scholarly journals Achievement of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative: recommended serum calcium, phosphate and parathyroid hormone values with parathyroidectomy in patients with secondary hyperparathyroidism

2013 ◽  
Vol 85 (1) ◽  
pp. 25 ◽  
Author(s):  
Woo Young Kim ◽  
Jae Bok Lee ◽  
Hoon Yub Kim ◽  
Sang Uk Woo ◽  
Gil Soo Son ◽  
...  
2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Tsung-Liang Ma ◽  
Peir-Haur Hung ◽  
Ing-Ching Jong ◽  
Chih-Yen Hiao ◽  
Yueh-Han Hsu ◽  
...  

Secondary hyperparathyroidism increases morbidity and mortality in hemodialysis patients. The Kidney Disease Outcomes Quality Initiative Guidelines recommend parathyroidectomy for patients with chronic kidney disease and parathyroid hormone concentrations exceeding 800 pg/mL; however, this concentration represents an arbitrary cut-off value. The present study was conducted to identify factors influencing mortality in hemodialysis patients with parathyroid hormone concentrations exceeding 800 pg/mL and to evaluate the effects of parathyroidectomy on outcome for these patients. Two hundred twenty-one hemodialysis patients with parathyroid hormone concentrations > 800 pg/mL from July 2004 to June 2010 were identified. 21.1% of patients (n = 60) received parathyroidectomy and 14.9% of patients (n = 33) died during a mean follow-up of 36 months. Patients with parathyroidectomy were found to have lower all-cause mortality (adjusted hazard ratio [aHR]: 0.34). Other independent predictors included age ≥ 65 years (aHR: 2.11) and diabetes mellitus (aHR: 3.80). For cardiovascular mortality, parathyroidectomy was associated with lower mortality (HR = 0.31) but with a marginal statistical significance (p = 0.061). In multivariate analysis, diabetes was the only significant predictor (aHR: 3.14). It is concluded that, for hemodialysis patients with parathyroid hormone concentrations greater than 800 pg/mL, parathyroidectomy is associated with reduced all-cause mortality.


Author(s):  
Stefania Sella ◽  
Luciana Bonfante ◽  
Maria Fusaro ◽  
Flavia Neri ◽  
Mario Plebani ◽  
...  

AbstractObjectivesKidney transplant (KTx) recipients frequently have deficient or insufficient levels of serum vitamin D. Few studies have investigated the effect of cholecalciferol in these patients. We evaluated the efficacy of weekly cholecalciferol administration on parathyroid hormone (PTH) levels in stable KTx patients with chronic kidney disease stage 1–3.MethodsIn this retrospective cohort study, 48 stable KTx recipients (37 males, 11 females, aged 52 ± 11 years and 26 months post-transplantation) were treated weekly with oral cholecalciferol (7500–8750 IU) for 12 months and compared to 44 untreated age- and gender-matched recipients. Changes in levels of PTH, 25(OH) vitamin D (25[OH]D), serum calcium, phosphate, creatinine and estimated glomerular filtration rate (eGFR) were measured at baseline, 6 and 12 months.ResultsAt baseline, clinical characteristics were similar between treated and untreated patients. Considering the entire cohort, 87 (94.6%) were deficient in vitamin D and 64 (69.6%) had PTH ≥130 pg/mL. Serum calcium, phosphate, creatinine and eGFR did not differ between groups over the follow-up period. However, 25(OH)D levels were significantly higher at both 6 (63.5 vs. 30.3 nmol/L, p < 0.001) and 12 months (69.4 vs. 30 nmol/L, p < 0.001) in treated vs. untreated patients, corresponding with a significant reduction in PTH at both 6 (112 vs. 161 pg/mL) and 12 months (109 vs. 154 pg/mL) in treated vs. untreated patients, respectively (p < 0.001 for both).ConclusionsWeekly administration of cholecalciferol can significantly and stably reduce PTH levels, without any adverse effects on serum calcium and renal function.


Author(s):  
Patrick Biggar ◽  
Hansjörg Rothe ◽  
Markus Ketteler

Chronic kidney disease-mineral and bone disorders (CKD-MBD), calcium, phosphate, and parathyroid hormone are biomarkers of mortality and cardiovascular risk. Hyperphosphataemia is a prominent and pathophysiologically most plausible risk indicator. Calcium balance and load appear to be more important than serum concentrations. Parathyroid hormone is a less reliable marker with a relatively wide range extending above that applicable for a normal population especially when used as a singular laboratory parameter without additional assessment of bone metabolism, for example, bone-specific alkaline phosphatase and bone biopsy. There is not a single prospective controlled hard-outcome study that provides us with unequivocal evidence that such an isolated laboratory parameter-based treatment approach will lead to significant clinical improvements. As CKD-MBD is complex, clinical decisions would be made easier by informative prospective trials.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Ryuta Fujimura ◽  
SHOGO SHIBATA ◽  
Takechiyo Tokuda ◽  
Ayako Tanaka ◽  
Aya Mizumoto ◽  
...  

Abstract Background and Aims Among patients with chronic kidney disease (CKD) at predialysis stage, there is a high incidence of secondary hyperparathyroidism. Metabolic changes associated with secondary hyperparathyroidism lead to renal osteodystrophy, including osteitis fibrosa, ectopic calcification, cardiovascular disease, and the risk of death, and serum parathyroid hormone levels are influenced by nutritional variables. Non-dialyzed CKD patients are especially prone to vitamin C deficiency because of dietary restrictions and malnutrition. Vitamin C is an important antioxidant and relates to the development and maintenance of bone tissues. However, the contribution of vitamin C deficiency to parathyroid hormone secretion is unknown. Here, we performed a single-center cross-sectional study in order to assess association of serum vitamin C and parathyroid hormone in non-dialyzed CKD patients. Method We had 280 consecutive patients who underwent serum vitamin C and serum intact parathyroid hormone (iPTH) measurement for screening purposes from January 1st, 2013 to November 30th, 2017. We analysed a total of 128 patients (71.3±11.6 year-old, 80 males) who had an estimated glomerular filtration rate (eGFR) that remained less than 60 mL/min/1.73m2 after 152 patients were excluded because of vitamin C or vitamin D supplementation, age &lt;20 years, dialysis, positive serostatus for HIV, hepatitis B or hepatitis C, chronic infection, or cancer. Results Twenty-three percent of the patients (n=29) had vitamin C levels&lt; 2.0 μg/mL (a range seen in very deficient subjects), 53% (n=68) had levels between 2.0 and 5.5 μg/mL, and 31 patients (24%) had vitamin C levels &gt;5.5 μg/mL, which is considered the upper limit of normal for the healthy population. Log(iPTH) significantly correlated with age (r=-0.238, p=0.00672), log(eGFR) (r=-0.625, p&lt;0.0001), serum calcium (r=-0.609, p&lt;0.0001), and serum phosphate (r=0.41, p&lt;0.0001), and had a tendency to correlate with serum albumin (r=-0.146, p=0.101). Low serum vitamin C was associated with higher serum iPTH (P=0.0005, one-way analysis of variance). In a multiple linear regression model with log(iPTH) as the dependent variable, and age, gender, log(eGFR), serum levels of calcium, phosphate, albumin, and vitamin C as independent variables, the inverse relationship of log(iPTH) and serum vitamin C was confirmed (R2 = 0.568, adjusted R2 = 0.543, P&lt;0.0001), along with other parameters influencing iPTH levels, including age, log(eGFR), serum calcium, and serum phosphate. Low vitamin C levels were also associated with increased serum alkaline phosphatase (r=-0.209, p=0.0179), a further indicator of the impact of vitamin C status on bone metabolism. Conclusion Vitamin C deficiency is prevalent in a significant proportion of non-dialyzed CKD patients. Low vitamin C levels contribute to secondary hyperparathyroidism, leading to increased bone turnover. This novel observation may result from effects of vitamin C on vitamin D metabolism, vitamin D binding in target tissues, and cAMP-linked signalling pathways in bone and parathyroid gland. Therapeutic intervention with supplemental vitamin C for secondary hyperparathyroidism might be a good strategy.


2017 ◽  
Vol 20 (2) ◽  
pp. 63-68 ◽  
Author(s):  
Lilit V. Egshatyan ◽  
Natalya G. Mokrisheva ◽  
Lyudmila Ya. Rozhinskaya

In the treatment of secondary hyperparathyroidism of end-stage chronic kidney disease, vitamin D receptor activation and allosteric modulators of the calcium-sensing receptor – inhibit glandular hyperplasia, reduce parathyroid hormone levels, impact on bone turnover and mineral density. But the use of calcimimetic and vitamin D analogs or mimetics did not reduce the need for parathyroidectomy for refractory hyperparathyroidism. The enlarged parathyroid gland and gland nodular transformation became refractory to medical therapy and patient need for parathyroidectomy. Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone after a long period of secondary hyperparathyroidism and renal transplantation. In this article, we present the case of a Caucasian male with chronic kidney disease (end-stage on chronic hemodialysis and after kidney transplantation) and different forms of hyperparathyroidism (secondary and tertiary). Our case study shows that only a multi-interventional strategy is likely to be more effective treatment in cases of severe and refractory to medical therapy hyperparathyroidism.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Maimoona Bahlol ◽  
Alan Scott Sacerdote ◽  
Gul Bahtiyar

Abstract •Our patient is a 63-year-old African American female with medical history significant for hypertension, class 1 obesity, osteoarthritis of knees who initially presented to the adult ambulatory clinic on 9/19/2013 with complaints of body aches and bone pain. Labs were remarkable for a serum calcium level of 9.8 mg/dl, serum phosphorous of 4.7 mg/dl, and serum parathyroid hormone level of 166 pg/ml (15-65 pg/ml), normal GFR and serum vitamin 25-OH D of 62. A DEXA scan was performed which showed mild osteopenia wof 1.0 (0.8-1.8), serum 1,25 - OH vitamin D of &lt;8 pg/ml, normal alpha and beta carotene level, negative endomysial antibodies and normal magnesium level. A diagnosis of secondary hyperparathyroidism with unclear etiology was made. Same treatment was continued and a follow up in 3 months with repeat labs was advised. Repeat PTH went up to 281pg/ml but serum calcium and phosphate remained normal. Based on normal serum 25 OH vitamin D and low 1, 25 OH vitamin D, patient was started on calcitriol 0.25 mg daily. On next follow up in 3 months PTH decreased to 203pg/ml and 1, 25 OH vitamin D level normalized (35pg/ml). MEN was excluded with normal serum free metanephrine and gastrin levels. On subsequent visits DEXA scan normalized and PTH further trended downward to 101.7 pg/ml. Patient was discharged from endocrine clinic back to the PCP. • •Patient continued to follow up in adult medicine clinic but calcitriol fall off of patient’s medication list likely due to an error. Patient was off of calcitriol for 6 months but continue to take calcium vitamin D.PTH trended up to 186pg/ml and then to 350pg/ml. A referral to endocrinology was made again and a parathyroid sestamibi scan was obtained which did not reveal any abnormal uptake. Serum calcium, phosphate, magnesium and vitamin OH 25 vitamin D remained normal. •Patient was started back on calcitriol 0.5 mg daily and PTH again started to trend downward. The last PTH was down to 82 on March 20th 2019 with normal serum calcium, phosphate, magnesium and eGFR. The final diagnosis was secondary hyperparathyroidism due to decrease 1 alpha hydroxylase activityith a T score of −1.5 at left forearm. A diagnosis of primary hyperparathyroidism was made by the PCP and patient was started on calcium vitamin D and Fosamax and was referred to endocrinology for further evaluation. • •Further testing in the endocrine clinic revealed 24-hour urine calcium of 49 mg (100-300) and urine creatinine. This case report concludes that low 1-alpha hydroxylase activity should be considered as a cause of secondary hyperparathyroidism in a patient with normal GFR and 25-OH vitamin D level


1995 ◽  
Vol 6 (5) ◽  
pp. 1371-1378
Author(s):  
A J Felsenfeld ◽  
A Jara ◽  
M Pahl ◽  
J Bover ◽  
M Rodriguez

Hemodialysis patients with predialysis intact parathyroid hormone (PTH) levels of more than 500 pg/mL are generally considered to have marked secondary hyperparathyroidism. Because the serum calcium level in these patients varies from low to high, it is not clear whether every hemodialysis patient with a PTH level > 500 pg/mL is part of a uniform group. The dynamics of PTH secretion in 21 hemodialysis patients with predialysis (basal) intact PTH levels > 500 pg/mL (range, 506 to 1978 pg/mL) has been evaluated. The basal/maximal PTH ratio, an indicator of the degree of relative PTH stimulation in the baseline state, was inversely correlated with the maximal PTH (r = -0.71), the basal serum calcium (r = -0.70), and the difference between the serum calcium at basal and maximal PTH (r = 0.81); the latter is the decrement in serum calcium from baseline necessary to maximally stimulate PTH. Because the basal PTH level appeared to be disproportionately influenced by hypocalcemia, the 21 patients were separated into two groups on the basis of the basal serum calcium (Group I < 9 mg/dL and Group II > 9 mg/dL). Basal PTH was not different between the two groups, even though maximally stimulated PTH (1,219 +/- 204 versus 2,739 +/- 412 pg/mL; P < 0.01) as induced by hypocalcemia and maximally suppressed PTH (217 +/- 37 versus 528 +/- 104; P = 0.05) as induced by hypercalcemia were less in Group I with the low basal calcium; moreover, the ratio of basal/maximal PTH was higher (73 +/- 6 versus 47 +/- 5%; P < 0.01) in Group I with the low basal calcium. These results suggest that the reason for a basal PTH > 500 pg/mL may be different among hemodialysis patients. In hypocalcemic patients, the low serum calcium appeared to be a major impetus for the high basal PTH level. In conclusion, (1) the maximally stimulated PTH appears to provide a better means of separating patients with marked secondary hyperparathyroidism than the basal PTH and (2) hemodialysis patients with basal PTH levels > 500 pg/mL may not be a uniform group.


2020 ◽  
Author(s):  
Raimunda Sheyla Carneiro Dias ◽  
Dyego José Araújo Brito ◽  
Joyce Santos Lages ◽  
Alcione Miranda Santos ◽  
Elisangela Milhomen Santos ◽  
...  

Abstract Background: Disorders of mineral metabolism occur in most patients with chronic kidney disease (CKD). The aim of this work was to correlate serum parathyroid hormone (PTH) levels with urinary magnesium excretion in patients with non-dialysis CKD.Methods: Cross-sectional study with patients with CKD undergoing non-dialysis treatment in stages 3A, 3B and 4. Concentrations of creatinine, magnesium, calcium, phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D [25(OH)D] and alkaline phosphatase (ALP) were determined in blood samples. The assessment of urinary magnesium levels was performed by means of total daily excretion and by the excretion fraction (FEMg). Results: The study evaluated 163 patients with a mean age of 60.7 ± 11.7 years and 51.0% were male. In the highest quartile of PTH (> 89.5pg / ml), the mean levels of FEMg and ALP were higher (p <0.05), as well as the levels of serum calcium and eGFR were lower (p <0.05). In the unadjusted regression analysis, the following variables were related to serum PTH levels: FEMg (odds ratio (OR) = 1.12; 95% confidence intervals (CI): 1.02–1.23), Calcium (OR = 0.45; 95% CI: 0.22-0.90), ALP (OR = 1.02; 95% CI: 1.00-1.03) and eTFG (OR = 0.92; 95% CI: 1.00-1.03). After an adjusted analysis, only one FEMg and ALP will remain correlated with PTH. Conclusion: In patients with non-dialysis CKD, with higher levels of PTH, higher mean columns of ALP and FEMg, and lower levels of serum calcium and eGFR. FEMg and ALP were some variables that remained associated with PTH.


Author(s):  
Sara Elizabeth Gonzalez ◽  
Ira G. Roth ◽  
Chad W. Schmiedt ◽  
Michelle H. Patrick ◽  
Alison G. Meindl

A 6 yr old neutered male mixed-breed cat presented for renal transplantation (RTx) for chronic kidney disease. Severe periodontal disease was identified, and before initiation of immunosuppressive therapy, a comprehensive oral health assessment and treatment procedure was performed to reduce the burden of existing oral infection. Dental radiography revealed diffuse, severe bone demineralization across the mandible and maxilla, with thinning of the cortices. Nasal turbinates were easily visualized owing to the decreased opacity of maxillary bone. Generalized bone resorption left teeth to appear minimally attached. A Vitamin D panel revealed a severely elevated parathyroid hormone level. Full mouth extractions were performed. Seven days following this procedure, RTx was performed. Serum creatinine concentration was within normal limits by 48 hr after surgery and remained normal until discharge 12 days after RTx. At 3.5 mo after RTx, the cat was mildly azotemic, and the parathyroid hormone level was elevated but significantly decreased from the original measurement. Secondary hyperparathyroidism is a common abnormality in cats with chronic kidney disease. However, clinical manifestations of hyperparathyroidism are rare in this species. This is a novel presentation of a cat demonstrating bone loss in the oral cavity as a result of renal secondary hyperparathyroidism.


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