scholarly journals Chlorthalidone Is Superior to Potassium Citrate in Reducing Calcium Phosphate Stones and Increasing Bone Quality in Hypercalciuric Stone-Forming Rats

2019 ◽  
Vol 30 (7) ◽  
pp. 1163-1173 ◽  
Author(s):  
Nancy S. Krieger ◽  
John R. Asplin ◽  
Ignacio Granja ◽  
Felix M. Ramos ◽  
Courtney Flotteron ◽  
...  
Keyword(s):  
Calcium Phosphate ◽  
Potassium Chloride ◽  
Bone Quality ◽  
Stone Formation ◽  
Potassium Citrate ◽  
Idiopathic Hypercalciuria ◽  
Mineral Density ◽  
Urine Calcium ◽  
Fixed Amount ◽  
Normal Calcium

BackgroundThe pathophysiology of genetic hypercalciuric stone-forming rats parallels that of human idiopathic hypercalciuria. In this model, all animals form calcium phosphate stones. We previously found that chlorthalidone, but not potassium citrate, decreased stone formation in these rats.MethodsTo test whether chlorthalidone and potassium citrate combined would reduce calcium phosphate stone formation more than either medication alone, four groups of rats were fed a fixed amount of a normal calcium and phosphorus diet, supplemented with potassium chloride (as control), potassium citrate, chlorthalidone (with potassium chloride to equalize potassium intake), or potassium citrate plus chlorthalidone. We measured urine every 6 weeks and assessed stone formation and bone quality at 18 weeks.ResultsPotassium citrate reduced urine calcium compared with controls, chlorthalidone reduced it further, and potassium citrate plus chlorthalidone reduced it even more. Chlorthalidone increased urine citrate and potassium citrate increased it even more; the combination did not increase it further. Potassium citrate, alone or with chlorthalidone, increased urine calcium phosphate supersaturation, but chlorthalidone did not. All control rats formed stones. Potassium citrate did not alter stone formation. No stones formed with chlorthalidone, and rats given potassium citrate plus chlorthalidone had some stones but fewer than controls. Rats given chlorthalidone with or without potassium citrate had higher bone mineral density and better mechanical properties than controls, whereas those given potassium citrate did not.ConclusionsIn genetic hypercalciuric stone-forming rats, chlorthalidone is superior to potassium citrate alone or combined with chlorthalidone in reducing calcium phosphate stone formation and improving bone quality.

scholarly journals Renal stone disease: causes, evaluation and medical treatment

2006 ◽  
Vol 50 (4) ◽  
pp. 823-831 ◽  
Author(s):  
Ita Pfeferman Heilberg ◽  
Nestor Schor
Keyword(s):  
Medical Treatment ◽  
Renal Stone ◽  
Salt Intake ◽  
Current Knowledge ◽  
Stone Formation ◽  
Potassium Citrate ◽  
Blood Analysis ◽  
Dietary Recommendations ◽  
Metabolic Disturbances ◽  
Mineral Density

The purpose of the present review is to provide an update about the most common risk factors or medical conditions associated with renal stone formation, the current methods available for metabolic investigation, dietary recommendations and medical treatment. Laboratory investigation of hypercalciuria, hyperuricosuria, hyperoxaluria, cystinuria, hypocitraturia, renal tubular acidosis, urinary tract infection and reduction of urinary volume is based on the results of 24-hr urine collection and a spot urine for urinary sediment, culture and pH. Blood analysis for creatinine, calcium and uric acid must be obtained. Bone mineral density has to be determined mainly among hypercalciurics and primary hyperparathyroidism has to be ruled out. Current knowledge does not support calcium restriction recommendation because it can lead to secondary hyperoxaluria and bone demineralization. Reduction of animal protein and salt intake, higher fluid intake and potassium consumption should be implemented. Medical treatments involve the use of thiazides, allopurinol, potassium citrate or other drugs according to the metabolic disturbances. The correction of those metabolic abnormalities is the basic tool for prevention or reduction of recurrent stone formation.

scholarly journals Impact of Thyroid Disease on Bone Mineral Density Preservation in Patients With Osteoporosis and Idiopathic Hypercalciuria

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A247-A248
Author(s):  
James W Chu
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
Fragility Fracture ◽  
Thyroid Disease ◽  
Medication Use ◽  
Fragility Fractures ◽  
Idiopathic Hypercalciuria ◽  
Mineral Density ◽  
Urine Calcium ◽  
Thyroid Medication

Abstract Background: Idiopathic hypercalciuria (IHC) is associated with reduced bone mineral density (BMD) and increased risk of osteoporotic fractures. It is not known if thyroid disease impacts the degree of urine and bone mineral abnormalities in patients with IHC and osteoporosis (OPO). Methods: Retrospective chart review from a private endocrinology clinic identified 62 consecutive patients with OPO (fragility fracture and/or t-score ≤-2.5 on bone density scan) and concomitant diagnosis of IHC (urine calcium > 4.0 mg/kg weight/d when intaking low-moderate calcium amounts). Patients were classified into two groups: those with thyroid disease (Thy+, if presence of autoimmune thyroid disease [AITD] with high antibody titers and/or long-term thyroid medication use) and those without (Thy-). Comparisons were made between the two groups for severity of renal disease (urine calcium) and bone disease (number of fragility fractures, and BMD response to therapy). Results: Of 55 women and 7 men identified with both OPO and IHC, 30 were Thy+ (4 with Graves’, 11 with confirmed Hashimoto’s, 13 taking levothyroxine for presumed Hashimoto’s and 2 with thyroid cancer), and 32 were Thy- (including 2 with type 1 DM, 1 with vitiligo, and 6 with non-toxic nodular goiters requiring biopsies). Thy+ were compared to Thy- with respect to: mean age (70.7 ± 7.3 vs. 70.8 ± 9.3 y), sex (97% vs. 81% women), 24-hr urine calcium at diagnosis (317 ± 75 vs. 311 ± 68 mg), presence of fragility fracture (50% vs. 59%), use of thiazide (83% vs. 78%), and use of anti-fracture pharmacotherapy (73% vs. 84%). 50 patients had adequate comparative longitudinal BMD data. A (+) BMD response was based on consistent increases in BMD and/or t-scores across all spine and hip sites, and a (-) BMD response was classified by decreased BMD and/or t-scores across all sites. For Thy+ vs. Thy- patients, there were 25% vs. 69% (+) BMD response, 38% vs. 12% (-) BMD response, 21% vs. 4% with no significant BMD response, and 17% vs. 15% with mixed BMD responses. Conclusions: In this group at high risk for future fragility fractures, much lower rates of BMD preservation was seen in the Thy+ as compared to the Thy- patients. Overall, AITD and medical thyroid disease was very common (48%) in this cohort of patients with IHC and OP. However, this high rate may be confounded by the selective nature of the specialty clinic population. Further research needs to delineate the impact of AITD and thyroid medication use on the progression and treatment of patients with IHC and OPO.

Does Potassium Citrate Medical Therapy Increase the Risk of Calcium Phosphate Stone Formation?

2007 ◽  
Author(s):  
Victor Leitao ◽  
George E. Haleblian ◽  
Marnie R. Robinson ◽  
Sean A. Pierre ◽  
Roger L. Sur ◽  
...  
Keyword(s):  
Calcium Phosphate ◽  
Medical Therapy ◽  
Stone Formation ◽  
Potassium Citrate

scholarly journals SUN-391 Denosumab Treatment of Patients with Osteoporosis and Idiopathic Hypercalciuria

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Winston S Chu ◽  
James W Chu
Keyword(s):  
Lumbar Spine ◽  
Femoral Neck ◽  
Osteoporotic Fractures ◽  
Retrospective Chart Review ◽  
Fragility Fractures ◽  
Idiopathic Hypercalciuria ◽  
Mineral Density ◽  
Urine Calcium ◽  
Total Hip ◽  
Denosumab Treatment

Abstract Background: Idiopathic hypercalciuria (IHC) is associated with reduced bone mineral density (BMD) and higher risk of osteoporotic fractures. Denosumab is a RANK-ligand inhibitor that prevents osteoporosis-related fractures. No previous published studies have specifically evaluated denosumab treatment of osteoporosis patients with IHC. Methods: Retrospective chart review from a private endocrinology clinic identified 31 consecutive patients with osteoporosis (prior fragility fracture and/or t-score ≤-2.5 on bone density scan) with concomitant diagnosis of IHC (defined as urine calcium > 4.0 mg/kg weight/d when intaking low-moderate calcium amounts), who had received at least 3 denosumab injections. Comparisons were made for BMD measurements determined by dual-energy x-ray absorptiometry done before denosumab initiation, and after the latest dose. Results: There were 28 women and 3 men, with average age of 71.9 ± 8.9 years. 20 subjects had prior total of 31 fragility fractures. Baseline 24-hr urine calcium was 331 ±65 mg/day. Average exposure to denosumab therapy was 9.0 ± 4.8 doses. 27 of these patients received concomitant thiazide diuretics during the course of their denosumab therapy. Baseline t-scores were -2.4 ± 0.8 at lumbar spine, -1.5 ± 0.7 at total hip and -1.8 ± 0.5 at femoral neck. After denosumab therapy, the t-scores were respectively -1.9 ± 0.9, -1.3 ± 0.8 and -1.6 ± 0.7. Mean increases in BMD were seen at the lumbar spine of 6.2 ± 8.4%, at the total hip of 3.2 ± 6.0%, and at the femoral neck of 2.5 ± 8.0% 19 patients were considered to have (+) BMD responses, based on consistent increases in BMD and/or t-scores across all spine and hip sites. 4 patients had (-) BMD responses, based on decreased BMD and/or t-scores across all sites. 6 patients had mixed responses and 2 did not have comparative BMD data. Baseline urine calcium did not seem to correlate with clinical responses. Those patients with longer duration of thiazide and/or denosumab use had higher likelihood of (+) BMD responses. However, during the course of follow-up, 4 subjects suffered 7 fragility fractures while treated with denosumab: 3 with (+) and 1 with (-) BMD responses. Conclusion: Denosumab can effectively increase BMD in a cohort of osteoporosis patients with IHC, the majority of whom also received thiazide. However, increased BMD response did not necessarily predict lower risks of fragility fractures. Further research needs to evaluate the role of denosumab therapy in such high-risk patients.

Calcium stones

2015 ◽  
Author(s):  
David A. Bushinsky ◽  
Orson Moe
Keyword(s):  
Risk Factors ◽  
Stone Formation ◽  
Epidemiological Studies ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Calcium Stones ◽  
Renal Tubular ◽  
Urine Calcium Excretion ◽  
Predisposing Conditions

Key predisposing factors in calcium stone formation are idiopathic hypercalciuria, primary hyperparathyroidism, and hyperoxaluria (dietary, enteric, idiopathic, sometimes genetic). These are described in detail. Other predisposing conditions include renal tubular acidosis, and risk factors identified in epidemiological studies such as hypocitraturia, increased urinary urate. is defined as an excess of urine calcium excretion without a discernible metabolic cause.

Is calcium oxalate nucleation in postprandial urine of males with idiopathic recurrent calcium urolithiasis related to calcium phosphate nucleation and the intensity of stone formation? Studies allowing insight into a possible role of urinary free citrate and protein

2004 ◽  
Vol 42 (3) ◽  
Author(s):  
Paul O. Schwille ◽  
Angelika Schmiedl ◽  
Mahimaidos Manoharan
Keyword(s):  
Clinical Trial ◽  
Calcium Phosphate ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Urine Volume ◽  
Control Group ◽  
Urine Calcium ◽  
Element Analysis ◽  
Protein Ratio ◽  
Whole Urine

AbstractIn idiopathic recurrent urolithiasis (IRCU) calcium oxalate and calcium phosphate are components of stones. It is not sufficiently known whether in urine the nucleation (liquid-solid transition) of each salt requires a different environment, if so which environment, and whether there is an impact on stone formation. Nucleation was induced by in vitro addition of oxalate or calcium to post-test meal load whole urine of male stone patients (n=48), showing normal daily and baseline fasting oxaluria. The maximally tolerated (until visible precipitates occur) concentration of oxalate (T-Ox) or calcium (T-Ca) was determined; additionally evaluated were other variables in urine, including total, complexed and free citrate (F-Cit), protein (albumin, non-albumin protein) and the clinical intensity (synonymous metabolic activity; MA) of IRCU. In the first of three trials the accumulation of substances in stone-forming urine was verified (trial-V); in the second (clinical trial 1) two strata of T-Ox (Low, High) were compared; in the third (clinical trial 2) IRCU patients (n=27) and a control group (n=13) were included to clarify whether in stone-forming urine the first crystal formed was calcium oxalate or calcium phosphate, and to identify the state of F-Cit. T-Ox was studied at the original pH (average<6.0), T-Ca at prefixed pH 6.0; the precipitates were subjected to electron microscopy and element analysis. Trial-V: Among the urinary substances accumulating at the indicated pHs were calcium, oxalate and phosphate, and the crystal-urine ratios were compatible with the nucleation of calcium oxalate, calcium-poor and calcium-rich calcium phosphate; citrate, protein and potassium also accumulated. Clinical trial 1: the two strata exhibited an inverse change of T-Ox and T-Ca, the ratio T-Ox/T-Ca and MA. The initial (before induction of Ox or Ca excess) supersaturation of calcium oxalate and brushite were unchanged, with the difference of proteinuria being borderline. Several correlations were significant (p≤0.05): urine pH with citrate and volume, protein with volume and MA, T-Ox with T-Ca and MA. Clinical trial 2: in patients with reduced urine volume and moderate urine calcium excess, the first precipitate appeared to be calcium oxalate, followed by amorphous calcium phosphate. Conversely, when the calcium excess was extreme, calcium-rich hydroxyapatite developed, followed by calcium oxalate; F-Cit, not total and complexed citrate, was decreased in IRCU vs. male controls; F-Cit rose pH-dependently, and the ratio F-Cit at original pH vs. F-Cit at pH 6.0 correlated inversely with the nucleation index T-Ox/T-Ca; MA correlated inversely with the ratio F-Cit at pH 6.0, respectively, original pH, but directly with the urinary albumin/non-albumin protein ratio. In summary 1) to study calcium oxalate and calcium phosphate nucleation in whole urine of IRCU patients is feasible; 2) at this crystallization stage the two substances, dominant in calcium stones, appear intimately linked, 3) in stone-forming urine, calcium phosphate may be ubiquitously present, likely as particles <0.22 μm; 4) together with co-precipitation of calcium oxalate and calcium phosphate, low F-Cit and alteration of proteinuria may act in concert and accelerate stones.

scholarly journals Effect of Age on Bone Structure Parameters in Laying Hens

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 570
Author(s):  
Masayoshi Yamada ◽  
Chongxiao Chen ◽  
Toshie Sugiyama ◽  
Woo Kyun Kim
Keyword(s):  
Cortical Bone ◽  
Bone Quality ◽  
Bone Mineral ◽  
Volume Fraction ◽  
Bone Structure ◽  
Bone Volume ◽  
Egg Laying ◽  
Medullary Bone ◽  
Mineral Density ◽  
Tibial Diaphysis

Changes in medullary and cortical bone structure with age remain unclear. Twenty Hy-Line W36 hens, 25 or 52 weeks of age, were euthanized, and both tibiae were collected when an egg was present in the magnum. Serial cross sections of the tibiae were stained with Alcian blue. The bones were scanned using micro-computed tomography. Trabecular width (Tb.Wi) was significantly higher (p < 0.05) in 25-week-old hens, whereas medullary bone tissue volume (TV) was significantly higher (p < 0.01) in 52-week-old hens. 25-week-old hens had significantly higher (p < 0.01) bone volume fraction (BVF = calcified tissue / TV). Moreover, the cortical bone parameters were significantly higher (TV and bone mineral content (BMC) at p < 0.05, and bone volume (BV) and BVF at p < 0.01) in younger hens. Open porosity and total porosity, which indicate less density, were significantly higher (p < 0.01) in older hens. Older hens showed significantly higher (p < 0.01) tibial diaphysis TV than younger hens. Younger hens had significantly higher (p < 0.01) BV, BVF and bone mineral density (BMD) of the tibial diaphysis. These findings reveal that reductions in medullary bone quality might be associated with age-related low estrogen levels and stimulation of osteoclastic bone resorption by parathyroid hormone. Cortical bone quality decreased with enlargement of the Haversian canals and loss of volume, with a longer egg-laying period leading to osteoporosis.

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