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.

scholarly journals Urine calcium excretion predicts bone loss in idiopathic hypercalciuria

2006 ◽  
Vol 70 (8) ◽  
pp. 1463-1467 ◽  
Author(s):  
J.R. Asplin ◽  
S. Donahue ◽  
J. Kinder ◽  
F.L. Coe
Keyword(s):  
Bone Loss ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Urine Calcium Excretion

Sucrose and Idiopathic Renal Stone

1987 ◽  
Vol 5 (1-2) ◽  
pp. 9-17 ◽  
Author(s):  
Norman J. Blacklock
Keyword(s):  
Risk Factors ◽  
Renal Stone ◽  
Stone Formation ◽  
Insulin Response ◽  
Western World ◽  
Blood Levels ◽  
Calcium Excretion ◽  
Renal Tubular Cell ◽  
Stone Formers ◽  
Renal Tubular

Idiopathic renal stone comprises more than SO per cent of kidney stone disease. Whilst the incidence rate in the Western World is high, that in Africa south of the Sahara is very low. Epidemiological studies point to a dietary aetiology as the basis for stone formation in the kidney. A number of dietary constituents increase the urinary risk factors for stone formation and one of these is sucrose. The sucrose effect is exaggerated when it is consumed in certain forms. There is also the evidence that a third of a normal population responds in an exaggerated manner in respect of an increased excretion of urinary risk factors when sucrose is consumed and this phenomenon has been noted in over 70 per cent of idiopathic stone formers. In studying the mechanism of this, insulin was found to influence distal renal tubular function to increased calcium excretion. Stone formers with an exaggerated urinary risk factor response to sucrose were found to have abnormally high and sustained blood levels of insulin following a standard glucose test meal. Where sucrose or sucrose products are in abundance, quite apart from its effect in increasing urinary risk factors in the population in general, there is particular vulnerability of a significant sub group within the population with this type of insulin response. Sucrose furthermore is known to induce nephrocalcinosis in the kidney of the rodent and similar calcific lesions have been found in the kidney substance of man and these have been observed to begin to appear within the first decade of life. Sucrose has also been observed in man to increase the excretion rate of an enzyme which is identified with renal tubular cell damage.

Effect of Diet Cola on Urine Calcium Excretion.

2010 ◽  
pp. P2-198-P2-198
Author(s):  
NS Larson ◽  
R Amin ◽  
C Olsen ◽  
MA Poth
Keyword(s):  
Calcium Excretion ◽  
Urine Calcium ◽  
Urine Calcium Excretion

Mechanism of chronic hypocalciuria with chlorthalidone: reduced calcium absorption

1984 ◽  
Vol 247 (5) ◽  
pp. F746-F752 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
F. L. Coe
Keyword(s):  
Serum Calcium ◽  
Calcium Absorption ◽  
Chronic Administration ◽  
Intestinal Calcium Absorption ◽  
Male Rats ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
X 24 ◽  
Filtered Load ◽  
Urine Calcium Excretion

Chlorthalidone, like other benzothiadiazides, lowers urine calcium excretion chronically. If intestinal calcium absorption did not fall or bone accretion did not increase, serum calcium and the filtered load of calcium would increase and urine calcium would return to pretreatment levels. To determine whether overall intestinal calcium absorption fell, we fed chlorthalidone (5 mg X kg body wt-1 X 24 h-1) to 10 adult male rats eating 15 g/day of a 0.6% calcium diet. Compared with 10 control rats, chlorthalidone reduced urine calcium [2.1 +/- 0.1 (SE) vs. 5.8 +/- 0.5 mg/6 days; P less than 0.001]. Fecal calcium rose (307 +/- 9 vs. 257 +/- 12; P less than 0.005) because percent intestinal calcium absorption fell (41 +/- 2 vs. 52 +/- 2; P less than 0.002). Twenty other rats given the same diet were injected subcutaneously with 1,25(OH)2D3 (50 ng/day). In these rats, chlorthalidone reduced urine calcium (23 +/- 3 vs. 59 +/- 3; P less than 0.001) and percent intestinal calcium absorption (60 +/- 1 vs. 66 +/- 1; P less than 0.01). With or without 1,25(OH)2D3, chronic administration of chlorthalidone reduces intestinal calcium absorption, and this reduction seems to be the mechanism that permits urine calcium excretion to remain low.

Urinary calcium indices in primary hyperparathyroidism (PHPT) and familial hypocalciuric hypercalcaemia (FHH): which test performs best?

2020 ◽  
pp. postgradmedj-2020-137718
Author(s):  
Muhammad Fahad Arshad ◽  
James McAllister ◽  
Azhar Merchant ◽  
Edmund Rab ◽  
Jacqueline Cook ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
International Workshop ◽  
Significant Proportion ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Clearance Ratio ◽  
Urine Calcium ◽  
Genetic Studies ◽  
Urine Calcium Excretion ◽  
Control Study

AimPrimary hyperparathyroidism (PHPT) is much more common than familial hypocalciuric hypercalcaemia (FHH), but there is considerable overlap in biochemical features. Urine calcium indices help with the differential diagnosis, but their reliability in making this distinction is not clear. The aim of this study was to compare urinary calcium values in patients with PHPT and FHH.MethodsThis was a case–control study of patients with PHPT who had successful surgery and genetically proven FHH between 2011 and 2016. Due to low FHH numbers, patients from neighbouring hospitals and outside study period (2017–2019) were allowed to improve power. Data on demographics and urinary calcium were obtained from electronic records and compared between the two groups.ResultsDuring the study period, 250 patients underwent successful PHPT surgery, while in the FHH arm, 19 genetically proven cases were included. The median (IQR) 24-hour urine calcium excretion (UCE) in the PHPT group was 8.3 (5.6–11.2) mmol/24 hours compared with 3.2 (2.1–6.1) mmol/24 hour in the FHH group (p<0.001). Median (IQR) calcium to creatinine clearance ratio (CCCR) in the PHPT and FHH groups was 0.020 (0.013–0.026) and 0.01 (0.002–0.02), respectively (p=0.001). The sensitivity of urinary tests for PHPT was 96% for UCE (cut-off ≥2.5 mmol/24 hour) and 47% for CCCR (cut-off >0.02). The specificity of the urinary tests for FHH was 29.4% for UCE (cut-off <2.5 mmol/24 hour) and 93% for CCCR (cut-off <0.02).Conclusions24-hour UCE is more sensitive in diagnosing PHPT; however, it is less specific in ruling out FHH as compared with CCCR, when the cut-offs suggested by the International guidelines from the fourth international workshop are used. A significant proportion of patients with PHPT would have also required genetic studies if the guidelines were followed.

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