Hypoparathyroidism versus hyperparathyroidism in pediatric dialysis patients; a single center study (original) (raw)

Assessment of Calcium, Phosphorous Parathyroid Hormone

Libyan Medical Journal , 2024

Abstract Dialysis is essential for patients with end-stage renal disease (ESRD), a potentially fatal illness. Nev-ertheless, Patients continue encountering significant metabolic issues, such as calcium and phos-phate imbalances, even with dialysis. These disorders raise the risk of cardiovascular disease, bone fragility, and death. Examples of these disorders include hypocalcemia, hyperphosphatemia, and sec-ondary hyperparathyroidism. Although many patients are aware of these problems, less focus has been placed on aspects that may be changed, like dietary choices, the use of supplements, and the way comorbid conditions like hypertension and diabetes mellitus (DM) exacerbate these imbalances. This study investigates the prevalence and factors contributing to calcium-phosphate imbalances in ESRD patients on dialysis. It examines how demographic, clinical, and lifestyle factors influence these metabolic disturbances, aiming to inform more individualized care. This cross-sectional study was conducted at Ibn Sina Teaching Hospital, Sirt, Libya from November 2023 to June 2024. A total of 99 ESRD patients undergoing dialysis. The measures obtained were Serum calcium, phosphate, and parathyroid hormone (PTH) levels. The study also collected data on6 age, gender, DM and hy-pertension, supplement use, and dairy consumption. Correlation analyses were performed to explore the relationships between these variables and mineral disturbances. The study found that 78.8% of patients had low calcium levels, and 70.7% had elevated phosphate levels despite dialysis. 57.6% of patients exhibited elevated PTH, indicating secondary hyperparathyroidism. DM was present in 39.4% of patients, and 80.8% of patients had hypertension. Notably, 56.6% of patients used supple-ments, and 53.5% consumed dairy products, but hypocalcemia persisted in the majority. The findings emphasize the difficulty of maintaining calcium and phosphate imbalances in ESRD patients receiving dialysis. These results highlight the necessity of patient-specific, customized approaches to regulating mineral metabolism, particularly in individuals with co-occurring diseases such as diabetes mellitus and hypertension. Reducing problems and raising ESRD patients' quality of life requires addressing these imbalances. Keywords: ESRD, PTH, Calcium, Phosphate, Diseases, DM.

Parathyroid gland function in dialysis patients

Journal of Parathyroid Disease, 2015

Parathyroid disorder, is a common consequence of end-stage kidney disease (ESRD) and maintenance dialysis patient. This article, aims to investigate parathyroid disorders consisting symptoms, signs, laboratory findings, prevention and its treatment in dialysis patients. Directory of Open Access Journals (DOAJ), Google Scholar, PubMed, and Web of Science has been searched. Secondary hyperparathyroidism is one of disorders in minerals metabolism in ESRD patients, resulted from calcium reduction in blood due to a decrease in synthesis of active vitamin D, acidosis, and an increase in blood phosphorus, and also 1-alpha-hydroxylase deficiency that can cause bone demineralization as well as renal osteodystrophy with symptoms such as bone pain and fractures, and even vessels and soft-tissue calcification which can affect duration of hospitalization, hospital costs and length and quality of life. The findings show that with accurate measurement of serum level of laboratory values of alkaline phosphatase, calcium, and phosphorous monthly, and parathormone every six months, training the dialysis patients, recommending a diet with low phosphorous and appropriated use of phosphate binding agents will improve the outcome of hemodialysis patients.

Secondary Hyperparathyroidism and Hypocalcaemia in Dialysis Patients in AKTH

The Aminu Kano Teaching Hospital (AKTH) is one of the tertiary health institutions in Nigeria where dialysis is provided to patients with chronic renal disease, but there had been no reported study on the prevalence of biochemical indicators of bone and mineral metabolism in these patients. We measured serum parathyroid hormone (PTH), total calcium (Ca), albumin (ALB) and phosphate (P) and calculated calcium-phosphate (CaP) ion product in order to evaluate parathyroid function and bone mineral status in dialysis patients seen at the AKTH, Kano. Forty five patients and fourty-five healthy age matched hospital staff who served as controls were studied. Intact PTH was measured with a commercial kit which is based on immunoassay (DRG International Incorp, USA) while serum calcium, phosphate and albumin were estimated also with commercial kits (Randox Laboratories, UK). Calcium was corrected for albumin.The mean PTH of 194 pg/mL in dialysis patients was significantly higher (P< 0.001) than 28 pg/mL found in controls. The corrected calcium was 1.81 mmol/L, phosphate 2.26 mrnol/L, albumin 27.09 g/L and CaP product 3.35 mmoF/U in dialysis patients compared to calcium of 2.46 mmol/L, phosphate 1.04 mmol/L, albumin 42.78 glL and CaP product of 2.55 mmoF/U in controls. Fourty eight percent of the patients had secondary hyperparathyroidism, 89% hypocalcaemia, 53% hyperphosphataernia, 82% hypoalbuminaemia and 29% elevated CaP product. This study has demonstrated significant abnormality of calcium, phosphate and parathyroid homeostasis in patients undergoing dialysis in Kano. As persistent elevations of PTH, phosphate, CaP product and co-existing hypocalcaemia are known to contribute to morbidity and mortality in dialysis patients, it is recommended that pharmacological correction and routine measurement ofthese biochemical indicators be instituted for management of haemodialysis patients in our hospitals.

Biochemical Effects of High Dialysate Calcium in Hemodialysis Patients with Hyperparathyroidism: A 10 Month Study

ASAIO Journal, 2003

In the past 15 years, there has been a trend to decrease dialysate calcium concentrations to prevent hypercalcemia. However, low dialysate calcium can provoke hyperparathyroidism. The time course of the effect of increasing dialysate calcium is not well characterized, and the effect on calciumphosphate product is unclear. Therefore, we studied the effect of increasing dialysate calcium from 1.5 to 1.75 mM in 21 stable patients on hemodialysis who had serum phosphate of less than 2 mM and serum calcium of less than 2.4 mM. Over 10 months, parathyroid hormone levels fell from 39.6 to 16.6 pM (p < 0.0001), whereas serum calcium increased from 2.27 to 2.41 mM. There were no significant changes in serum phosphate or the calcium-phosphate product. Three patients became hypercalcemic when their parathyroid hormone levels were suppressed to less than 10 pM. We conclude that in carefully selected patients, increasing dialysate calcium can safely treat hyperparathyroidism with minimal risk of complications. This treatment has the advantage over the use of vitamin D therapy of being less expensive, independent of patient compliance, and less likely to cause increases in serum phosphate or calcium-phosphate product.

Are we overconcerned about secondary hyperparathyroidism and underestimating the more common secondary hypoparathyroidism in our dialysis patients?

The Journal of the Association of Physicians of India, 2012

The aim of the study was to determine the prevalence of hyper and hypo-parathyroid state in prevalent dialysis patients. The second part of the study was to look for the prevalence of vascular calcification (abdominal aortic) and factors predicting calcification in these patients. All adult patients, who were more than 1 month on dialysis, were included in the study. A total of 68 patients, of which 75% were on hemodialysis and 25% on peritoneal dialysis, were finally studied. Patients' parathyroid status was defined as per target recommendation of KDOQI--hypoparathyroid with iPTH < or = 150 pg/ml and hyperparathyroid with iPTH > 300 pg/ml. Vascular calcification was determined by X ray of lateral lumbar spine to look for abdominal aortic calcification (AAC). The AAC was scored as validated. The prevalence of hyper- and hypoparathyroidism in dialysis patients was determined as percentage of total dialysis patients. The prevalence of AAC and factors predicting it was analyz...

Intravenous calcitriol for treatment of hyperparathyroidism in children on hemodialysis

Pediatric Nephrology, 2005

This double-blind, placebo-controlled study evaluated the safety and efficacy of intravenous (IV) calcitriol (Calcijex) for treatment of secondary hyperparathyroidism (2HPT) in pediatric end-stage renal disease (ESRD) patients on hemodialysis (HD). After a 2 to 6-week washout period of all vitamin D compounds, patients with two consecutive PTH values >400 pg mL 1 , calcium levels 10.5 mg dL 1 and calciumphosphorus product values 70 mg 2 dL 2 were eligible for the treatment phase. Patients received a bolus injection of calcitriol or placebo three times a week, immediately after dialysis for up to 12 weeks. Initial doses (0.5-1.5 mg) were based on the severity of 2ºHPT. The dose was increased every two weeks by 0.25 mg until there was at least a 30% decrease in PTH from baseline, or Ca>11.0 mg dL 1 , or CaP>75 mg 2 dL 2 . Overall, 11/21 (52%) patients in the calcitriol group had two consecutive !30% decreases from baseline in serum PTH compared with 5/26 (19%) patients in the placebo group (P=0.03). The mean total alkaline phosphatase decreased from 274 to 232 IU L 1 in the calcitriol group and increased from 547 to 669 IU L 1 in the placebo group (P=0.002). The mean bone-specific alkaline phosphatase decreased from 72.5 to 68 mg L 1 in the calcitriol group and increased from 105.3 to 148.5 mg L 1 in the placebo group (P=0.03). The incidence of two consecutive occurrences of elevated calciumphosphorus (CaP>75 mg 2 dL 2 ) product was higher in the calcitriol group than in the placebo group (P=0.01). Two consecutive occurrences of phosphorus >6.5 mg dL 1 occurred in 71% of the calcitriol group and 46% of the placebo group (P=0.14). Calcium levels >10.5 mg dL 1 were more common in the calcitriol group than in the placebo group (P=0.01). There was a direct relationship between serum phosphorus concentration and the percentage change in PTH from baseline in both the calcitriol group (r=0.46; P<0.0001) and the placebo group (r=0.21; P=0.0005). This study demonstrates that IV calcitriol, at initial doses of 0.5-1.5 mg, effectively reduces PTH levels in pediatric HD patients and that patients should be closely monitored for hyperphosphatemia and elevated CaP product.

The set point of calcium and the reduction of parathyroid hormone in hemodialysis patients

Kidney International, 1996

The set point of calcium and the reduction of parathyroid hormone in hemodialysis patients. Since in some studies in hemodialysis patients calcitriol treatment has resulted in a reduction of both parathyroid hormone (PTH) levels and the set point of calcium, it has been suggested that the set point of calcium reflects a reduction in the magnitude of hyperparathyroidism. However, others have maintained that the set point of calcium is primarily an indicator of the serum calcium at which PTH is secreted and may be dissociated from the magnitude of hyperparathyroidism. The present study was designed to evaluate how a reduction in PTH levels associated with an increase in the predialysis (basal) serum calcium would affect the set point of calcium. Two different treatments were used to produce a reduction in PTH that was associated with an increase in predialysis serum calcium. In the first group, hemodialysis patients received 2 rg of intravenous calcitriol and were dialyzed with a 3.5 mEq/liter calcium dialysate for six weeks; in the second group, hemodialysis patients were dialyzed with a 4 mEq/liter calcium dialysate and had oral calcium supplementation increased for six weeks. In both groups, low and high calcium studies were performed to determine the PTH-calcium relationship before treatment, at the end of six weeks of treatment, and six weeks after the discontinuation of treatment. In the calcitriol group, the predialysis calcium increased from 9.62 0.34 to 10.56 0.31 mgldl, P < 0.05 and the Set point of calcium increased from 9.34 0.23 to 9.79 0.25 mgldl, P < 0.05 at the same time as maximally stimulated PTH decreased from 2637 687 to 1555 617 pg/mI, P < 0.05. In the high calcium dialysate group, the predialysis serum calcium increased from 9.19 0.31 to 9.84 0.28 mg/dl, P < 0.05, and set point of calcium increased from 9.01 0.28 to 9.39 0.22 mg/dl, P < 0.05 at the same time as maximally stimulated PTH decreased from 1642 450 to 1349 513 pg/mI, P < 0.05. Discontinuation of treatment for six weeks resulted in a return to pretreatment values. In conclusion, our results would suggest that the Set point of calcium may not be a reliable indicator of the magnitude of hyperparathyroidism during calcitriol treatment, and (2) PTH secretion may adapt to the ambient serum calcium concentration. In most studies in hemodialysis patients, calcitriol treatment has resulted in a reduction in parathyroid hormone (PTH) levels [1-41. However, while ealcitriol treatment of dialysis patients with secondary hyperparathyroidism has been shown to reduce PTH levels, the effect of calcitriol on the set point of calcium, defined as the serum calcium concentration at which maximal PTH secretion is reduced by 50% [5], is controversial inasmuch as some studies have reported a reduction in the set point of calcium [3, 6, 7], while in other studies, the set point of calcium did not change despite a reduction in PTH levels [2, 4, 8, 9]. Moreover, it has been suggested that the set point of calcium reflects the reduction in the magnitude of hyperparathyroidism, and thus an inability to reduce the set point of calcium indicates a refractoriness to treatment that may require a parathyroidectomy [3, 7, 91.