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      Hypoparathyroidism and pseudohypoparathyroidism: etiology, laboratory features and complications

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          ABSTRACT

          Objectives

          To identify a clinical profile and laboratory findings of a cohort of hypoparathyroidism patients and determine the prevalence and predictors for renal abnormalities.

          Materials and methods

          Data from medical records of five different visits were obtained, focusing on therapeutic doses of calcium and vitamin D, on laboratory tests and renal ultrasonography (USG).

          Results

          Fifty-five patients were identified, 42 females and 13 males; mean age of 44.5 and average time of the disease of 11.2 years. The most frequent etiology was post-surgical. Levels of serum calcium and creatinine increased between the first and last visits (p < 0.001 and p < 0.05, respectively); and serum levels of phosphate decreased during the same period (p < 0.001). Out of the 55 patients, 40 had USG, and 10 (25%) presented with kidney calcifications. There was no significant difference in the amount of calcium and vitamin D doses among patients with kidney calcifications and others. No correlation between serum and urinary levels of calcium and the presence of calcification was found. Urinary calcium excretion in 24h was significantly higher in patients with kidney calcification (3.3 mg/kg/d) than in those without calcification (1.8 mg/kg/d) (p < 0.05).

          Conclusions

          The reduction of hypocalcemia and hyperphosphatemia suggest an effectiveness of the treatment, and the increase in serum creatinine demonstrates an impairment of renal function during follow-up. Kidney calcifications were prevalent in this cohort, and higher urinary calcium excretion, even if still within the normal range, was associated with development of calcification. These findings suggest that lower rates of urinary calcium excretion should be aimed for in the management of hypoparathyroidism.

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          Most cited references44

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          Prediction of Creatinine Clearance from Serum Creatinine

          A formula has been developed to predict creatinine clearance (C cr ) from serum creatinine (S cr ) in adult males: Ccr = (140 – age) (wt kg)/72 × S cr (mg/100ml) (15% less in females). Derivation included the relationship found between age and 24-hour creatinine excretion/kg in 249 patients aged 18–92. Values for C cr were predicted by this formula and four other methods and the results compared with the means of two 24-hour C cr’s measured in 236 patients. The above formula gave a correlation coefficient between predicted and mean measured Ccr·s of 0.83; on average, the difference between predicted and mean measured values was no greater than that between paired clearances. Factors for age and body weight must be included for reasonable prediction.
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            • Article: not found

            Gender differences in autoimmune disease.

            Autoimmune diseases are a range of diseases in which the immune response to self-antigens results in damage or dysfunction of tissues. Autoimmune diseases can be systemic or can affect specific organs or body systems. For most autoimmune diseases there is a clear sex difference in prevalence, whereby females are generally more frequently affected than males. In this review, we consider gender differences in systemic and organ-specific autoimmune diseases, and we summarize human data that outlines the prevalence of common autoimmune diseases specific to adult males and females in countries commonly surveyed. We discuss possible mechanisms for sex specific differences including gender differences in immune response and organ vulnerability, reproductive capacity including pregnancy, sex hormones, genetic predisposition, parental inheritance, and epigenetics. Evidence demonstrates that gender has a significant influence on the development of autoimmune disease. Thus, considerations of gender should be at the forefront of all studies that attempt to define mechanisms that underpin autoimmune disease. Copyright © 2014. Published by Elsevier Inc.
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              • Article: not found

              Calcium metabolism in health and disease.

              This brief review focuses on calcium balance and homeostasis and their relationship to dietary calcium intake and calcium supplementation in healthy subjects and patients with chronic kidney disease and mineral bone disorders (CKD-MBD). Calcium balance refers to the state of the calcium body stores, primarily in bone, which are largely a function of dietary intake, intestinal absorption, renal excretion, and bone remodeling. Bone calcium balance can be positive, neutral, or negative, depending on a number of factors, including growth, aging, and acquired or inherited disorders. Calcium homeostasis refers to the hormonal regulation of serum ionized calcium by parathyroid hormone, 1,25-dihydroxyvitamin D, and serum ionized calcium itself, which together regulate calcium transport at the gut, kidney, and bone. Hypercalcemia and hypocalcemia indicate serious disruption of calcium homeostasis but do not reflect calcium balance on their own. Calcium balance studies have determined the dietary and supplemental calcium requirements needed to optimize bone mass in healthy subjects. However, similar studies are needed in CKD-MBD, which disrupts both calcium balance and homeostasis, because these data in healthy subjects may not be generalizable to this patient group. Importantly, increasing evidence suggests that calcium supplementation may enhance soft tissue calcification and cardiovascular disease in CKD-MBD. Further research is needed to elucidate the risks and mechanisms of soft tissue calcification with calcium supplementation in both healthy subjects and CKD-MBD patients.

                Author and article information

                Journal
                Arch Endocrinol Metab
                Arch Endocrinol Metab
                aem
                Archives of Endocrinology and Metabolism
                Sociedade Brasileira de Endocrinologia e Metabologia
                2359-3997
                2359-4292
                07 November 2016
                Nov-Dec 2016
                : 60
                : 6
                : 532-536
                Affiliations
                [1 ] orgnameUniversidade Federal do Paraná Curitiba PR Brasil original Serviço de Endocrinologia e Metabologia do Paraná (SEMPR), Universidade Federal do Paraná (UFPR), Curitiba, PR, Brasil
                [2 ] orgdiv1Departamento de Medicina Interna orgnameUniversidade Federal do Paraná Curitiba PR Brasil originalDepartamento de Medicina Interna da Universidade Federal do Paraná (UFPR), Curitiba, PR, Brasil
                [3 ] orgdiv1Divisão de Histomorfometria Óssea orgnameFundação Pró-Renal Curitiba PR Brasil original Laboratório P. R .O., Divisão de Histomorfometria Óssea, Fundação Pró-Renal, Curitiba, PR, Brasil
                Author notes
                Correspondence to: Carolina A. Moreira Av. Agostinho Leão Jr, 285 80030-110 – Curitiba, PR, Brasil carolina.aguiar.moreira@ 123456gmail.com

                Disclosure: no potential conflict of interest relevant to this article was reported.

                Article
                2359-3997000000221
                10.1590/2359-3997000000221
                10522163
                27901178
                b0d0591d-6f73-4f20-810b-ee73552b586f

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 February 2016
                : 27 May 2016
                Page count
                Figures: 2, Tables: 1, Equations: 0, References: 24, Pages: 1
                Categories
                Articles

                hypoparathyroidism,renal complication,renal calcification,hypocalcemia,pseudohypoparathyroidism

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