Increase In Calcium Excretion Research Articles

Features of Bone Mineral Density, Calcium-Phosphorus Metabolism and Bone Remodeling in Patients with Systemic Lupus Erythematosus

Introduction. Systemic lupus erythematosus (SLE) is a complex autoimmune disease with variable clinical manifestations associated with multiple autoantibodies formation and deposition of immune complexes, and other immune processes. Despite significant advances in treatment, the disease remains disabling, in particular, due to increased bone fragility and low-energy fractures. The study of bone remodeling in patients with SLE should help to improve the therapy and quality of their treatment. The aim of the study. To investigate the features of bone mineral density, calcium-phosphorus metabolism and bone remodeling in patients with systemic lupus erythematosus. Materials and methods. The study involved 123 women with SLE aged 21-51 years. The comparison group (CG) consisted of 25 women without SLE in premenopausal status of the appropriate age. The control group included 25 practically healthy women. In order to study bone mineral density (BMD), dual-energy X-ray densitometry (DXA) of the lumbar spine was performed using a dual-energy X-ray absorptiometer. For the study of calcium-phosphorus metabolism (CPM), total calcium (Ca), ionized Ca, phosphorus (P) in blood and Ca, P, creatinine in daily urine, as well as parathyroid hormone (PTH) and 25-hydroxyvitamin D in serum were determined. Markers of bone remodeling (osteocalcin, procollagen type 1 amino-terminal propeptide (P1NP) and isomerized C-terminal telopeptide (β-crosslaps) in serum were measured. To achieve the stated goal, the first step included the determination of bone damage prevalence in patients with the diagnosed SLE; the second step was directed towards the characterization the particular bone condition in patients with SLE based on the results of BMD, CPM indices and markers of bone remodeling assessment. Results and discussion. According to the results of DXA of the lumbar spine, 88 (71.54 %) women of the SG and only 8 (32.00 %) women of the CG had a decrease in BMD (p < 0.001). According to the mean values, the studied CPM indices of the SG patients, CG and control group wemen exposed no significant differences. Similarly, no significant differences were detected in the mean values of urinary phosphorus and in between blood PTH values in SG, CG, and control. The level of 25-hydroxyvitamin D was significantly lower in SG (15.14 ± 0.80 ng/ml) than in CG (19.62 ± 0.46 ng/ml) and control (22.38 ± 1.34 ng/ml) p < 0.05. The mean value of osteocalcin in woman with SLE was significantly lower than in CG and control (11.81 ± 0.49 ng/ml versus 18.61 ± 0.75 ng/ml and 19.28 ± 1.88, p < 0.001). No significant difference were detected in between the mean values of P1NP in SG, CG and control. The mean values of β-cross laps were significantly higher in patients with SLE (0.51 ± 0.02 ng/ml) compared to GC (0.26 ± 0.02 ng/ml) and control (0.28 ± 0.02 ng/ml), p < 0.001. Conclusions. Bone mineral density, calcium-phosphorus metabolism and bone remodeling in patients with systemic lupus erythematosus have peculiarities as follows: a significant decrease in bone mass in 71.54 % of patients, namely 18, 70 % - grade I osteopenia, 21.14 % - grade II osteopenia, 14.63 % - grade III osteopenia; 17.07 % - osteoporosis, increased calcium excretion, vitamin D deficiency, decreased osteoblastic and enhansed osteoclastic functions.

Метаболические факторы риска и формирование мочевых камней. Исследование IX: Особенности литогенеза камней мономинерального и смешанного состава у мужчин и женщин.

Introduction. The study of lithogenic substances excretion in stone formers with pure monomineral stones allows us to identify characteristic metabolic changes, the long-term effect of which determines the originality of the pathogenetic mechanism features of the formation of urinary stones consisting of pure minerals. The problem of studying lithogenesis of «pure» (monomineral) stones in stone formers is of great clinical importance, since it assumes the existence of various approaches to prevention and metaphylaxis of urolithiasis in patients with «pure» stones and mixed stones. Materials and methods. We examined 982 patients with urolithiasis (439 men and 543 women aged from 18 to 79 years. Of these, 837 patients (384 men and 453 women) had «pure» urinary stones of various types, represented by one mineral. Metabolic parameters of excretion in patients were studied men and women with monomineral urinary stones of various chemical types. Results. In oxalate stones, the most active accumulation of the calcium oxalate mineral component and an increase in the number of «pure» oxalate stones by 1.25 times was observed in men than in women (p=0.046). Increased calcium excretion activates oxalate lithogenesis in men, as opposed to women, contributing to the accumulation of veddelite in pure oxalate stones. In contrast to women, the accumulation of calcium oxalate in stones in men is associated with increased excretion of uric acid, phosphates, and partly magnesium (p<0.01). In uric acid stones consisting of pure uric acid and uric acid dihydrate, pure uric acid stones were 1.52 times more common in women than in men (p<0.01), and did not depend on the level of uricosuria. Patients with pure uric acid stones had lower urine pH than patients with pure calcium-oxalate stones. The accumulation of uric acid in stones to the level of pure uric acid stones was accompanied in the groups of men by an increase in phosphaturia (p=0.021), and in the groups of women – with an increase in body mass index (p=0.028). Men with 100% uric acid stones had higher levels of excretion of calcium, uric acid and phosphates compared to female patients by 1.21 times, 1.3 times and 1.26 times, respectively (p<0.05). Urinary stones from pure carbonate apatite were rare in men and women. In women, stones of mixed composition with 80-90% carbonatapatite were more often detected, and in men with 60-70% of this mineral. In men, compared with women, with the accumulation of carbonatapatite in stones, an increase in the excretion of calcium, uric acid, phosphates and magnesium was observed (p<0.05). About 80% of mixed stones in stone formers men and women are pure calcium oxalate-phosphate bimineral stones consisting only of carbonate apatite and calcium oxalate. In men, in contrast to women, there was a predominance of calcium oxalate (1.24 times), the accumulation of which in these stones was higher. It is associated with increased excretion of calcium, uric acid, phosphates, and magnesium (1.41-fold, 1.32-fold, 1.35-fold, and 1.33-fold, respectively (p<0.05). Men with calcium oxalate-phosphate stones had higher calcium excretion than those with pure calcium oxalate or carbonate apatite stones and lower urine pH values than those with carbonate apatite stones (p<0.01). In women, level of calciuria did not play a big role in the genesis of pure calcium oxalate-phosphate, calcium oxalate and carbonate apatite stones. A more important factor in their lithogenesis was the alkaline reaction of urine, which led to the activation of carbonate apatite stone formation. Conclusion. The formation of urinary stone and the distribution of its mineral components depend on the interaction of various metabolic factors. The study of groups of patients with pure (100%) monomineral stones and patients with stones of mixed composition, in which main mineral is only the predominant part, allows us to identify characteristic complexes of lithogenic metabolic factors that distinguish these groups of patients from each other. This approach is important both for understanding the pathogenetic mechanisms of stone formation, and for choosing the directions of empirical therapy for urolithiasis and developing further metaphylactic measures that also take into account the gender of patients.

Injection of luteinizing hormone or human chorionic gonadotropin increases calcium excretion and serum PTH in males

Animal and human studies have suggested that sex steroids have calciotropic actions, and it has been proposed that follicle-stimulating hormone (FSH) may exert direct effects on bone. Here, we demonstrate the expression of the receptor for Luteinizing hormone (LH) and human choriogonadotropin (hCG), LHCGR, in human kidney tissue, suggesting a potential influence on calcium homeostasis. To investigate the role of LHCGR agonist on calcium homeostasis in vivo, we conducted studies in male mice and human subjects. Male mice were treated with luteinizing hormone (LH), and human extrapolation was achieved by injecting 5000 IU hCG once to healthy men or men with hypergonadotropic or hypogonadotropic hypogonadism. In mice, LH treatment significantly increased urinary calcium excretion and induced a secondary increase in serum parathyroid hormone (PTH). Similarly, hCG treatment in healthy men led to a significant increase in urinary calcium excretion, serum PTH levels, and 1,25 (OH)2D3, while calcitonin, and albumin levels were reduced, possibly to avoid development of persistent hypocalcemia. Still, the rapid initial decline in ionized calcium coincided with a significant prolongation of the cardiac QTc-interval that normalized over time. The observed effects may be attributed to LH/hCG-receptor (LHCGR) activation, considering the presence of LHCGR expression in human kidney tissue, and the increase in sex steroids occurred several hours after the changes in calcium homeostasis. Our translational study shed light on the intricate relationship between gonadotropins, sex hormones and calcium, suggesting that LHCGR may be influencing calcium homeostasis directly or indirectly.

Protective effect of pomegranate seed oil against salt toxicity in rat kidneys

Consuming too much salt can have a negative impact on your kidneys. The kidneys play an important role in regulating sodium levels in the body, and excess salt can lead to water retention and increased blood pressure, which in turn can have a negative impact on the kidneys. Excess salt in the diet can contribute to the formation of kidney stones. This is because excess sodium can lead to increased calcium excretion in the urine, which in turn increases the risk of stone formation. An experiment was conducted on rats to study the effect of salt on kidney function. During the experiment, a group of rats received a high dose of salt for a certain period of time, while another group received a regular amount of salt. The results showed that rats that consumed more salt had increased blood pressure and negative changes in kidney function. They also faced problems with fluid retention and the formation of kidney stones. This experiment confirmed that excess salt consumption can negatively affect kidney function and lead to the development of various diseases. Therefore, controlling your salt intake is an important aspect of maintaining a healthy kidney system. Kidney contamination from salt can lead to various diseases such as kidney stones, kidney failure and other genitourinary problems. One way to correct this problem may be to use pomegranate oil. Pomegranate oil contains antioxidants that help reduce inflammation and protect kidney cells from damage. It also improves blood circulation and helps cleanse the kidneys of toxins and waste. Research has shown that consuming pomegranate oil may help improve kidney function, reduce inflammation, and prevent the formation of kidney stones. It can also help lower blood pressure and improve the overall health of the kidney system.

Effect of circadian clock and claudin regulations on inulin-induced calcium absorption in the mouse intestinal tract.

Dietary calcium supplementation has been shown to be an effective adjunct therapy in an inflammatory bowel disease model. Soluble dietary fiber reduces intestinal pH and is known to enhance calcium absorption. Although many circadian clock regulations of nutrient absorption in the intestinal tract have been reported, the effects of clock regulation on calcium absorption have yet to be understood. In this study, we investigated the timing of efficient calcium intake by measuring urinary calcium excretion in mice. The diurnal variations in channel-forming tight junctions (claudins) were detected in both the jejunum and ileum. Following 2 days of feeding with a Ca2+-free diet, Ca2+-containing diets with or without soluble fiber (inulin) were fed at specific timings, and urine was subsequently examined every 4 hr. There was an evident increase in urinary calcium concentration when the inulin diet was fed at the beginning of the resting period. The Claudin 2 (Cldn2) expression level also showed a significant day-night change, which seemed to be a mechanism for the increased calcium excretion after inulin intake. This diurnal rhythm and enhanced Cldn2 expression were abolished by disruption of the suprachiasmatic nucleus, the central clock in the hypothalamus. This study suggests that intestinal calcium absorption might be modulated by the circadian clock and that the intake of inulin is more effective at the beginning of the resting period in mice.

Angiotensin II Modulates Calcium/Phosphate Excretion in Experimental Model of Hypertension: Focus on Bone.

A link between hypertension and long-term bone health has been suggested. The aim of this study was to investigate the effects of chronic angiotensin II administration on urinary calcium/phosphate excretion, bone mineral density, bone remodeling and osteoblast population in a well-established experimental model of hypertension, in the absence of possible confounding factors that could affect bone metabolism. Male Sprague-Dawley rats, divided in the following groups: (a) Angiotensin II (Ang II, 200 ng/kg/min, osmotic minipumps, sub cutis, n = 8); (b) Ang II+losartan (Los, 50 mg/kg/day, per os, n = 6); (c) control group (physiological saline, sub cutis, n = 9); and (d) control+losartan (n = 6) were treated for four weeks. During the experimental period, 24-hour diuresis, urinary calcium, phosphate and sodium excretion were measured prior to the treatment, at two weeks of treatment, and at the end of the treatment. Systolic blood pressure was measured by plethysmography technique (tail cuff method). At the end of the experimental protocol, the rats were euthanized and peripheral quantitative computed tomography at the proximal metaphysis and at the diaphysis of the tibiae and quantitative bone histomorphometry on distal femora were performed. Angiotensin II-dependent hypertension is associated with increased calcium and phosphate excretion. AT1 receptor blockade prevented the increase of blood pressure and phosphate excretion but did not affect the increase of calcium excretion. These changes took place without significantly affecting bone density, bone histology or osteoblast population. In conclusion, in our experimental conditions, angiotensin II-dependent hypertension gave rise to an increased urinary excretion of calcium and phosphate without affecting bone density.

Acclimatization of fish to the higher calcium levels in the water environment

It is established that calcium concentration changes (variations) in the water environment significantly influence its intake and distribution in tissues and organs of hydrobionts. The decrease in calcium concentration in water from 100 to 60 mg.L-1 significantly reduces its content in fish liver. In the gills glandular apparatus of fish acclimated to the environment with lower calcium level (in comparison with control one), its concentration on the first day of the acclimation period slightly exceeded the initial level, thus testifying to its possible excretion of endogenous calcium by gills. The increase of calcium excretion through the renal and digestive systems in fish acclimates to the higher water level, and specific changes in phosphates excretion dynamics accompany oral intake. Long keeping fish in water with 100 mg.L-1 calcium is accompanied by the increase of total phosphorus in urine (by 2 – 2.5 times), and its day excretion increases by 1.9 – 2.4 times. During fish acclimation to higher calcium levels in the water environment, the excretion of total phosphorus with faecal matter increases. The increase of calcium in the water environment to 100 mg.L-1 leads to a temporary increase in total phosphorus excretion with faecal issues. The rise in cation concentration to 200 mg.L-1 increases significantly during long-time fish stay in such an environment.

The influence of habitual salt intake on bone remodelling in young healthy people

Introduction: Sodium alters calcium metabolism by increasing calcium excretion, thus possibly influencing bone metabolism. The hypothesis of the present study is that amount of dietary sodium intake affects the bone remodelling. This study aimed to assess whether a habitual intake of sodium has an effect on peak bone mass and biochemical indicators of bone metabolism.
 Subjects and Methods: In a cross-sectional study that involved 41 young men and women, six biochemical markers were assessed from blood samples using ELISA: osteocalcin, C-terminal procollagen type I peptide, receptor activator kappa B ligand, pyridinoline, parathyroid hormone, and osteoprotegerin, while bone mineral density (BMD) and bone mineral content (BMC) were measured by dual x-ray absorptiometry. Subjects were divided into two groups according to habitual sodium intake (low-Na and high-Na group) assessed by questionnaire.
 Results: No difference was found between groups of low and high Na intake in BMD and BMC, or in biochemical markers of bone metabolism. Since the groups differed in Ca intake, energy and vitamin D, adjustments were made for those cofounders. Regression analysis showed that only the dietary intake of vitamin D was associated with dual femur BMD and BMC, and no correlation was found between bone remodelling indicators and Na intake after adjustment for vitamin D intake.
 Conclusion: The present results could not confirm that habitual sodium intake above recommended levels affects bone remodelling processes or decreases bone mineral density in young healthy people if combined with adequate calcium intake.

The effect of high-dose, short-term caffeine intake on the renal clearance of calcium, sodium and creatinine in healthy adults.

The consumption of caffeine has been linked to osteoporosis, believed to be due to enhanced bone resorption as a result of increased calcium excretion in the urine. However, the amount of calcium in the urine may not necessarily reflect the true effect of caffeine on calcium clearance. This study therefore examined the impact of high-dose, short-term caffeine intake on renal clearance of calcium, sodium and creatinine in healthy adults. In a double-blind clinical study, participants chewed caffeine (n = 12) or placebo (n = 12) gum for 5 minutes at 2-hour intervals over a 6-hour treatment period (800 mg total caffeine). Caffeine increased renal calcium clearance by 77%. Furthermore, the effect was positively correlated with sodium clearance and urine volume, suggesting that caffeine may act through inhibition of sodium reabsorption in the proximal convoluted tubule. This study confirmed that caffeine does increase renal calcium clearance and fosters further investigation into safe consumption of caffeine.

Clinical Spectrum of Hereditary Hypophosphatemic Rickets With Hypercalciuria (HHRH).

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) represents an FGF23-independent disease caused by biallelic variants in the solute carrier family 34-member 3 (SLC34A3) gene. HHRH is characterized by chronic hypophosphatemia and an increased risk for nephrocalcinosis and rickets/osteomalacia, muscular weakness, and secondary limb deformity. Biochemical changes, but no relevant skeletal changes, have been reported for heterozygous SLC34A3 carriers. Therefore, we assessed the characteristics of individuals with biallelic and monoallelic SLC34A3 variants. In 8 index patients and 5 family members, genetic analysis was performed using a custom gene panel. The skeletal assessment comprised biochemical parameters, areal bone mineral density (aBMD), and bone microarchitecture. Pathogenic SLC34A3 variants were revealed in 7 of 13 individuals (2 homozygous, 5 heterozygous), whereas 3 of 13 carried monoallelic variants of unknown significance. Whereas both homozygous individuals had nephrocalcinosis, only one displayed a skeletal phenotype consistent with HHRH. Reduced to low-normal phosphate levels, decreased tubular reabsorption of phosphate (TRP), and high-normal to elevated values of 1,25-OH2 -D3 accompanied by normal cFGF23 levels were revealed independently of mutational status. Interestingly, individuals with nephrocalcinosis showed significantly increased calcium excretion and 1,25-OH2 -D3 levels but normal phosphate reabsorption. Furthermore, aBMD Z-score <-2.0 was revealed in 4 of 8 heterozygous carriers, and HR-pQCT analysis showed a moderate decrease in structural parameters. Our findings highlight the clinical relevance also of monoallelic SLC34A3 variants, including their potential skeletal impairment. Calcium excretion and 1,25-OH2 -D3 levels, but not TRP, were associated with nephrocalcinosis. Future studies should investigate the effects of distinct SLC34A3 variants and optimize treatment and monitoring regimens to prevent nephrocalcinosis and skeletal deterioration. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study.

ContextAlthough dietary potassium and sodium intake may influence calcium-phosphate metabolism and bone health, the effects on bone mineral parameters, including fibroblast growth factor 23 (FGF23), are unclear.ObjectiveHere, we investigated the effects of potassium or sodium supplementation on bone mineral parameters.Design, setting, participantsWe performed a post hoc analysis of a dietary controlled randomized, blinded, placebo-controlled crossover trial. Prehypertensive individuals not using antihypertensive medication (n = 36) received capsules containing potassium chloride (3 g/d), sodium chloride (3 g/d), or placebo. Linear mixed-effect models were used to estimate treatment effects.ResultsPotassium supplementation increased plasma phosphate (from 1.10 ± 0.19 to 1.15 ± 0.19 mmol/L, P = 0.004), in line with an increase in tubular maximum of phosphate reabsorption (from 0.93 ± 0.21 to 1.01 ± 0.20 mmol/L, P < 0.001). FGF23 decreased (114.3 [96.8-135.0] to 108.5 [93.5-125.9] RU/mL, P = 0.01), without change in parathyroid hormone and 25-hydroxy vitamin D3. Fractional calcium excretion decreased (from 1.25 ± 0.50 to 1.11 ± 0.46 %, P = 0.03) without change in plasma calcium. Sodium supplementation decreased both plasma phosphate (from 1.10 ± 0.19 to 1.06 ± 0.21 mmol/L, P = 0.03) and FGF23 (from 114.3 [96.8-135.0] to 108.7 [92.3-128.1] RU/mL, P = 0.02). Urinary and fractional calcium excretion increased (from 4.28 ± 1.91 to 5.45 ± 2.51 mmol/24 hours, P < 0.001, and from 1.25 ± 0.50 to 1.44 ± 0.54 %, P = 0.004, respectively).ConclusionsPotassium supplementation led to a decrease in FGF23, which was accompanied by increase in plasma phosphate and decreased calcium excretion. Sodium supplementation reduced FGF23, but this was accompanied by decrease in phosphate and increase in fractional calcium excretion. Our results indicate distinct effects of potassium and sodium intake on bone mineral parameters, including FGF23.Clinical Trial Registration numberNCT01575041

Metabolic effects of cholecalciferol supplementation in patients with calcium nephrolithiasis and vitamin D deficiency.

In this paper, we investigated whether cholecalciferol supplementation may increase the risk of stone recurrence in patients with calcium nephrolithiasis and Vitamin D deficiency. Thirty-three stone formers (56 ± 17years old, 12 males) with 25(OH)D < 20ng/mL were considered. Calcium excretion and urine supersaturation with calcium oxalate (ßCaOx) and brushite (ßbsh) were evaluated, both before and after cholecalciferol supplementation. Values of ß > 1 mean supersaturation. Cholecalciferol was prescribed as oral bolus of 100,000-200,000 IU, followed by weekly (5000-10,000 IU) or monthly (25,000-50,000 IU) doses. Calcium intake varied between 800 and 1000mg/day. In urine, total nitrogen (TNE) was taken as an index of protein intake, sodium as a marker of dietary intake, and net acid excretion (NAE) as an index of acid-base balance. TNE, sodium, and NAE did not change during the study (p = ns). Compared to baseline values, after cholecalciferol, both serum calcium and phosphate did not vary (p = ns); 25(OH)D increased from 11.8 ± 5.5 to 40.2 ± 12.2ng/mL (p < 0.01); 1.25(OH)2D increased from 41.6 ± 17.6 to 54 ± 16pg/mL (p < 0.01); PTH decreased from 75 ± 27.2 to 56.7 ± 21.1pg/mL (p < 0.01); urinary calcium increased from 2.7 ± 1.5 to 3.6 ± 1.6mg/Kg b.w. (p < 0.01); ßbsh increased from 0.9 ± 0.7 to 1.3 ± 1.3 (p = 0.02); whereas ßCaOx varied but not significantly. Before cholecalciferol supplementation, 6/33 patients were hypercalciuric (i.e., urine Ca ≥ 4mg/Kg b.w.) and increased to 13/33 after cholecalciferol supplementation (pX2 = 0.03). Cholecalciferol supplementation may increase calcium excretion, or reveal an underlying condition of absorptive hypercalciuria. This may increase both urine supersaturation with calcium salts and stone-forming risk.

Calcium-sensing receptor: evidence and hypothesis for its role in nephrolithiasis.

Calcium-sensing receptor (CaSR) is a plasma-membrane G protein-coupled receptor activated by extracellular calcium and expressed in kidney tubular cells. It inhibits calcium reabsorption in the ascending limb and distal convoluted tubule when stimulated by the increase of serum calcium levels; therefore, these tubular segments are enabled by CaSR to play a substantial role in the regulation of serum calcium levels. In addition, CaSR increases water and proton excretion in the collecting duct and promotes phosphate reabsorption and citrate excretion in the proximal tubule. These CaSR activities form a network in which they are integrated to protect the kidney against the negative effects of high calcium concentrations and calcium precipitates in urine. Therefore, the CaSR gene has been considered as a candidate to explain calcium nephrolithiasis. Epidemiological studies observed that calcium nephrolithiasis was associated with polymorphisms of the CaSR gene regulatory region, rs6776158, located within the promoter-1, rs1501899 located in the intron 1, and rs7652589 in the 5'-untranslated region. These polymorphisms were found to reduce the transcriptional activity of promoter-1. Activating rs1042636 polymorphism located in exon 7 was associated with calcium nephrolithiasis and hypercalciuria. Genetic polymorphisms decreasing CaSR expression could predispose individuals to stones because they may impair CaSR protective effects against precipitation of calcium phosphate and oxalate. Activating polymorphisms rs1042636 could predispose to calcium stones by increasing calcium excretion. These findings suggest that CaSR may play a complex role in lithogenesis through different pathways having different relevance under different clinical conditions.

Association between bone mineral density and metabolic syndrome in postmenopausal Turkish women

14.3% bazedoxifeno, 14.3% ibandronate and 7.1% risedronate). 62.5% of patients with high urinary calcium took some of these drugs, while only 16.7% of those who had normal urinary calcium took them. These differences were statistically significant (p=0.012). No significant differences between different antiosteoporotic drugs regarding calciuria (denosumab vs bisphosphonate or bisphosphonates vs bazedoxifeno) were observed. When they were analyzed separately bisphosphonates showed raised calciuria significantly with respect to osteoporotic patients not taking drugs, which does not occur in any significant way with other drugs. Conclusions: Treatment with anti-osteoporotic drugs is associated with increased calcium excretion in urine, at the expense of bisphosphonates.

Effects of coffee intake and intraperitoneal caffeine on bone repair process--a histologic and histometric study.

Studies have suggested that caffeine acts on bone promoting an increase of calcium excretion, inhibition of osteoblast proliferation and delay in tissue repair process, raising the risk of fractures, osteoporosis, periodontal disease and affecting the success of bone reconstructive procedures. The aim of this study was to analyze histomorphometrically the process of alveolar bone healing after tooth extraction in rats subjected to daily intake of boiled coffee or intraperitoneal administration of caffeine. Forty-five male rats were divided according to the treatment in Control group (C); Coffee group (CO) - treated with coffee since birth; and Caffeine (CAF) - intraperitoneal injection of aqueous solution of caffeine 1.5% (0.2 mL/100g body weight) for 30 days. When weighing between 250-300 g they were anesthetized, subjected to extraction of the maxillary right incisor, and euthanized 7, 21 and 42 days after surgery for histological assessments of bone volume and the quality of formed bone in the dental socket. The qualitative results demonstrated larger amounts of blood clot and immature bone in animals under treatment of pure caffeine compared to coffee and control. Histometric analysis revealed that coffee treatment led to a 40% drop in bone formation, and caffeine a 60% drop in comparison to control animals (ANOVA p≤0.01). It was concluded that both the daily ingestion of coffee and the intraperitoneal administration of caffeine in rats delayed the alveolar bone reparative process after tooth extraction, and this effect was more aggressive when pure caffeine was used.

Does the use of chitosan contribute to oxalate kidney stone formation?

Chitosan is widely used in the biomedical field due its chemical and pharmacological properties. However, intake of chitosan results in renal tissue accumulation of chitosan and promotes an increase in calcium excretion. On the other hand, the effect of chitosan on the formation of calcium oxalate crystals (CaOx) has not been described. In this work, we evaluated the antioxidant capacity of chitosan and its interference in the formation of CaOx crystals in vitro. Here, the chitosan obtained commercially had its identity confirmed by nuclear magnetic resonance and infrared spectroscopy. In several tests, this chitosan showed low or no antioxidant activity. However, it also showed excellent copper-chelating activity. In vitro, chitosan acted as an inducer mainly of monohydrate CaOx crystal formation, which is more prevalent in patients with urolithiasis. We also observed that chitosan modifies the morphology and size of these crystals, as well as changes the surface charge of the crystals, making them even more positive, which can facilitate the interaction of these crystals with renal cells. Chitosan greatly influences the formation of crystals in vitro, and in vivo analyses should be conducted to assess the risk of using chitosan.

Increasing urinary calcium excretion after ceftriaxone and cephalothin therapy in adults: possible association with urolithiasis

In children, stone formation after ceftriaxone (CTRX) therapy by increasing calcium excretion was showed in the literature. In this study, we investigated the effect of CTRX, cephalothin (CP) and ampicillin (AS) therapy on urinary calcium excretion in adults. 180 participants included in the study who divided into six equal groups. The groups were; (1) CTRX therapy in stone free patients, (2) CTRX therapy in patients who have urinary stone; (3) CP therapy in stone free patients, (4) CP therapy in patients with urinary stone, (5) AS therapy in stone free patients, (6) AS therapy in patients with urinary stone. The patients received 2 g/day intravenous CTRX, CP and AS for 5 days in all groups respectively. There were no significant differences in demographic characteristics and blood biochemistry between the groups. Before and 5 days after the antibiotic therapies, the participants were evaluated by 24-h urinary calcium to creatinine ratio. Results were compared between the groups statistically by ANOVA and Tukey test. After drug therapies in group 2 and 4, the excretion of calcium to creatinine ratio in 24-h urine was more than the other groups. We found that both groups of two drugs therapy with or without stones (groups 1, 2, 3, 4), have significantly increased calcium to creatinine ratio in 24-h urine (p < 0.05). We did not find statistically difference in groups 5 and 6, after AS therapy. As a result of the study, we suggest that the patients who have taken antibiotic therapy with CTRX or CP, have an increased risk for the urolithiasis. In addition, we think that these drugs should be used carefully especially in patients with urolithiasis.

Do the other nutrients except calcium and vitamin D prevent the incidence of osteoporosis

Osteoporosis as a skeletal disorder characterize by compromised bone strength predisposing a person to an increased risk of fracture. All people should be encouraged to take efforts to prevent bone loss and fractures. Nutrition is one of several factors that can be modified to reduce osteoporosis risk. The purpose of this review article is assessment the role of the other nutrients the exception of calcium and vitamin D on bone health and prevention of osteoporosis.The search was undertaken in three databases (PubMed, google scholar and science direct) for publications from 2005 onwards using key words as follows. Initial searches yielded approximately 2467 results. After considering additional exclusion criteria, 33 clinical trial and meta- analysis papers remained.According to investigations, high intake of dietary protein increase bone resorption and calcium excretion and low protein intake can prevent calcium absorption and decrease strength and bone mass. Omega-3 supplementation also can decrease bone resorption and α-linleic acid (for men and women) and arashidonic acid (in men) and isoflavones can significantly diminish the risk of hip fracture. Adequate intake of some nutrients like zinc, vitamin A, boron and manganese in bone formation and copper, fluoride and strontium in bone mineralization have positive effects. However, high intake of vitamin A and fluoride result in hip fracture incretion. Vitamin K (in form of K 2 ) along with calcium and vitamin D induce bone fracture decrease. If intake of phosphate, iron and sodium be more than the recommended values, they may present negative effects on bone mineralization.In conclusion, risk of osteoporosis incidence may be diminished with an adequate and balanced diet containing variety of foods to meet needs and a healthy lifestyle. Nutrition education and training the other preventive factors should be carrying out in childhood to achieve the peak bone mass in youth and aging.

Calcium-sensing receptor gene polymorphisms in patients with calcium nephrolithiasis

The calcium-sensing receptor gene (CaSR, chr. 3q13.3-21) is a candidate to explain nephrolithiasis. This review analyzes the potential role of CaSR in lithogenesis according to findings of functional and genetic studies. CaSR is a cation receptor located in the tubular cell plasma membrane. Its activation decreases calcium reabsorption in the ascending limb and distal convoluted tubule, but increases phosphate reabsorption in proximal tubules and decreases water and proton reabsorption in collecting ducts. Its effects in proximal tubules and collecting ducts can limit the calcium phosphate precipitation risk induced by the increase in calcium excretion. The nonconservative CaSR gene Arg990Gly polymorphism was associated with nephrolithiasis and hypercalciuria in different populations. Arg990Gly is located on exon 7 and produces a gain of the CaSR function. rs7652589 and rs1501899 were also associated with nephrolithiasis in patients with normal citrate excretion. These polymorphisms are located in the CaSR gene regulatory region and may modify CaSR gene promoter activity. The activating Arg990Gly polymorphism may predispose to nephrolithiasis by increasing calcium excretion. Polymorphisms at the regulatory region may predispose to nephrolithiasis by changing tubular expression of the CaSR. CaSR genotype may be a marker to identify patients prone to develop calcium nephrolithiasis.

Biochemical indices in the blood of rats at different terms of reparative osteogenesis in conditions of hyperhomocysteinaemia

The effects, produced by hyperhomocysteinaemia (HHcy) and its correction with Decamevit and Glutargin on bone tissue metabolism in rats with femur fractures in different terms of reparative osteogenesis, were studied. It was established, that HHcy caused enhancement of bone tissue resorption, increase of calcium excretion with urine, inhibition of collagen biosynthesis in rats with femur fractures. HHcy induced dysregulation of reparative osteogenesis by lowering the transforming growth factor beta -1 (TGF- β1) levels in the first 2 weeks after trauma and by an excessive increase of this index on days 30-45 after the trauma. Decamevit and Glutargin reduced HHcy-induced imbalance between the processes of resorption and biosynthesis of bone tissue, and normalized the staging changes of TGF- β1 levels in blood serum of rats with femur fractures.