Management Of Hypoparathyroidism Research Articles

Challenges in management of hypoparathyroidism and severe hypocalcaemia in autoimmune polyendocrine syndrome -Is recombinant human parathyroid hormone or PTH pump an option?

Challenges in management of hypoparathyroidism and severe hypocalcaemia in autoimmune polyendocrine syndrome -Is recombinant human parathyroid hormone or PTH pump an option?

Calcium- alkali syndrome: an endocrine complication in the management of hypoparathyroidism

Calcium- alkali syndrome: an endocrine complication in the management of hypoparathyroidism

Revealing the therapeutic potential of teriparatide: a review

Teriparatide is an FDA-approved medication for osteoporosis that presents promising results in treating various musculoskeletal conditions. It helps in improving the bone mineral density and preventing fractures in individuals with osteoporosis. Its effectiveness in treating non-union and delayed union fractures, atypical femoral fractures, and spinal fusion procedures makes it valuable in improving bone healing and reducing complications. Teriparatide also improves bone density and strength in individuals with osteogenesis imperfecta, helps prevent and treat hypocalcaemia post-thyroidectomy, and helps in the management of hypoparathyroidism. In MRONJ, teriparatide improves lesion resolution and reduces bony defects. Furthermore, it potentially prevents bone metastasis in cancer patients without stimulating tumour growth. Nevertheless, teriparatide may cause short-term side effects like nausea and long-term concerns pertaining to the risk of osteosarcoma. Recent European alliance of associations for rheumatology guidelines have highlighted teriparatide's superior effectiveness in achieving bone mineral density thresholds and reducing fracture risks. Further clinical trials are necessary to determine optimal dosages and treatment durations of teriparatide. The off-label use of teriparatide should be considered only under the guidance of a healthcare professional when standard options are unavailable or inadequate.

Endocrine manifestations in adults with 22q11.2 deletion syndrome: a retrospective single-center cohort study

Introduction and objectivePatients with the 22q11.2 deletion syndrome (22q11DS) frequently display cardiological and psychiatric diseases, but are also at increased risk for endocrine manifestations. The aim of this study was to evaluate the screening, prevalence, and management of hypoparathyroidism and thyroid disease in patients with 22q11DS, to evaluate the metabolic profile, and to compare these results with current literature and guidelines.DesignWe performed a retrospective study of patients with genetically confirmed 22q11DS, followed at the center for human genetics of the University Hospitals Leuven, resulting in a cohort of 75 patients. Medical history, medication, and laboratory results concerning hypoparathyroidism, thyroid dysfunction, and the metabolic profile were collected.ResultsOf the total cohort, 26 patients (35%) had at least one hypocalcaemic episode. During hypocalcaemia, parathyroid hormone (PTH) was measured in only 12 patients with 11 having normal or low PTH, confirming a diagnosis of hypoparathyroidism. Recurrent episodes of hypocalcaemia occurred in seventeen patients (23%). Adherence to the guidelines was low, with 13% of patients having a yearly serum calcium evaluation, 12% receiving daily calcium supplements, and 20% receiving non-active vitamin D. Hypothyroidism was present in 31 patients (44%) and hyperthyroidism in 6 patients (8%). Information on body mass index (BMI) was available in 52 patients (69%), of which 38% were obese (BMI ≥ 30 kg/m2).ConclusionHypoparathyroidism, hypothyroidism, and obesity are common endocrine manifestations in patients with 22q11DS but are probably underdiagnosed and undertreated, indicating the need for multidisciplinary follow-up including an endocrinologist.

Management of hypoparathyroidism: a Position Statement of the Expert Group of the Polish Society of Endocrinology.

Over the past few years, there have been significant advances in our understanding of hypoparathyroidism (HypoPT) in terms of its epidemiology, clinical presentation, etiology, and skeletal and renal complications. Moreover, the available treatment options for HypoPT have changed. This position statement of the Expert Group of the Polish Society of Endocrinology summarizes the current state of knowledge and provides recommendations for optimal management to assist clinicians in the diagnosis, treatment, and monitoring of HypoPT in Poland. The specific aspects of HypoPT management in children, pregnant and lactating women, and patients with chronic kidney disease are also discussed. HypoPT is a rare disorder characterized by hypocalcemia and the lack or deficiency of parathyroid hormone (PTH). Hypoparathyroidism can be associated with complications, including nephrocalcinosis, nephrolithiasis, renal insufficiency, cataract, seizures, cardiac arrhythmia, depression, and an increased risk of infection. Minimizing complications of HypoPT requires careful evaluation and close monitoring of laboratory parameters. Conventional management of HypoPT has focused on maintaining serum calcium levels using oral calcium and active vitamin D. However, this approach is limited because it does not restore normal PTH function, is often associated with inadequate biochemical control, and raises concerns as to long-term side effects. HypoPT is the only classic endocrine insufficiency that is not commonly treated with the substitution of the missing hormone. Recently, recombinant human PTH(1-84) has become available, offering hope that the use of the missing hormone in the treatment of HypoPT will help achieve better control and reduce the risk of complications. However, this treatment is currently unavailable in Poland.

SAT225 An Unexpected Case Of Hypocalcemia

Abstract Disclosure: M. Nogueira Cordeiro: None. Calcitriol and oral calcium supplementation remains the standard of care in the management of hypoparathyroidism. The targeted serum calcium level for this condition is quite narrow, typically at the lower end of the reference range to avoid hypercalciuria, but above the calcium level from which a patient may develop symptoms. Pharmacokinetic and pharmacodynamic properties vary among different over-the-counter (OTC) calcium salt preparations, therefore it is important for the provider and patient to understand the differences in calcium formulations to meet therapy goals. We present a case of symptomatic hypocalcemia related to a patient unknowingly switching from calcium carbonate to tricalcium phosphate supplementation. A 71 year-old woman with a history of thyroid cancer status post total thyroidectomy complicated by permanent hypoparathyroidism, CKD stage III, nephrolithiasis and hypercalciuria presented for a follow up visit complaining of perioral numbness for approximately one month. Laboratory evaluation revealed hypocalcemia, hyperphosphatemia, hypomagnesemia and a normal 25-OH-vitamin D level: Ca 7.3 mg/dL (8.5-10.5 mg/dL), Phos 5.6 mg/dL (2.5-4.5 mg/dL), Mg 1.1 mg/dL (1.7-2.8 mg/dL), 25-OH-vit D 45 ng/mL (30-60 ng/mL). Prior to this, her serum calcium had been well controlled, avoiding symptomatic hypocalcemia and hypercalciuria, for years. She had remained on her usual dose of calcitriol, but had changed her calcium supplement to 500 mg of tricalcium phosphate three times per day from calcium carbonate 650 mg three times a day. Rather than adjust her calcitriol, she was recommended to stop tricalcium phosphate and restart the previous regimen of calcium carbonate; serum calcium and phosphorus improved within 72 hours (Ca 7.7 mg/dL, Phos 3.8 mg/dL) and two weeks later her calcium level was back at goal (8.2 mg/dL), phosphate level had normalized (4.5 mg/dL) and she was no longer symptomatic. Tricalcium phosphate is not generally recommended for patients with hypoparathyroidism given they are less available and not as well tested. Previous studies have shown conflicting outcomes for serum calcium elevation after an oral load of tricalcium phosphate when compared with calcium carbonate. Elderly individuals might also experience an elevation in phosphate levels after a tricalcium phosphate load. Additionally, the elemental calcium in OTC tricalcium formulations is often less than what is available in similar appearing calcium carbonate or citrate supplements. Although calcium carbonate and citrate are the most commonly prescribed calcium supplements, other preparations are available OTC and it is difficult to tell these apart. Given the narrow goal of serum calcium for patients with hypoparathyroidism, providers should confirm the calcium formulation at each visit and counsel the patient to notify them if any changes are made in their oral calcium supplementation. Presentation: Saturday, June 17, 2023

Postoperative hypoparathyroidism after thyroid operation and exploration of permanent hypoparathyroidism evaluation.

To investigate the risk factors for hypoparathyroidism, discuss the prevention of postoperative hypoparathyroidism, and explore permanent postoperative hypoparathyroidism evaluation (PPHE). A total of 2,903 patients with thyroid nodules were treated between October 2012 and August 2015. Serum calcium and intact parathyroid hormone (iPTH) levels were measured at 1 day, 1 month, and 6 months postoperatively. The incidence and management of hypoparathyroidism were analyzed. The PPHE was established based on the risk factors and clinical practice. A total of 637 (21.94%) patients developed hypoparathyroidism, and 92.15% of them had malignant nodules. The incidence rates of transient and permanent hypoparathyroidism were 11.47% and 10.47%, respectively. The iPTH level was lower in patients with malignant nodules who underwent total thyroidectomy (TT) and central-compartment neck dissection (CND). These factors were independently associated with the recovery rate of parathyroid function. The formula for PPHE is as follows: {iPTH} + {sCa} + {surgical procedure} + {reoperation} + {pathologic type}. A scoring system was developed, and we scored low, middle, and high risk of permanent postoperative hypoparathyroidism as 4-6, 7-9, and 10-13, respectively. The differences in the recovery rates of parathyroid function in several risk groups were statistically significant (p < 0.001). Simultaneous TT and CND is a risk factor for hypoparathyroidism. The reoperation is not associated with hypoparathyroidism. Identification of parathyroid glands in situ and preservation of their vascular pedicles are key factors in managing hypoparathyroidism. PPHE can forecast the risk of permanent postoperative hypoparathyroidism well.

Development of a Hypoparathyroid Male Rodent Model for Testing Delayed-Clearance PTH Molecules.

Parathyroid hormone (PTH) replacement is a promising approach in the management of hypoparathyroidism but long-acting analogues need to be developed. To date, animal models for testing PTH required parathyroidectomy by surgery. We have developed a nonsurgical rodent hypoparathyroid model and tested a delayed-clearance PTH molecule (DC-PTH). The aim of this study was to use cinacalcet to suppress calcium levels in normal rats and to reverse these effects with the administration of PTH or PTH analogues. Male Wistar rats were gavaged with either 30 mg/kg cinacalcet-HCl (cinacalcet) or vehicle only. Animals were then dosed with either single or repeated subcutaneous doses of PTH 1-34 or a DC-PTH at 20 nmol/kg. Control animals received vehicle only. Serum samples were analyzed for ionized calcium (iCa), phosphate, PTH, and DC-PTH. A pharmacokinetic-pharmacodynamic (PK-PD) model was built for cinacalcet, PTH 1-34, and DC-PTH using Phoenix64. Cinacalcet reduced iCa levels between 2 and 24 hours, returning to baseline by 72 hours post dose with nadir at 8 hours (analysis of variance P < .001), associated with a fall in rat PTH. For phosphate there was a variable biphasic response. Single-dose PTH abrogated the cinacalcet-induced fall in iCa for up to 2 hours. DC-PTH prevented the fall in iCa from 4 hours post dose and gave a prolonged response, with iCa levels quicker to return to baseline than controls. DC-PTH has a half-life of 11.5 hours, approximately 44 times longer than human PTH 1-34. The PK-PD models defined the reproducible effect of cinacalcet on iCa and that DC-PTH had prolonged biological activity. The administration of cinacalcet provides a robust and reproducible nonsurgical animal model of hypoparathyroidism. DC-PTH holds promise for the treatment of hypoparathyroidism in the future.

Hypoparathyroidism in Pregnancy and Lactation: Current Approach to Diagnosis and Management

Background: Hypoparathyroidism is an uncommon endocrine disorder. During pregnancy, multiple changes occur in the calcium-regulating hormones, which may affect the requirements of calcium and active vitamin D during pregnancy in patients with hypoparathyroidism. Close monitoring of serum calcium during pregnancy and lactation is ideal in order to optimize maternal and fetal outcomes. In this review, we describe calcium homeostasis during pregnancy in euparathyroid individuals and also review the diagnosis and management of hypoparathyroidism during pregnancy and lactation. Methods: We searched the MEDLINE, CINAHL, EMBASE, and Google scholar databases from 1 January 1990 to 31 December 2020. Case reports, case series, book chapters, and clinical guidelines were included in this review. Conclusions: During pregnancy, rises in 1,25-dihydroxyvitamin D (1,25-(OH)2-D3) and PTH-related peptide result in suppression of PTH and enhanced calcium absorption from the bowel. In individuals with hypoparathyroidism, the requirements for calcium and active vitamin D may decrease. Close monitoring of serum calcium is advised in women with hypoparathyroidism with adjustment of the doses of calcium and active vitamin D to ensure that serum calcium is maintained in the low-normal to mid-normal reference range. Hyper- and hypocalcemia should be avoided in order to reduce the maternal and fetal complications of hypoparathyroidism during pregnancy and lactation. Standard of care therapy consisting of elemental calcium, active vitamin D, and vitamin D is safe during pregnancy.

Canadian national hypoparathyroidism registry: an overview of hypoparathyroidism in Canada.

To evaluate the epidemiology, presentation and management of hypoparathyroidism in Canada. Hypoparathyroidism is associated with significant morbidity and poor quality of life. We present baseline results from the Canadian National Hypoparathyroidism Registry, a prospective observational study evaluating hypoparathyroidism in Canada. Our study enrolled 130 patients with hypoparathyroidism. Patients were followed every 6 months with clinical and lab assessments. We present baseline data in this manuscript. Seventy percent (91/130) of patients had postsurgical hypoparathyroidism, 30% (39/130) of patients had nonsurgical hypoparathyroidism due to autoimmune, genetic or idiopathic causes, and a molecular diagnosis was confirmed in 11 of these 39 patients. Pseudohypoparathyroidism was confirmed in 4/39 patients, DiGeorge syndrome in 2/39 patients, Barakat syndrome with a mutation in the GATA3 gene in 1/39, and activating mutations of the CASR gene in 3/39 patients with nonsurgical hypoparathyroidism. Renal complications with nephrocalcinosis or nephrolithiasis were present in 27% (14/52) of patients with postsurgical disease and 17% (4/24) of patients with nonsurgical hypoparathyroidism. Basal ganglia calcification was noted on imaging in 15% (n = 5/34) of patients with postsurgical hypoparathyroidism and 37% (n = 7/19) of patients with nonsurgical hypoparathyroidism. Hypercalciuria was more commonly seen in those with renal complications of nephrocalcinosis, nephrolithiasis or CKD, and hyperphosphatemia was more commonly seen in those with basal ganglia calcification. Hospitalization occurred in 28% of those with postsurgical hypoparathyroidism and 46% of those with nonsurgical hypoparathyroidism. Hypoparathyroidism is associated with significant morbidity. Effective strategies to reduce the short-and long-term complications of hypoparathyroidism need to be developed and evaluated.

Methodology for the Guidelines on Evaluation and Management of Hypoparathyroidism and Primary Hyperparathyroidism.

To develop guidelines for hypoparathyroidism and primary hyperparathyroidism, the panel assembled a panel of experts in parathyroid disorders, general endocrinologists, representatives of the Hypoparathyroidism Association, and systematic review and guideline methodologists. The guideline panel referred to a formal process following the Recommendations, Assessment, Development, and Evaluation Working Group (GRADE) methodology to issue GRADEd recommendations. In this approach, panelists and methodologists formatted the questions, conducted systematic reviews, evaluated risk of bias, assessed certainty of evidence, and presented a summary of findings in a transparent fashion. For most recommendations, the task forces used a less structured approach largely based on narrative reviews to issue non-GRADEd recommendations. The panel issued Eight GRADEd recommendations (seven for hypoparathyroidism and one for hyperparathyroidism). Each GRADEd recommendation is linked to the underlying body of evidence and judgments regarding the certainty of evidence and strength of recommendations, values and preferences, and costs, feasibility, acceptability and equity. This article summarizes the methodology for issuing GRADEd and non-GRADEd recommendations for patients with hypoparathyroidism or hyperparathyroidism. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

Recent advances in understanding and managing hypoparathyroidism

Hypoparathyroidism is a rare endocrine disorder which leads to hypocalcemia, hypercalciuria, and hyperphosphatemia. Complications include nephrocalcinosis with renal dysfunction, reduced quality of life, and abnormal skeletal properties. Conventional therapy with calcium and vitamin D analogs addresses hypocalcemia but has important limitations. Parathyroid hormone (PTH) therapy is a fundamental advance, although the effects of PTH on long-term complications require additional testing. Continuous PTH therapy is likely to be particularly advantageous for addressing renal, quality of life, and skeletal complications. Overall, much progress has been made, yet more information is needed to improve our understanding and management of hypoparathyroidism.

Management of hypoparathyroidism during pregnancy

Hypoparathyroidism during pregnancy is an uncommon clinical problem, By presenting a case of post-surgical hypoparathyroidism during pregnancy, this paper reviewed calcium physiology in pregnancy, as well as characteristics of pregnant women with hypoparathyroidism which differ from those of normal pregnant women in order to help readers better undarstand the complexity of this problem and management of hypoparathyroidism during pregnancy. Key words: Hypoparathyroidism; Pregnancy; Calcium metabolism; Treatment

Standards of care for hypoparathyroidism in adults: a Canadian and International Consensus.

Purpose: To provide practice recommendations for the diagnosis and management of hypoparathyroidism in adults. Methods: Key questions pertaining to the diagnosis and management of hypoparathyroidism were addressed following a literature review. We searched PubMed, MEDLINE, EMBASE and Cochrane databases from January 2000 to March 2018 using keywords ‘hypoparathyroidism, diagnosis, treatment, calcium, PTH, calcidiol, calcitriol, hydrochlorothiazide and pregnancy’. Only English language papers involving humans were included. We excluded letters, reviews and editorials. The quality of evidence was evaluated based on the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. These standards of care for hypoparathyroidism have been endorsed by the Canadian Society of Endocrinology and Metabolism. Results: Hypoparathyroidism is a rare disease characterized by hypocalcemia, hyperphosphatemia and a low or inappropriately normal serum parathyroid hormone level (PTH). The majority of cases are post-surgical (75%) with nonsurgical causes accounting for the remaining 25% of cases. A careful review is required to determine the etiology of the hypoparathyroidism in individuals with nonsurgical disease. Hypoparathyroidism is associated with significant morbidity and poor quality of life. Treatment requires close monitoring as well as patient education. Conventional therapy with calcium supplements and active vitamin D analogs is effective in improving serum calcium as well as in controlling the symptoms of hypocalcemia. PTH replacement is of value in lowering the doses of calcium and active vitamin D analogs required and may be of value in lowering long-term complications of hypoparathyroidism. This manuscript addresses acute and chronic management of hypoparathyroidism in adults. Main conclusions: Hypoparathyroidism requires careful evaluation and pharmacologic intervention in order to improve serum calcium and control the symptoms of hypocalcemia. Frequent laboratory monitoring of the biochemical profile and patient education is essential to achieving optimal control of serum calcium.

Management of hypoparathyroidism against European guidelines: Experience of a large teaching hospital

Management of hypoparathyroidism against European guidelines: Experience of a large teaching hospital

Advances in the treatment of hypoparathyroidism with PTH 1-34.

Hypoparathyroidism is a rare disorder of calcium metabolism which is treated with calcium and vitamin D analogs. Although conventional therapy effectively raises serum calcium, it bypasses the potent calcium reabsorption effects of PTH on the kidney which leads to hypercalciuria and an increased risk of nephrocalcinosis and renal insufficiency. Twenty-five years ago, we launched the first systematic investigation into synthetic human PTH 1-34 replacement therapy in both adults and children. These studies led to our current understanding of the complex nature of PTH 1-34 therapy and to the challenges we still face in our pursuit of a safe and effective physiologic replacement therapy for hypoparathyroidism. The normalization and minimal fluctuation of serum and urine calcium levels were the primary management goals. As the frequency of PTH 1-34 injections increased, the total daily dose required to normalize calcium homeostasis decreased and episodes of hypercalcemia and hypercalciuria diminished, producing a more physiologic biochemical profile. Twice-daily injections achieved simultaneous normalization of serum and urine calcium levels in many patients but the persistent elevation of bone markers and the difficulty in reducing urine calcium to normal levels in the more severe cases, suggested an alternative to PTH 1-34 injections was needed. The studies with PTH 1-34 delivered by insulin pump represent an important advance in the management of hypoparathyroidism. PTH 1-34 delivered by insulin pump normalized serum and urine calcium and markers of bone turnover. Additionally, pump delivery of PTH 1-34 produced stable magnesium values within the normal range and reduced magnesium excretion. Currently, PTH 1-34 delivery by pump is the only alternative to PTH injections that has been tested in both adults and children and proven to achieve a physiologic biochemical profile.

The Management of Permanent Primary Hypoparathyroidism in Children and Adolescents: A Complex Task.

Management of hypoparathyroidism (hypoPT), depends on the etiology and the severity of hypocalcemia. Treatment goals include control of hypocalcemic symptoms preserving serum calcium in the low-normal range and phosphate in the high normal range. While correction of serum calcium to low-normal range does not fully correct mineral and bone metabolism it may be associated with increased risk of complications such as nephrolithiasis, nephrocalcinosis and soft tissue calcifications. Therefore, it is imperative to find out ways to individualize treatment of patients with hypoPT to achieve the best prognosis while minimizing complications. Replacement therapy with recombinant human PTH (rhPTH) was recently tested for optimizing treatment of hypoPT in a small number of patients. For children and adolescents, further studies are needed to evaluate the long-term effects and safety of rhPTH. In this short review we summarize current knowledge on the management of hypoPT and debate our gaps on the long-term management of children and adolescents with hypoPT.

Hypoparathyroidism: is it that easy to treat?

Hypoparathyroidism is a relatively rare endocrine disease characterised by either null or inappropriately low secretion of parathyroid hormone (PTH) for serum calcium levels. The other main laboratory findings include hypocalcaemia, inappropriately normal or high urine calcium excretion and hyperphosphataemia with low urine phosphate excretion. The management of hypoparathyroidism should be tailored to each individual case, which makes it a demanding undertaking in everyday clinical practice. In this review, we sought to focus on the diagnostic approach of hypoparathyroidism and the therapeutic challenges of the disease from a clinical perspective. Conventional treatment with vitamin D analogues and calcium salts is no longer the only available treatment, since replacement treatment with PTH(1-84) has recently been approved for the disease. However, the optimal treatment schedule is yet to be defined.

Hypoparathyroidism – Review of the Literature 2018

Hypoparathyroidism is a rare endocrine disorder characterized by low calcium and high phosphate levels, in the setting of a low or inappropriately normal PTH level. Given its rarity, it has been classified as an orphan disease in the United States and by the European Commission. The first international conference on the management of hypoparathyroidism was convened in Florence Italy 2015 and resulted in the publication of detailed guidelines on the epidemiology, presentation, clinical features and management of hypoparathyroidism. Hypoparathyroidism may be associated with a spectrum of clinical manifestations, ranging from asymptomatic in the setting of mild hypocalcemia, to life threatening cardiac arrythmias, seizures or laryngospasm, in the setting of severe acute hypocalcemia. The most common cause is postsurgical hypoparathyroidism following anterior neck surgery, followed by autoimmune disorders and rarely genetic disorders. Establishing a diagnosis of hypoparathyroidism is important as it is associated with the development of kidney stones, renal insufficiency, cataracts, basal ganglia calcifications, as well as a reduced health-related quality of life. Most patients with chronic hypoparathyroidism require lifelong high dose calcium and activated vitamin D supplements. The goals of treatment are 3 fold, namely, relieve symptoms of hypocalcemia, raise calcium concentration to the low-normal range and avoid hypercalciuria. For those individuals who cannot maintain a stable serum and urine calcium with conventional calcium and activated Vitamin D regimens, the addition of recombinant PTH (1-84) is currently an option. The approval of recombinant PTH (1-84) represents a significant step forward in the management of this disorder.

Hypoparathyroidism and pseudohypoparathyroidism: etiology, laboratory features and complications.

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