scholarly journals Association of Urinary Calcium Excretion with Serum Calcium and Vitamin D Levels

2014 ◽  
Vol 10 (3) ◽  
pp. 452-462 ◽  
Author(s):  
Anita Rathod ◽  
Olivier Bonny ◽  
Idris Guessous ◽  
Paolo M. Suter ◽  
David Conen ◽  
...  
2005 ◽  
Vol 90 (4) ◽  
pp. 2122-2126 ◽  
Author(s):  
Andrew Grey ◽  
Jenny Lucas ◽  
Anne Horne ◽  
Greg Gamble ◽  
James S. Davidson ◽  
...  

Abstract Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium <12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] <20 μg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 μg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P < 0.01) and 26% at 12 months (P < 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = −0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion.


1971 ◽  
Vol 49 (5) ◽  
pp. 469-478 ◽  
Author(s):  
William H. Shaw

The relationship between urinary calcium excretion and serum calcium was studied at stable serum calcium levels, both normal and elevated. The linearity of this relationship being known, the slope of this line could be determined by sampling only at its lower and upper ends, that is, by measuring urine and serum calcium at a resting level and at a constant level of hypercalcemia produced by a calcium infusion. This method permitted three sets of measurements at each of the two levels, and also tended to eliminate the factor of renal delay time. The procedure was performed with normal subjects, with normals given vitamin D2 or parathyroid extract, and with subjects having hyperparathyroidism, sarcoidosis, and recurrent renal calculi. In the normal subjects the gradient of the slope appeared to indicate that there is no maximal tubular reabsorptive capacity for calcium, in the range sampled at any rate. The slopes of the various abnormal subjects mostly did not differ markedly from those of the normals. One incidental finding was that resting levels of urinary calcium excretion were significantly depressed 24 h following vitamin D2 administration, despite unchanged serum calcium levels.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A215-A216
Author(s):  
Ru H New ◽  
Matthew J L Hare ◽  
Diana MacKay ◽  
Vidya Kasireddy ◽  
Elna Ellis ◽  
...  

Abstract Introduction: While transient parathyroid insufficiency is not an uncommon complication of thyroidectomy, severe and prolonged hypocalcemia attributed to a combination of post-surgical hypoparathyroidism, hungry bone syndrome (HBS) and hypovitaminosis D is unusual. Clinical Case: A 17-year-old female from a remote community in Australia with Graves’ disease, complicated by exophthalmos and atrial flutter, underwent total thyroidectomy due to challenges with medication adherence leading to persistent thyrotoxicosis. FT4 was >150 pmol/L (normal 10–20 pmol/L) almost two years after diagnosis. Pre-operatively, she received Lugol’s iodine, carbimazole and beta-blockade. The operation was uncomplicated and three parathyroid glands were preserved. Within six hours of thyroidectomy, she developed symptomatic hypocalcemia with corrected calcium 1.9 mmol/L (7.6 mg/dL) (normal 2.2–2.65 mmol/L). PTH level was 0.8 pmol/L (normal 1.4–9.0 pmol/L). Magnesium and phosphate levels were initially normal but hyperphosphatemia developed the following day. 25-OH vitamin D was low (29 nmol/L, normal 50–150 nmol/L) and was corrected with high dose cholecalciferol. Despite use of continuous intravenous calcium gluconate in addition to oral calcium carbonate, as well as both intravenous and oral calcitriol and magnesium, urinary calcium excretion remained undetectable. Teriparatide 20 mcg BD was commenced on post-operative day 14 with no demonstrable improvement in serum calcium. Less than 48 hours after cessation of parenteral calcium on day 18 post-operation, corrected calcium and ionised calcium declined to 1.47 mmol/L (5.9 mg/dL) and 0.46 mmol/L (normal 1.15–1.33 mmol/L) respectively, prompting recommencement of calcium infusion. Her remarkably high requirement for calcium replacement with negligible urinary calcium excretion for at least one month in spite of parenteral calcium infusion for a total of three weeks’ duration is highly suggestive of HBS which became evident due to post-surgical hypoparathyroidism. She had elevated ALP (618 U/L, normal 35–140 U/L) and increased bone resorption marker (N-telopeptide/creatinine 262 nmol BCE/mmol, normal <100 nmol BCE/mmol), with osteopenia at lumbar spine (Z-score -1.7) and femur (Z-score -1.3). Additionally, vitamin D deficiency is likely to have contributed to the severity of hypocalcemia. 60 days after surgery, she was still requiring calcium carbonate 2500 mg QID (4 g/day elemental calcium) and calcitriol 1 mcg TDS. Her phosphate level had normalised and ALP gradually declined to 241 U/L. Clinical Lesson: This case highlights the importance of attaining euthyroid status as early as possible pre-operatively to allow near-complete reversal of thyrotoxicosis-induced osteodystrophy, as indicated by normalisation of serum ALP, and ensuring vitamin D levels are replete prior to thyroidectomy for Graves’ disease.


2019 ◽  
Vol 104 (11) ◽  
pp. 5601-5610 ◽  
Author(s):  
Yu-Kwang Donovan Tay ◽  
Gaia Tabacco ◽  
Natalie E Cusano ◽  
John Williams ◽  
Beatriz Omeragic ◽  
...  

Abstract Context Conventional treatment of hypoparathyroidism is associated with decreased renal function and increased bone mineral density (BMD). Objective To evaluate the effects of 8 years of recombinant human parathyroid hormone (1-84) [rhPTH(1-84)] therapy on key biochemical and densitometric indices. Design Prospective open-label trial. Setting Tertiary medical center. Participants Twenty-four subjects with hypoparathyroidism. Intervention Treatment with rhPTH(1-84) for 8 years. Main Outcome Measures Supplemental calcium and vitamin D requirements, serum calcium and phosphorus levels, calcium-phosphate product, urinary calcium excretion, estimated glomerular filtration rate (eGFR) and BMD. Results PTH therapy was associated with progressive reduction in supplemental calcium (57%; P < 0.01) and active vitamin D (76%; P < 0.001) requirements over 8 years. Serum calcium concentration was stable; urinary calcium excretion declined 38% (P < 0.01). eGFR remained stable and was related to baseline eGFR and serum calcium levels. Calcium-phosphate product was below the recommended limit; serum phosphorus remained within normal range. Lumbar spine and total hip BMD increased, peaking at 4 (mean ± SE, 4.6% ± 1.5%; P = 0.01) and 8 years (2.6% ± 1.1%; P = 0.02), whereas femoral neck BMD did not change and one-third radius BMD decreased (mean ± SE, −3.5% ± 1.1%; P = 0.001). BMD at all sites was higher throughout the 8 years than in the age- and sex-matched reference population. Hypercalcemia and hypocalcemia were uncommon. Conclusion rhPTH(1-84) is a safe and effective treatment for hypoparathyroidism for 8 years. Long-term reductions in supplemental requirements and biochemical improvements with stable renal function are maintained.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Luigi Petramala ◽  
Laura Zinnamosca ◽  
Amina Settevendemmie ◽  
Cristiano Marinelli ◽  
Matteo Nardi ◽  
...  

Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%;P<0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.


2010 ◽  
Vol 17 (04) ◽  
pp. 698-701
Author(s):  
MUHAMMAD ISHAQ ◽  
ISRAR AHMED AKHUND ◽  
MOULA BUX LAGHARI ◽  
Muhammad Sabir

Aims & Objectives: To evaluate the effects of Serum Calcium and Urinary Calcium excretion on upper urinary tract stone diseases in the Peshawar (a high stone incidence belt). Subjects & Methods: One hundred patients (age 20-60years) who were suffering severely from upper urinary tract stone disease were selected from LRH and Hayatabad Medical Complex Hospitals of Peshawar, same numbers of healthy controls from the same region were also selected for the study. Results: When results were summed up and testParameters were compared, it was seen that mean Serum Calcium in stone formers was greater than that of non-stone formers (P<0.001). Same pattern was also observed (P< 0.001) in both groups regarding mean urinary calcium excretion. Conclusions: We concluded that calcium is a definitive risk factor in upper urinary tract stone disease. However we suggest further work and research on wide scale population inorder to evaluate this relation. 


2009 ◽  
Vol 104 (10) ◽  
pp. 1512-1516 ◽  
Author(s):  
Kristina L. Penniston ◽  
Andrea N. Jones ◽  
Stephen Y. Nakada ◽  
Karen E. Hansen

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