{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T21:51:23Z","timestamp":1777758683120,"version":"3.51.4"},"reference-count":0,"publisher":"S. Karger AG","license":[{"start":{"date-parts":[[2008,10,28]],"date-time":"2008-10-28T00:00:00Z","timestamp":1225152000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"},{"start":{"date-parts":[[2008,10,28]],"date-time":"2008-10-28T00:00:00Z","timestamp":1225152000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am J Nephrol"],"abstract":"<jats:p>We studied 21 dialysis patients who became hypercalcemic without vitamin D or calcium therapy and compared them to 28 dialysis patients who were not hypercalcemic. In the hypercalcemic group, the mean ionized-calcium level was elevated compared to normal subjects (5.4 \u00b1 0.4 vs. 4.9 \u00b1 0.1; p &lt; 0.001), while the ionized-calcium level in the control dialysis patients was below normal (4.5 \u00b1 0.4 vs. 4.9 \u00b1 0.1; p &lt; 0.001). Bone biopsies were performed in all patients. Two thirds of the hypercalcemic patients had low-turnover osteodystrophy (LTO, predominantly osteomalacia), a fraction significantly higher than in the control dialysis patients (13\/21 vs. 8\/28, respectively; p &lt; 0.05). The hypercalcemic patients with LTO had markedly elevated surface bone aluminum (63 \u00b1 24% of all trabecular surfaces). In contrast, the nonhypercalcemic dialysis patients with LTO and all patients with osteitis fibrosa had minimal surface bone aluminum. Hypercalcemic patients with osteitis fibrosa had a significantly lower mean N-terminal parathyroid hormone (PTH) value than did nonhypercalcemic patients with osteitis fibrosa (149 \u00b1 81 vs. 278 \u00b1 135 pg\/ml, respectively; p &lt; 0.005). Both mean values were markedly elevated in comparison with those obtained in normal subjects (16 \u00b1 5 pg\/ml). In contrast, patients with LTO, irrespective of the calcium level, had mean PTH values that were not significantly different from those of normal subjects. A PTH level greater than 100 pg\/ml was 95% sensitive and 87% specific for osteitis fibrosa, as demonstrated by histomorphometry in nonhypercalcemic dialysis patients. However, this level was only 62% sensitive and 77% specific for a diagnosis of osteitis fibrosa in hypercalcemic dialysis patients. The hypercalcemic patients had an increased mortality at 1 year of follow-up compared to control dialysis patients, after controlling for the difference in age. Mortality at 1 year was 38% in those hypercalcemic patients who were more than 50 years of age. The majority of the deaths occurred in hypercalcemic patients with aluminum-related bone disease. In addition, this group of patients had the greatest disability.In summary, we found that hypercalcemic patients had increased disability and mortality and that aluminum-related bone disease was more common in this group of patients than was osteitis fibrosa. The N-terminal PTH level was not helpful in the differential diagnosis of the type of bone disease present in those patients who were hypercalcemic.<\/jats:p>","DOI":"10.1159\/000167964","type":"journal-article","created":{"date-parts":[[2008,10,31]],"date-time":"2008-10-31T11:35:40Z","timestamp":1225452940000},"page":"190-197","source":"Crossref","is-referenced-by-count":6,"title":["Elevated Bone Aluminum and Suppressed Parathyroid Hormone Levels in Hypercalcemic Dialysis Patients"],"prefix":"10.1159","author":[{"given":"Beth","family":"Piraino","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tai","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jules B.","family":"Puschett","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2008,10,28]]},"container-title":["American Journal of Nephrology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/karger.com\/article-pdf\/doi\/10.1159\/000167964","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T13:11:57Z","timestamp":1777468317000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000167964"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2008,10,28]]},"references-count":0,"URL":"https:\/\/doi.org\/10.1159\/000167964","archive":["Portico"],"relation":{},"ISSN":["0250-8095","1421-9670"],"issn-type":[{"value":"0250-8095","type":"print"},{"value":"1421-9670","type":"electronic"}],"subject":[],"published":{"date-parts":[[2008,10,28]]}}}