obtained in controls and patients with CKD or PHPT: estimated GFR (eGFR); concentrations of PTH 1-84, 1,25-dihydroxyvitamin D, and ultrafilterable and ionized calcium ([PTH], [1,25(OH)2D], [Ca]uf, [Ca]i); and ratios of calcium excreted or reabsorbed per volume of filtrate (ECa/Ccr, TRCa/Ccr). Pertinent linear regressions were examined. RESULTS: In CKD, [PTH] was increased, but ECa/Ccr, TRCa/Ccr, [Ca]uf, and [Ca]i equaled control values. [PTH] was inversely related to eGFR but unrelated to [1,25(OH)2D]. TRCa/Ccr was constant at all [PTH]. In PHPT, [PTH] was no higher than in CKD, but TRCa/Ccr, [Ca]uf, and [Ca]i were increased. [1,25(OH)2D] correlated with [PTH]. In controls, TRCa/Ccr varied directly with [1,25(OH)2D] and inversely with [PTH]. CONCLUSIONS: In controls, calcium reabsorption rose with [1,25(OH)2D], and [PTH] fell in response. In PHPT, [PTH] determined [1,25(OH)2D]; together, the hormones increased calcium reabsorption and caused hypercalcemia. In CKD, normal calcium reabsorption required high [PTH].
AIMS: Primary hyperparathyroidism (PHPT) causes hypercalcemia by increasing tubular calcium reabsorption. Because chronic kidney disease (CKD) is associated with normocalcemia, we inferred that calcium reabsorption is also normal, and hypothesized that normal reabsorption requires excessive parathyroid hormone (PTH) in CKD. METHODS: The following were obtained in controls and patients with CKD or PHPT: estimated GFR (eGFR); concentrations of PTH 1-84, 1,25-dihydroxyvitamin D, and ultrafilterable and ionizedcalcium ([PTH], [1,25(OH)2D], [Ca]uf, [Ca]i); and ratios of calcium excreted or reabsorbed per volume of filtrate (ECa/Ccr, TRCa/Ccr). Pertinent linear regressions were examined. RESULTS: In CKD, [PTH] was increased, but ECa/Ccr, TRCa/Ccr, [Ca]uf, and [Ca]i equaled control values. [PTH] was inversely related to eGFR but unrelated to [1,25(OH)2D]. TRCa/Ccr was constant at all [PTH]. In PHPT, [PTH] was no higher than in CKD, but TRCa/Ccr, [Ca]uf, and [Ca]i were increased. [1,25(OH)2D] correlated with [PTH]. In controls, TRCa/Ccr varied directly with [1,25(OH)2D] and inversely with [PTH]. CONCLUSIONS: In controls, calcium reabsorption rose with [1,25(OH)2D], and [PTH] fell in response. In PHPT, [PTH] determined [1,25(OH)2D]; together, the hormones increased calcium reabsorption and caused hypercalcemia. In CKD, normal calcium reabsorption required high [PTH].
Authors: Jin Xia; Wanzhu Tu; JoAnn E Manson; Hongmei Nan; Aladdin H Shadyab; Jennifer W Bea; Ting-Yuan D Cheng; Lifang Hou; Yiqing Song Journal: Am J Clin Nutr Date: 2020-08-01 Impact factor: 7.045
Authors: D Miyaoka; Y Imanishi; M Ohara; N Hayashi; Y Nagata; S Yamada; K Mori; M Emoto; M Inaba Journal: Osteoporos Int Date: 2018-09-05 Impact factor: 4.507
Authors: Dirk Hendrik Nicolaas van den Broek; Rebecca F Geddes; Nicola S Lötter; Yu-Mei Chang; Jonathan Elliott; Rosanne E Jepson Journal: J Vet Intern Med Date: 2022-05-24 Impact factor: 3.175
Authors: Soisungwan Satarug; Kanyarat Boonprasert; Glenda C Gobe; Ronnatrai Ruenweerayut; David W Johnson; Kesara Na-Bangchang; David A Vesey Journal: Clin Kidney J Date: 2018-11-21