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Metabolic Bone Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
24-hour urinary calcium excretion: is a vital investigation. FHH is due to loss of function in the calcium sensing receptors of the parathyroid gland leading to the same biochemical profile as primary hyperparathyroidism with the main difference being a low urinary calcium excretion (elevated in primary hyperparathyroidism)
Investigation of Hypercalcaemia
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
A ratio less than 0.01 is present in 80% of patients with FHH, while the ratio is greater than 0.02 in patients with HPTH. It also important to exclude other causes of low urinary calcium, such as low vitamin D and use of thiazide diuretics, because they can affect the sensitivity of the ratio. Patients with low vitamin D should have the vitamin replaced before their Ca/Cr excretion ratio is calculated.
Renal Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Scott and co-workers219 found that 22 of 27 coppersmiths exposed to cadmium had hypercalciuria. Five of these workers had developed renal stones. In another study221 it was reported that the urinary calcium concentrations were mainly in the range of 6 to 15 mmol/ℓ, with a “normal” range of 3 to 6 mmol/ℓ. The workers had normal serum calcium values indicating that the cause of the hypercalciuria was renal functional change.
Bioavailability of Calcium from Chia (Salvia hispanica L.) in Ovariectomized Rats Fed a High Fat Diet
Published in Journal of the American College of Nutrition, 2021
Marcella Duarte Villas Mishima, Bárbara Pereira da Silva, Renata Celi Lopes Toledo, Neuza Maria Brunoro Costa, Hércia Stampini Duarte Martino
Regarding calcium bioavailability, no difference in the values of urinary calcium, fecal calcium and calcium in the femur were observed in the SHAM and OVX groups. For the SHAM and OVX groups, serum calcium increased with the consumption of a high fat diet, but it was not altered by chia consumption. Also, calcium balance and absorption were not altered by a high fat diet (HFD + CC X SD + CC) or by chia consumption (SD + CC X SD + chia and HFD + CC X HFD + chia). In the OVX group, chia with a standard diet (SD + CC X SD + chia), and a high fat diet (HFD + CC X SD + CC) decreased calcium retention while in the SHAM group, we observed no difference in calcium retention between the groups. Bone strength was not altered between the animals. Regarding surgery, the OVX groups on standard diet (SD + CC or SD + chia) had lower concentrations of serum calcium when compared to the SHAM group fed the same diet (Table 2).
Clinical burden and healthcare resource utilization among patients with chronic hypoparathyroidism, overall and by adequately vs not adequately controlled disease: a multi-country chart review
Published in Journal of Medical Economics, 2019
Kristina Chen, Alan Krasner, Nanxin Li, Cheryl Q Xiang, Todor Totev, Jipan Xie
Using the collected data from patients’ medical records, patients were classified as NAC retrospectively based on the treatment targets suggested in two international clinical guidelines for hypoparathyroidism (the European Society of Endocrinology’s Clinical Guideline and First International Conference on the Management of Hypoparathyroidism)10,11. The criteria adapted from these guidelines were: (1) most recent serum calcium levels <2.0 mmol/L (<8.0 mg/dL) despite using activated vitamin D (≥3 µg/day of alfacalcidol or ≥1.5 µg/day of calcitriol); or (2) most recent serum phosphate levels >1.45 mmol/L (>4.5 mg/dL); or (3) most recent 24-hour urinary calcium excretion >7.5 mmol (300 mg)/24 h in males or >6.25 mmol (250 mg)/24 h in females; or (4) at least one of the following symptoms during the study period: blepharospasm, facial spasm, hypoesthesia, irritability, muscle fatigue, muscle spasms, muscle tightness, muscle twitching, musculoskeletal pain, musculoskeletal stiffness, myalgia, nervousness, esophageal spasm, paresthesia, throat tightness, or tremor. Patients who were not classified as NAC hypoparathyroidism were considered as AC with conventional therapy (calcium and activated vitamin D supplements). In addition, the endocrinologists who reviewed the medical charts were requested to provide their classification of whether the patients were AC or NAC, based on all the information available in the charts.
Elevated admission serum calcium phosphate product as an independent risk factor for acute kidney injury in hospitalized patients
Published in Hospital Practice, 2019
Charat Thongprayoon, Wisit Cheungpasitporn, Michael A. Mao, Andrew M. Harrison, Stephen B. Erickson
In the setting of acute phosphate nephropathy, previously termed acute nephrocalcinosis, injuries to the distal tubules and collecting ducts due to calcium phosphate deposits have been demonstrated [12,35,36]. As CaP levels increase, precipitation of calcium phosphate crystals may occur [22,23]. Acute phosphate nephropathy has not only been described after phosphate containing bowel preparation [37–39], but also been reported in patients who received oral or intravenous phosphate replacement [40,41]. Elevated serum calcium levels are associated with an increase in urinary calcium excretion due to compensatory increase in the filtered load and a decrease in the tubular reabsorption of calcium [42,43]. Consequently, hyperphosphatemia in patients with elevated calcium level may result in increased phosphate and calcium load in the distal tubules, resulting in acute phosphate nephropathy. AKI can also occur, or be exacerbated, by elevated serum calcium levels, which can cause renal vasoconstriction, leading to renal ischemia and tubular injury [44–46]. Based on the findings of our study, we demonstrate a linear trend of higher AKI incidence with increasing CaP levels.