Calcium nephrolithiasis and bone demineralization

Arrabal-Polo, Miguel Ángel; Cano-García, María del Carmen; Canales, Benjamin K.; Arrabal‐Martín, Miguel

doi:10.1097/mou.0000000000000111

Cited by 25 publications

(16 citation statements)

References 46 publications

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“…The urine metabolic profile was interpreted on the basis of the reference values used to assess the mineral metabolism [ 19 , 20 , 21 , 36 ]. At baseline, it was found that potassium excretion was <50 mEq in 90% of the 24 h urine samples, and 85% of women exhibited alteration in pH and/or citrate excretion.…”

Section: Resultsmentioning

confidence: 99%

“…While the nutritional hypothesis has been amended in systematic reviews and meta-analyses [ 11 , 16 , 17 ], the relationship between renal function, and the risk of osteoporosis or hip fracture has been confirmed in many studies. Recent findings have demonstrated that increased acid excretion [ 18 ], dysregulation of calcium homeostasis [ 19 ] and a decrease in urinary citrate [ 20 , 21 , 22 ] are recognizable in patients who exhibit osteopenia/osteoporosis and high bone turnover, thus, suggesting that urinary metabolic profiling may have significant implications for monitoring bone health status.…”

Section: Introductionmentioning

confidence: 99%

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Potassium Citrate Supplementation Decreases the Biochemical Markers of Bone Loss in a Group of Osteopenic Women: The Results of a Randomized, Double-Blind, Placebo-Controlled Pilot Study

et al. 2018

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The relationship involving acid-base imbalance, mineral metabolism and bone health status has previously been reported but the efficacy of the alkalizing supplementation in targeting acid overload and preventing bone loss has not yet been fully elucidated. In this randomized, double-blind, placebo-controlled study, the hypothesis that potassium citrate (K citrate) modifies bone turnover in women with postmenopausal osteopenia was tested. Three hundred and ten women were screened; 40 women met the inclusion criteria and were randomly assigned to the treatment or the placebo group. They were treated with K citrate (30 mEq day−1) or a placebo in addition to calcium carbonate (500 mg day−1) and vitamin D (400 IU day−1). At baseline and time points of 3 and 6 months, serum indicators of renal function, electrolytes, calciotropic hormones, serum bone turnover markers (BTMs) (tartrate-resistant acid phosphatase 5b (TRACP5b), carboxy-terminal telopeptide of type I collagen (CTX), bone alkaline phosphatase (BAP), procollagen type 1 N terminal propeptide (PINP)), and urine pH, electrolytes, and citrate were measured. The follow-up was completed by 17/20 patients in the “K citrate” group and 18/20 patients in the “placebo” group. At baseline, 90% of the patients exhibited low potassium excretion in 24 h urine samples, and 85% of cases had at least one urine parameter associated with low-grade acidosis (low pH, low citrate excretion). After treatment, CTX and BAP decreased significantly in both groups, but subjects with evidence of low-grade acidosis gained significant benefits from the treatment compared to the placebo. In patients with low 24h-citrate excretion at baseline, a 30% mean decrease in BAP and CTX was observed at 6 months. A significant reduction was also evident when low citrate (BAP: −25%; CTX: −35%) and a low pH (BAP: −25%; CTX: −30%) were found in fasting-morning urine. In conclusion, our results suggested that K citrate supplementation improved the beneficial effects of calcium and vitamin D in osteopenic women with a documented potassium and citrate deficit, and a metabolic profile consistent with low-grade acidosis.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potassium Citrate Supplementation Decreases the Biochemical Markers of Bone Loss in a Group of Osteopenic Women: The Results of a Randomized, Double-Blind, Placebo-Controlled Pilot Study

et al. 2018

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“…Following the first report of a correlation between BMD and KS by Alhava et al [ 21 ], many studies have demonstrated that patients with KS have increased risks of low BMD, osteoporosis, and bone fractures [ 3 , 4 , 22 – 24 ]. CaKS is considered to be a multisystem disease [ 25 ], and various mechanisms can result in CaKS formation [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Hyponatremia and the risk of kidney stones: A matched case-control study in a large U.S. health system

et al. 2018

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Kidney stones impose a large and increasing public health burden. Previous studies showed that hyponatremia is associated with an increased risk of osteoporosis and bone fractures, which are also known to be associated with kidney stones. However, the relation between hyponatremia and kidney stones is not known. To assess the relation between hyponatremia and kidney stones, we designed a matched case-control study by using the electronic health records of the MedStar Health system with more than 3.4 million unique patient records as of March 2016. Data were extracted for clinical factors of patients with kidney stones (cases) and those without kidney stones (controls). Cases (n = 20,199) and controls (n = 20,199) were matched at a 1:1 ratio for age, sex, race, and the duration of encounter window. Case and control exposures for each of the hyponatremia variables were defined by serum sodium laboratory measurements reported within the encounter windows, and divided into 3 categories: prior hyponatremia, recent hyponatremia, and persistent hyponatremia. In the final conditional logistic models adjusted for potential confounders, the risk of kidney stones significantly increased in both recent and persistent hyponatremia categories: prior hyponatremia odds ratio (OR) 0.93 (95% confidence interval [CI], 0.86–1.00); recent hyponatremia OR 2.02 (95% CI, 1.76–2.32); persistent hyponatremia OR 6.25 (95% CI, 3.27–11.96). In conclusion, chronic persistent hyponatremia is a significant and clinically important risk factor for kidney stones in patients in the U.S.

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“…Moreover, these [ 105 ] and other authors [ 107 , 108 , 109 , 110 , 111 ] found that patients who formed calcium kidney stones exhibited lower bone mineral density, suggesting that bone demineralization, which often accompanies hypercalcemia [ 112 ], may be linked to calcium stone formation. In fact, a previous study found increased occurrences of osteopenia and osteoporosis in patients with recurrent calcium nephrolithiasis and hypercalciuria [ 113 ]. Interestingly, as Gambaro et al has pointed out, lower bone density has also been linked to abnormal arterial stiffness, partially due to calcification, which is a strong indicator of cardiovascular mortality [ 114 ].…”

Section: Vascular Calcification and Stone Formation Similarities Tmentioning

confidence: 99%

Vascular Calcification and Stone Disease: A New Look towards the Mechanism

Yiu

Callaghan

Sultana

et al. 2015

JCDD

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Calcium phosphate (CaP) crystals are formed in pathological calcification as well as during stone formation. Although there are several theories as to how these crystals can develop through the combined interactions of biochemical and biophysical factors, the exact mechanism of such mineralization is largely unknown. Based on the published scientific literature, we found that common factors can link the initial stages of stone formation and calcification in anatomically distal tissues and organs. For example, changes to the spatiotemporal conditions of the fluid flow in tubular structures may provide initial condition(s) for CaP crystal generation needed for stone formation. Additionally, recent evidence has provided a meaningful association between the active participation of proteins and transcription factors found in the bone forming (ossification) mechanism that are also involved in the early stages of kidney stone formation and arterial calcification. Our review will focus on three topics of discussion (physiological influences—calcium and phosphate concentration—and similarities to ossification, or bone formation) that may elucidate some commonality in the mechanisms of stone formation and calcification, and pave the way towards opening new avenues for further research.

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Calcium nephrolithiasis and bone demineralization

Cited by 25 publications

References 46 publications

Potassium Citrate Supplementation Decreases the Biochemical Markers of Bone Loss in a Group of Osteopenic Women: The Results of a Randomized, Double-Blind, Placebo-Controlled Pilot Study

Potassium Citrate Supplementation Decreases the Biochemical Markers of Bone Loss in a Group of Osteopenic Women: The Results of a Randomized, Double-Blind, Placebo-Controlled Pilot Study

Hyponatremia and the risk of kidney stones: A matched case-control study in a large U.S. health system

Vascular Calcification and Stone Disease: A New Look towards the Mechanism

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