Literature DB >> 24527717

Predictors of renal function in primary hyperparathyroidism.

Marcella D Walker1, Thomas Nickolas, Anna Kepley, James A Lee, Chiyuan Zhang, Donald J McMahon, Shonni J Silverberg.   

Abstract

CONTEXT: Current guidelines for parathyroidectomy in primary hyperparathyroidism (PHPT) include an estimated glomerular filtration rate (eGFR) less than 60 mL/min per 1.73 m(2). Although the biochemical abnormalities associated with PHPT could impair renal function, there are currently no data examining whether more severe hypercalcemia, hypercalciuria, or nephrolithiasis are associated with chronic kidney disease (CKD) in mild PHPT.
OBJECTIVE: This cross-sectional study evaluated predictors of renal function in PHPT.
DESIGN: This is a case series of PHPT patients with (eGFR < 60 mL/min per 1.73 m(2)) and without (eGFR ≥ 60 mL/min per 1.73 m(2)) CKD. SETTINGS AND PARTICIPANTS: We studied 114 PHPT patients in a university hospital setting. OUTCOME MEASURES: We identified predictors of renal function using multiple linear regression.
RESULTS: eGFR was associated with age, hypertension, antihypertensive medication use, fasting glucose, and 25-hydroxyvitamin D. eGFR was positively rather than negatively associated with several PHPT disease severity indices including history of nephrolithiasis, 24-hour urinary calcium excretion, and 1,25-dihydroxyvitamin D but not serum calcium or PTH levels. An eGFR less than 60 mL/min per 1.73 m(2) was observed in 15% (n = 17), all of whom had stage 3 CKD (eGFR 30-59 mL/min per 1.73 m(2)). Those with CKD were older, had higher 25-hydroxyvitamin D levels and lower 1,25-dihydroxyvitamin D levels, and were more likely to be hypertensive than those without CKD. There were no between-group (<60 vs ≥60 mL/min per 1.73 m(2)) differences in serum calcium, PTH, nephrolithiasis, or meeting surgical criteria other than eGFR. Multiple linear regression indicated that age and diastolic blood pressure were negatively associated with eGFR, whereas serum calcium, kidney stones, and alcohol use were positive predictors. Calculation of eGFR using either the Modification of Diet in Renal Disease or Chronic Kidney Disease Epidemiology Collaboration equation yielded similar results.
CONCLUSIONS: PHPT patients with stage 3 CKD do not have biochemical or clinical evidence of more severe hyperparathyroidism compared with those without CKD. Traditional risk factors, rather than clinical or biochemical indices of PHPT, are associated with lower eGFR in mild PHPT.

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Year:  2014        PMID: 24527717      PMCID: PMC4010697          DOI: 10.1210/jc.2013-4192

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  27 in total

Review 1.  Clinical practice. Primary hyperparathyroidism.

Authors:  Claudio Marcocci; Filomena Cetani
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2.  Pre- and postoperative evaluation of renal function with five different tests in patients with primary hyperparathyroidism.

Authors:  A Kristoffersson; C Backman; K Granqvist; J Järhult
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Review 3.  Primary hyperparathyroidism and the kidney: biochemical and clinical spectrum.

Authors:  Munro Peacock
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4.  Increased circulating levels of FGF23: an adaptive response in primary hyperparathyroidism?

Authors:  Janneke E Witteveen; Antoon H van Lierop; Socrates E Papapoulos; Neveen A T Hamdy
Journal:  Eur J Endocrinol       Date:  2011-10-07       Impact factor: 6.664

5.  Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.

Authors:  D S Rao; R J Wilson; M Kleerekoper; A M Parfitt
Journal:  J Clin Endocrinol Metab       Date:  1988-12       Impact factor: 5.958

Review 6.  Hypercalciuria and stones.

Authors:  J Lemann; E M Worcester; R W Gray
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7.  Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience.

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Journal:  Neurology       Date:  1997-05       Impact factor: 9.910

8.  Association between serum 25-hydroxyvitamin D level and subclinical cardiovascular disease in primary hyperparathyroidism.

Authors:  Marcella D Walker; Elaine Cong; Anna Kepley; Marco R Di Tullio; Tatjana Rundek; Shunichi Homma; James A Lee; Rui Liu; Polly Young; Chiyuan Zhang; Donald J McMahon; Shonni J Silverberg
Journal:  J Clin Endocrinol Metab       Date:  2013-11-27       Impact factor: 5.958

9.  Fibroblast growth factor (FGF)-23 in patients with primary hyperparathyroidism.

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Journal:  Eur J Endocrinol       Date:  2004-07       Impact factor: 6.664

10.  Influence of renal function on clinico-pathological features of primary hyperparathyroidism.

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1.  Occult urolithiasis in asymptomatic primary hyperparathyroidism.

Authors:  Yu-Kwang Donovan Tay; Minghao Liu; Leonardo Bandeira; Mariana Bucovsky; James A Lee; Shonni J Silverberg; Marcella D Walker
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2.  Subclinical urolithiasis in patients with asymptomatic primary hyperparathyroidism.

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4.  Commentary on silent renal stones in primary hyperparathyroidism: prevalence and clinical features.

Authors:  Cristiana Cipriani; John P Bilezikian
Journal:  Endocr Pract       Date:  2014-11       Impact factor: 3.443

5.  CLINICAL FEATURES OF HYPERCALCEMIC CRISIS IN PRIMARY HYPERPARATHYROIDISM.

Authors:  U Turan; H Kilavuz; O Irkorucu
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Review 6.  Primary hyperparathyroidism.

Authors:  Marcella D Walker; Shonni J Silverberg
Journal:  Nat Rev Endocrinol       Date:  2017-09-08       Impact factor: 43.330

7.  Heart block and acute kidney injury due to hyperparathyroidism-induced hypercalcemic crisis.

Authors:  Taylor C Brown; James M Healy; Mary J McDonald; Joni H Hansson; Courtney E Quinn
Journal:  Yale J Biol Med       Date:  2014-12-12

8.  Surgery or no surgery: What works best for the kidneys in primary hyperparathyroidism? A study in a multi-ethnic Asian population.

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9.  "Silent" kidney stones in "asymptomatic" primary hyperparathyroidism-a comparison of multidetector computed tomography and ultrasound.

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Journal:  Langenbecks Arch Surg       Date:  2016-10-12       Impact factor: 3.445

10.  Disrupted tubular parathyroid hormone/parathyroid hormone receptor signaling and damaged tubular cell viability possibly trigger postsurgical kidney injury in patients with advanced hyperparathyroidism.

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Journal:  Clin Kidney J       Date:  2019-01-28
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