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There is controversy about the choice of dialysate calcium concentration (DCa), with strong arguments both in favor of and against the use of a low or high DCa, as they can both be potentially harmful. Evidence suggests that calcium mass balance is positive with a DCa 3.5 mEq/L, negative or neutral with the use of DCa 2.5 mEq/L, whereas both positive and negative balances have been observed with the use of DCa 3.0 mEq/L. Overall, the use of DCa >2.5 mEq/L is usually associated with an increase in serum calcium level and a decrease in serum PTH level and use of lower vitamin D analogue dose, with the opposite effects usually observed with the use of lower DCa. Most of the available evidence is from small-sized and crossover studies; hence, evidence should be regarded with caution and applied in a patient-specific manner. As there are a lot of significant unanswered questions regarding calcium balance and the optimal DCa in hemodialysis patients, further high-quality research is needed to clarify many still unclear aspects of calcium homeostasis and balance in these patients. In conclusion, with the existing evidence the choice of DCa needs to be individualized and contextualized in the setting of each patient's calcium balance needs and homeostatic response, taking also into account oral calcium intake (dietary and medicinal), any other relevant therapy administered, such as vitamin D analogues, the type of renal mineral bone disorder, and associated cardiovascular comorbidity.

Glucocorticoids are known to affect calcium balance but are not thought to cause clinically significant hypocalcemia. This case adds to a list of isolated reports noting significant hypocalcemia developing post administration of glucocorticoids in a patient with known hypoparathyroidism, postulating PTH deficiency as a risk factor of decompensated calcium homeostasis.\ud

We studied the role of calcium-regulating structures of slow- (m. soleus, SOL) and fast-twitch (m. extensor digitorum longus, EDL) skeletal muscles of rats during adaptation to exhausting physical activity and the possibility of modulating this adaptation with decaffeinated green tea extract. It was established that EDL adaptation is mainly aimed at Са2+ elimination from the sarcoplasm by Са-ATPase and its retention in the reticulum by calsequestrin. Administration of green tea extract increased endurance due to involvement of slow-twitch muscles whose adaptation is associated with enhanced expression of all the studied genes responsible for the regulation of Ca2+ balance.

Although the implications of long-term high Ca intakes have been well documented in growing dogs, the health consequences of Ca excess in adult dogs remain to be established. To evaluate the impact of feeding a diet containing 7·1 g/4184 kJ (1000 kcal) Ca for 40 weeks on Ca balance and health parameters in adult dogs, eighteen neutered adult Labrador Retrievers, (nine males and nine females) aged 2·5–7·4 years were randomised to one of two customised diets for 40 weeks. The diets were manufactured according to similar nutritional specifications, with the exception of Ca and P levels. The diets provided 1·7 and 7·1 g/4184 kJ (1000 kcal) (200(SD26) and 881(SD145) mg/kg body weight0·75 per d, respectively) Ca, respectively, with a Ca:P ratio of 1·6. Clinical examinations, ultrasound scans, radiographs, health parameters, metabolic effects and mineral balance were recorded at baseline and at 8-week intervals throughout the study. Dogs in both groups were healthy throughout the trial without evidence of urinary, renal or orthopaedic disease. In addition, there were no clinically relevant changes in any of the measures made in either group (all P>0·05). The high-Ca diet resulted in a 3·3-fold increase in faecal Ca excretion (PP>0·05). Ca intakes of up to 7·1 g/4184 kJ (1000 kcal) are well tolerated over a period of 40 weeks, with no adverse effects that could be attributed to the diet or to a high mineral intake.

Purpose of Review The kidneys play a critical role in the balance between the internal milieu and external environment. Kidney failure is known to disrupt a number of homeostatic mechanisms that control serum calcium and normal bone metabolism. However, our understanding of calcium balance throughout the stages of chronic kidney disease is limited and the concept of balance itself, especially with a cation as complex as calcium, is often misunderstood. Both negative and positive calcium balance have important implications in patients with chronic kidney disease, where negative balance may increase risk of osteoporosis and fracture and positive balance may increase risk of vascular calcification and cardiovascular events. Here, we examine the state of current knowledge about calcium balance in adults throughout the stages of chronic kidney disease and discuss recommendations for clinical strategies to maintain balance as well as future research needs in this area. Recent Findings Recent calcium balance studies in adult patients with chronic kidney disease show that neutral calcium balance is achieved with calcium intake near the recommended daily allowance. Increases in calcium through diet or supplements cause high positive calcium balance, which may put patients at risk for vascular calcification. However, heterogeneity in calcium balance exists among these patients. Summary Given the available calcium balance data in this population, it appears clinically prudent to aim for recommended calcium intakes around 1000 mg/day to achieve neutral calcium balance and avoid adverse effects of either negative or positive calcium balance. Assessment of patients’ dietary calcium intake could further equip clinicians to make individualized recommendations for meeting recommended intakes.

Vitamin D and its active metabolite 1,25 - dihydrooxyvitaminD (1,25(OH) 2D) has been generally recognized as repertoireof many classical (calcium balance and bone metabolism)and non-classical effects (non-calcium actions) such aspromotion of insulin secretion and its action,immunomodulation. Absorption of calcium and phosphorusdepends on sufficient vitamin D levels. Its low level leadsto demineralization of bone both in children and adults.Vitamin D has also a significant role and has potential toinfluence many factors in the developing fetus. Newbornsare at high risk of developing hypocalcaemic tetany as aconsequence of maternal deficiency of vitamin D.

Background: Dysregulated serum calcium and FGF23 are associated with increased mortality and morbidity rates in patients receiving hemodialysis. Preliminary data suggest serum calcium regulates FGF23 secretion independently of serum phosphate, parathyroid hormone, and 25-OH vitamin D. It is unclear to what extent dietary and prescription sources of calcium influence calcium and FGF23 levels, and whether they confound this relationship. In this cross-sectional analysis of a multi-ethnic cohort of prevalent hemodialysis patients, association of dietary calcium and prescribed calcium were examined against serum calcium and FGF23. Bi- and multivariable linear regression was used for all analyses. Results: 81 patients (mean age 58 years, dialysis vintage 2 years, 51 men) participated. Dietary calcium was inversely associated with FGF23 (p = 0.04) however association of FGF23 with prescribed calcium did not reach statistical significance (0.08). In multivariable models, dietary calcium and prescribed calcium were associated in opposing directions with serum calcium (prescribed calcium, &szlig, coefficient = &minus, 0.35, p = 0.005 versus dietary calcium, coefficient = 0.35, p = 0.03). FGF23 was independently associated with serum calcium (p = 0.007). Conclusions: We found differing, sometimes opposing, associations between serum calcium and FGF23 levels when considering prescribed versus dietary sources of calcium. Serum calcium and FGF23 were strongly correlated regardless of possible confounders examined in this hemodialysis cohort. Dietary calcium was associated with higher serum calcium and lower FGF23 concentrations, while prescribed calcium was only inversely associated with serum calcium. Further studies are required to confirm these associations and determine causality.

We developed a model of calcium homeostasis in the rat to better understand the impact of dysfunctions such as primary hyperparathyroidism and vitamin D deficiency on calcium balance. The model accounts for the regulation of calcium intestinal uptake, bone resorption, and renal reabsorption by parathyroid hormone (PTH), vitamin D3, and Ca2+itself. It is the first such model to incorporate recent findings regarding the role of the calcium-sensing receptor (CaSR) in the kidney, the presence of a rapidly exchangeable pool in bone, and the delayed response of vitamin D3synthesis. Accounting for two (fast and slow) calcium storage compartments in bone allows the model to properly predict the effects of bisphophonates on the plasma levels of Ca2+([Ca2+]p), PTH, and vitamin D3. Our model also suggests that Ca2+exchange rates between plasma and the fast pool vary with both sex and age, allowing [Ca2+]pto remain constant in spite of sex- and age-based hormonal and other differences. Our results suggest that the inconstant hypercalciuria that is observed in primary hyperparathyroidism can be attributed in part to counterbalancing effects of PTH and CaSR in the kidney. Our model also correctly predicts that calcimimetic agents such as cinacalcet bring down [Ca2+]pto within its normal range in primary hyperparathyroidism. In addition, the model provides a simulation of CYP24A1 inactivation that leads to a situation reminiscent of infantile hypercalcemia. In summary, our model of calcium handling can be used to decipher the complex regulation of calcium homeostasis.

Our previous studies found that different extracts or fractions of Fructus ligustri lucidi (FLL) played different roles in altering the regulation of bone and mineral metabolism in different animal models. The present study was designed to compare the actions of FLL ethanol (EE) and water extracts (WE) on bone and mineral metabolism in a 6-month-old mature ovariectomized (OVX) rat model. Our results showed that FLL extracts did not significantly improve systematic Ca balance in mature OVX rats. However, EE, but not WE treatment, significantly increased serum 1,25(OH)2D3levels in mature OVX rats. An in vitro study using human proximal tubule (HKC-8) cells showed that EE, but not WE, significantly enhanced renal 25-dihydroxyvitamin D3-1[Formula: see text]-hydroxylase (1-OHase) mRNA expressions and simultaneously repressed renal 25-dihydroxyvitamin D3-24-hydroxylase (24-OHase) mRNA expressions. Further investigation indicated that EE could significantly induce the protein expression of 1-OHase, but did not alter 24-OHase expression in HKC-8 cells. Our results demonstrated that EE increased circulating 1,25(OH)2D3levels in OVX rats, possibly via upregulation of renal 1-OHase expressions in renal proximal tubule cells. Our study indicates that FLL is a natural oral agent that could directly regulate renal vitamin D metabolism in vivo and in vitro.

Background Online hemodiafiltration (oHDF) is increasingly used in children; we treated 28 children since 2009, adapting this technique to pediatric patients. Methods In this service evaluation audit, we assessed plasma electrolytes to evaluate the evolution of total (tCa) and ionized (iCa) during a session, as well as dialysate calcium (dCa) concentrations. Results Using a 1.25 mmol Ca/L-dialysate, both tCa and iCa decreased during the session, with iCa falling below 1.1 mmol/L in 4/5 patients. In contrast, using a 1.5 mmol Ca/L-dialysate, iCa remained normal in all patients. Major discrepancies were observed between the expected and the measured dCa: 1.25 vs. 1.01 (0.83–1.04), and 1.5 vs. 1.47 (0.85–1.75) mmol/L, respectively (results presented as median [range]). These differences were explained by the modality of reconstituting dialysate: increasing bicarbonates and/or decreasing sodium requested in the dialysate decreases calcium extraction from the acid preparation. Proof of concept was given when requesting in an “ex-vivo” setting modifications in the requested sodium and bicarbonate in dialysate directly on the Fresenius machine. Conclusion Nephrologists should be aware that “high bicarbonate and/or low sodium” requirements in oHDF decrease calcium in the dialysate.

The physiological role of vitamin D depends on calcium supply and calcium balance. When the calcium balance is normal, the major target of vitamin D is intestine. Vitamin D stimulates mainly active intestinal calcium transport mechanism. During a negative calcium balance, bone effects of vitamin D become dominant. Thus, the role of vitamin D in maintaining normocalcemia appears to have priority over skeletal integrity in these situations.

A case of Pseudohypoparathyroidism 1b is reported, who presented with signs and symptoms of hypocalcemia. Causes, diagnosis and management with new insight into genetic novel mutations in PHP are discussed. The objectives are to provide information regarding problems of Calcium balance, causes and making diagnosis of pseudohypoparathyroidism, learn complexities of PTH cellular interactions and calcium homeostasis and learn the genetic novel mutations of various types of PHP. Keywords: Hyperphosphatemia, hypocalcemia Isolated PTH resistance, Pseudohypoparathyroidism, Secondary hyperparathyroidism. | PubMed

The purpose of this study was to investigate the antihypertensive mecha-nisms of piperitenone oxide in spontaneously hypertensive rat (SHR). Compared to control SHR, piperitenone oxide reduced the systolic blood pressure and serum endothelium-1 (ET-1). The nitric oxide (NO) production and ET-1 secretion were significantly inhibited in the noradrenaline-exposed bovine aortic endothelial cells. Piperitenone oxide showed endothelium-independent but concentration-dependent relaxation of the artery rings. The responsible mechanisms appear to be related to the modulation of ET-1 and NO levels. The vasorelaxant effect of piperitenone oxide is independent of endothelium-derived mediators, which is associated with interfering intracellular calcium homeostasis by blocking Ca2+ influx, as well as intracellular Ca2+ release. Video Clip of Methodology: 2 min 58 sec: Full Screen Alternate

A variety of genetic, mechano-response-related, endocrine-metabolic, and nutritional determinants impact bone health. Among the nutritional influences, protein intake and dietary acid load are two of the factors most controversially discussed. Although in the past high protein intake was often assumed to exert a primarily detrimental impact on bone mass and skeletal health, the majority of recent studies indicates the opposite and suggests a bone-anabolic influence. Studies examining the influence of alkalizing diets or alkalizing supplement provision on skeletal outcomes are less consistent, which raises doubts about the role of acid-base status in bone health. The present review critically evaluates relevant key issues such as acid-base terminology, influencing factors of intestinal calcium absorption, calcium balance, the endocrine-metabolic milieu related to metabolic acidosis, and some methodological aspects of dietary exposure and bone outcome examinations. It becomes apparent that for an adequate identification and characterization of either dietary acid load's or protein's impact on bone, the combined assessment of both nutritional influences is necessary.

In children with chronic kidney disease (CKD) optimal control of mineral and bone disorder (MBD) is essential not only for the prevention of debilitating skeletal complications and for achieving adequate growth, but also for preserving long-term cardiovascular health. The growing skeleton is particularly vulnerable to the effects of CKD, and bone pain, fractures and deformities are common in children on dialysis. Defective bone mineralisation has been linked with ectopic calcification, which in turn leads to significant morbidity and mortality. Despite national and international guidelines for the management of CKD-MBD, the management of mineral dysregulation in CKD can be extremely challenging, and a significant proportion of patients have calcium, phosphate or parathyroid hormone levels outside the normal ranges. Clinical and experimental studies have shown that, in the setting of CKD, low serum calcium levels are associated with poor bone mineralisation, whereas high serum calcium levels can lead to arterial calcification, even in children. The role of calcium in CKD-MBD is the focus of this review.

The transition cow is in a negative nutrient balance, recognized largely as a negative energy and calcium balance. In response to the negative energy state, the body begins to mobilize body fat. In response to the negative calcium balance, the body begins to mobilize calcium stores from bone. A negative protein balance has also been documented, and results in mobilization of protein reserves from skeletal muscles. Total serum protein has been associated with cow health, but serum albumin is more specific and plays an important role in transporting triglycerides and calcium. Albumin has been proposed as a potential biomarker for health in the transition cow. The objective of this study was to determine whether low serum albumin concentrations 2 days after calving would result in an increased risk of developing acute puerperal metritis (APM). A secondary objective was to establish whether total or ionized calcium levels 48 hours post calving were associated with serum albumin levels early postpartum., American Association of Bovine Practitioners Proceedings of the Annual Conference, 2016

Protein and calcium metabolisms interact at multiple levels. It is well known that an increase in the protein content of the diet causes an increase of the calcium concentration in the urine. However, the exact consequences of protein intake on the calcium economy are debated. Indeed, there are two explanations for increased calciuria: increased calcium absorption or increased bone resorption. Currently, there is no clear answer; however, there is increasing evidence that protein intake is not harmful to bone. In fact, an increased protein intake would probably be beneficial for bone. This chapter reviews the different aspects of the protein–calcium interaction and discusses the proposed mechanisms. The consequences for health are also considered, especially on bone strength and kidney-stone formation.

Animal models fed low calcium diets demonstrate a negative calcium balance and gross bone loss while the combination of calcium deficiency and oophorectomy enhances overall bone loss. Following oophorectomy the dietary calcium intake required to remain in balance increases some 5 fold, estimated to be approximately 1.3% dietary calcium. In the context of vitamin D and dietary calcium depletion, osteomalacia occurs only when low dietary calcium levels are combined with low vitamin D levels and osteoporosis occurs with either a low level of dietary calcium with adequate vitamin D status or when vitamin D status is low in the presence of adequate dietary calcium intake. Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. This anabolic effect occurs without a change to intestinal calcium absorption, suggesting dietary calcium and vitamin D have activities in addition to promoting a positive calcium balance. Each of the major bone cell types, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25 hydroxyvitamin D (25D) to 1,25 dihydroxyvitamin D (1,25D) to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes. Each of these activities is consistent with the actions of adequate circulating levels of 25D observed in vivo. Refereed/Peer-reviewed

Editor's Note: This paper is one of the first suggesting that idiapathic osteoporosis may be n disorder of calcium metabolism for which increased intakes calcium mas be preventative.

Combined calcium balance and 47Ca turnover studies in sarcoidosis (4 patients) and vitamin D intoxication (1 patient) disclosed three different patterns of calcium metabolism. One patient with sarcoidosis had a normal metabolism of calcium, and two patients presented the usual pattern of intestinal hyperabsorption, hypercalcemia, and hypercalciuria. The fourth patient with sarcoidosis and the patient with vitamin D intoxication, both studied during spontaneous remissions, presented the third pattern. The main features here were hypercalcemia despite normal intestinal absorption of calcium, enlarged exchangeable calcium pool, accelerated accretion and resorption rates, hypercalciuria, and a distinctly negative calcium balance. This pattern of remission seems to represent a mobilization of extraosseous or metastatic calcifications, rather than a resorption of bone calcium.

Jejuno-ileostomy was performed in eight women because of severe alimentary obesity. Their calcium phosphate and bone metabolism was studied an average of 31 months post-operatively. This revealed secondary intestinal hyperparathyroidism due to an artificial malabsorption syndrome. While most of the significant metabolic factors were within normal limits, examination of calcium balance and kinetics indicated a marked disorder of calcium and bone metabolism. Calcium balance averaged-138 mg daily, corresponding to a yearly loss of skeletal mass of 4-5%.

Calcium balance during hemodialysis (HD) is important in determining short-term cardiovascular function, this influences the hemodynamic tolerability of dialysis. In the longer term, calcium flux during HD is an important determinant of overall calcium balance in a patient and may also influence the development and progression of vascular calcification, with its attendant consequences. This article aims to review the assessment and mechanisms of calcium flux during HD, choice of dialysate calcium concentration, influence of HD modality, and potential consequences of therapy choices (cardiovascular and skeletal) resulting from an inappropriate intradialytic calcium balance.

Calcium regulation in sturgeon is of special interest because they are a representative of the ancient fishes possessing mainly cartilaginous skeletons and a supposedly low calcium demand. The present study aimed to characterize the effect of a chronic absence of dietary calcium and the effect of parathyroid hormone-related protein (PTHrPA) (1-34) ( 7 ) on calcium balance in juvenile sturgeon ( Acipenser naccarii). At rest, sturgeon juveniles are in net positive calcium balance, since whole body calcium uptake is significantly higher than efflux and calcium accumulates in the body. To study the importance of dietary calcium, the sturgeon were kept on a calcium-free diet for 8 wk. This manipulation impaired growth as measured by failure to gain weight or increase in length and indicates that dietary calcium is important for growth in sturgeon. An increased whole body calcium uptake partially compensated dietary calcium deficiency and was associated with increased gill chloride cell number in lamellae and filaments in parallel with increased gill Na+K+-ATPase activity. In addition, a single injection of piscine PTHrP(1-34) significantly increased whole body calcium uptake and decreased whole body calcium efflux. Administration of PTHrP significantly increased circulating plasma calcium 4–24 h postinjection. The increase in net calcium transport and increased plasma levels of calcium is consistent with the actions of a hypercalcemic factor. It would appear that the sturgeon rely on calcium for growth and tightly regulate calcium transport. The action in calcium balance is consistent with PTHrP acting as a hypercalcemic factor in sturgeon.

Information on the pathophysiology of glucocorticoid-induced osteoporosis (GIO) is limited, since its clinical picture often reflects a combined effect of glucocorticoids (GC) and the treated systemic disease (i.e., inflammation and immobility). In 50 healthy adult (30-mo-old) primiparous Göttingen minipigs, we studied the short-term (8 mo, n = 30) and long-term (15 mo, n = 10) effect of GC on bone and mineral metabolism longitudinally and cross-sectionally compared with a control group ( n = 10). All animals on GC treatment received prednisolone orally at a dose of 1.0 mg·kg body wt−1·day−1for 8 wk and thereafter at 0.5 mg/kg body wt−1·day−1. In the short term, GC reduced bone mineral density (BMD) at the lumbar spine by −47.5 ± 5.1 mg/cm3from baseline ( P < 0.001), which was greater ( P < 0.05) than the loss [not significant (NS)] in the control group of −11.8 ± 12.6 mg/cm3. Calcium absorption decreased from baseline by −2,488 ± 688 mg/7 days ( P < 0.001) compared with −1,380 ± 1,297 mg/7 days (NS) in the control group. Plasma bone alkaline phosphatase (BAP) decreased from baseline by −17.8 ± 2.2 U/l ( P < 0.000), which was significantly different ( P < 0.05) from the value of the control group of −1.43 ± 4.8 U/l. In the long term, the loss of BMD became more pronounced and bone mineral content (BMC), trabecular thickness, mechanical stability, calcium absorption, 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and parathyroid hormone tended to be lower compared with the control group. There was a negative association between the cumulative dose of GC and BMD, which was associated with impaired osteoblastogenesis. In conclusion, the main outcomes after GC treatment are comparable to symptoms of GC-induced osteoporosis in human subjects. Thus the adult Göttingen miniature pig appears to be a valuable animal model for GC-induced osteoporosis.

Acidosis is common in patients with AKI in the ICU and often associated with acidemia. It is typically secondary to the accumulation of lactate, chloride and unmeasured anions. Its correction appears desirable and can be more reliably and safely achieved with CRRT. Use of bicarbonate-based fluids is safest as the initial approach. However, lactate- and citrate-buffered fluids can also correct acidosis if appropriately metabolized by the liver and other key organs. CRRT can also be used to correct extreme acidosis in the absence of a major degree of renal impairment. As CRRT controls volume status easily, it would additionally enable bicarbonate infusion to occur for more rapid correction of acidemia.

The aim of this study was to evaluate the effect of Fructus Ligustri Lucidi (FLL), a kidney-tonifying Chinese herbal medicine, on the biochemical markers of bone turnover, calcium metabolism and balance in osteoporotic rat model developed by ovariectomy. Four weeks after surgical operation, animals were randomly assigned to one of the four treatments for 14 weeks: sham-operated control treated with vehicle (sham, n=8), ovariectomized group treated with vehicle (OVX, n=8), OVX group treated with 17beta-estradiol (E(2), n=10, 2 microg/kg/d) and OVX group treated with FLL extracts (FLL, n=10, 550 mg/kg/d). Serum osteocalcin and urinary deoxypyridinoline levels were upregulated in rats in response to OVX, suggesting that the bone turnover rate was accelerated in these animals. Treatment of OVX rats with FLL extract could prevent OVX-induced increase in bone turnover by suppression of both serum osteocalcin (p0.05, vs. OVX) and urinary deoxypyridinoline (p0.05, vs. OVX) levels. In addition, FLL extract could prevent OVX-induced loss of calcium in rats by increasing the intestinal calcium absorption rate (p0.01, vs. OVX), suppressing urinary Ca excretion (p0.05, vs. OVX) as well as increasing bone calcium content (p0.05, vs. OVX). Our study is the first to report that FLL can modulate bone turnover and calcium balance in OVX rats and it might be a potential candidate for prevention and treatment of postmenopausal osteoporosis.

Objective: The purpose of this study was to examine the effects of vitamin K2 administration on calcium balance and bone mass in young rats fed a normal or low calcium di

Contains fulltext : 57350.pdf (Publisher’s version ) (Open Access) Juvenile gilthead sea bream (Sparus auratus L.; 10-40 g body mass) were acclimatized in the laboratory to full strength (34 per thousand) or dilute (2.5 per thousand) seawater and fed normal, calcium-sufficient or calcium-deficient diet for nine weeks. Mean growth rate, whole-body calcium and phosphorus content and accumulation rates were determined, as well as plasma levels of ionic and total calcium, cortisol and parathyroid hormone related protein (PTHrP; a hypercalcemic hormone in fish). When confronted with limited calcium access (low salinity and calcium-deficient diet), sea bream show growth arrest. Both plasma cortisol and PTHrP increase when calcium is limited in water or diet, and a positive relationship was found between plasma PTHrP and plasma ionic calcium (R(2)=0.29, N=18, P

We examined the effect of vitamin D supplementation on bone growth in young rats fed a normal or low calcium diet.Fifty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into five groups with 10 rats in each group: baseline control, 0.5% (normal) or 0.1% (low) calcium diet, and 0.5 or 0.1% calcium diet + vitamin D (25 microg/100 g, food intake). Duration of the experiment was 10 weeks.Vitamin D supplementation stimulated intestinal calcium absorption and increased urinary calcium excretion in rats fed a low or normal calcium diet. Vitamin D supplementation prevented the reduction in periosteal bone gain but enhanced enlargement of the marrow cavity and reduced the maturation-related cancellous bone gain in rats fed a low calcium diet, and increased the maturation-related cancellous and cortical bone gains in rats fed a normal calcium diet.This study shows the differential effects of vitamin D supplementation on born growth in young rats fed a normal or low calcium diet.

Calcium supplements for prevention and treatment of mineral and bone disorders in chronic kidney disease (CKD) have been alternately praised and damned. Clinical evidence in favor of either attitude has been lacking. The calcium balance study by Spiegel and Brady in patients with late stage 3 and stage 4 CKD suggests that CKD subjects ingesting 2000mg of elemental calcium per day are in marked positive balance. Methodological limitations such as unproven steady state warrant caution and confirmatory studies.

Objectives To assess selenium intakes, absorption, retention, and status in healthy adolescent girls and the effect of calcium supplementation on selenium parameters. Design Annual 2-week study conducted each year for 3 consecutive years in which yearly selenium intakes, absorption, and retention and blood selenium status were measured. Setting A metabolic unit in a large metropolitan hospital located in Columbus, Ohio—a low selenium region of the United States. Subjects Healthy white girls aged 11 to 14 years (n=16) enrolled in a calcium balance study and randomly assigned to receive a placebo of methylcellulose (n=9) or a calcium supplement containing 1,000mg supplemental calcium as calcium citrate malate (n=7). Interventions Each subject consumed a diet with ∼100μg selenium/day during the yearly 2-week balance studies. Results Selenium status measurements (serum and erythrocyte selenium and glutathione peroxidase activity) were all within normal ranges for adults during the study. Apparent selenium absorption averaged 71%, 76%, and 74% for years 1,2, and 3 of the study, respectively, and did not vary significantly ( P >.05). Average daily selenium retention did not differ among the years of the study ( P >.05) and indicated that the usual selenium intake was ∼100μg daily. Measurements of selenium status and retention did not differ between calcium-supplemented and placebo groups. Conclusions An intake of ∼100μg selenium/day is the typical intake of the mineral among the subjects and appeared adequate to maintain selenium status in these healthy adolescent girls; in addition, calcium supplementation of 1,000mg daily does not have a negative impact on selenium parameters. J Am Diet Assoc. 2002;102:1082-1087.

Background: A positive calcium balance may contribute to vascular calcification, while a negative balance increases iPTH. We explored the impact of different dialysate calcium concentrations on bone and mineral metabolism parameters according to pre-dialysis serum calcium levels. Results: Fifty-six hemodialysis patients were dialyzed with 3.0 or 2.5 mEq/l dialysate [calcium] in a crossover study of two weeks. Bone mineral metabolites were measured prior to and following the hemodialysis session. A 3.0 mEq/l dialysate [calcium] increased more post-dialysis total calcium and ionized calcium than 2.5 mEq/l dialysate [calcium]. The mildest dialysis-induced changes in calcium and PTH were observed in patients with pre-dialysis serum calcium 9.15 mg/dl dialyzed with 3.0 mEq/l calcium dialysate. Conclusion: In conclusion, the individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium may prevent major excursions in post-dialysis serum calcium and iPTH levels. Short Summary: High calcium dialysate may increase serum calcium in hemodialysis patients, while low dialysate calcium may increase PTH. Individualization of dialysate calcium according to predialysis serum calcium levels may prevent or decrease unwanted excursions of both serum calcium and PTH.

The growing interest in a personalized choice of dialysate calcium concentration faces some important unsolved questions. First, the desired aims to be achieved should be clarified, as different d-Ca concentrations might differentially impact dialysis calcium balance and serum calcium concentration. A second point to be addressed is how to achieve the desired goals; the kinetics of calcium during dialysis treatment are complex. This is not an easy task and probably only an automatic device able to read serum calcium concentration in real-time and adjust d-Ca to it might supply an effective method for individualizing d-Ca. Finally, it is not even clear whether individualizing d-Ca is worth doing; cost-effectiveness studies might give some further insights into this intricate issue.

Background: Variation in absorption efficiency explains more of the variability in calcium balance than does actual calcium intake. Several investigators have suggested that the relatively high phosphorus and protein intakes of the diets of industrialized nations reduce calcium absorption and thereby aggravate the problem of calcium deficiency. Objective: My objective was to test whether variation in phosphorus and protein intakes is associated with variation in calcium absorption. Design: One hundred ninety-one Roman Catholic nuns aged 48.7 ± 7.0 y were studied 3 times each over a >20-y period with a full metabolic balance regimen; controlled, chemically analyzed diets; and double-tracer measurement of calcium absorption. Results: Although the expected associations with absorption were found for age, calcium intake, and estrogen status, no association was observed for intakes of either phosphorus or protein. Conclusion: Phosphorus and protein intakes do not contribute to the wide variability in calcium absorption efficiency.

Prior to the advent of calcitriol therapy, haemodialysis (HD) patients were often in negative calcium (Ca) balance between dialyses because of severely impaired Ca absorption [1] that led to the recommendation of dialysate inlet Ca concentration (CdiCa++) 3.0–3.5 mEq/L, higher than plasma concentration [2]. Over the past 25 years since the advent of calcitriol, virtually all haemodialysis patients absorbed a substantial portion of dietary and phosphate binder calcium ingested between dialyses and yet CdiCa++ 3.0 mEq/L has continued to be widely used. The total Ca absorbed between dialyses (CaAbsT) must be removed by the dialyser (JdCaT) to achieve net zero Ca mass balance over the dialysis cycle and prevent chronic Ca overload that likely contributes to the high rate of vascular calcification in haemodialysis patients [3–5]. From this perspective, it follows that the CdiCa++ prescribed should result in neutral Ca mass balance and thus total Ca removed during dialysis (JdCa++), the sum of diffusive (JDiffCa++) and convective Ca++ (JConvCa++) removal, should equal CaAbs in accordance with

Study of morphometric parameters of podocyte foot processes showed that the increase of parathyroid hormone blood level causes dilatation of podocyte foot processes resulting from accumulation of calcium in the cells. Influence of the hormone on filtration processes in glomeruli as a result of its effect on podocytes is discussed.

Animal studies have indicated that calcium absorption is increased by lactulose, a synthetic disaccharide. Therefore, the influence of lactulose on calcium absorption was measured in postmenopausal women who may benefit from the possible enhancing effect of lactulose on calcium absorption. Twelve postmenopausal women drank 100 ml of water containing 5 or 10 g of lactulose or a reference substance at breakfast for 9 days. The three treatments were given according to a randomized, double-blind, cross-over design, separated by two 19-day wash-out periods. On the 8th day of each treatment period, 44Ca dissolved in orange juice was drunk immediately after the solution with the study substance and just before a standard breakfast with 162 mg of carrier calcium. Within half an hour, 48Ca was given intravenously. Based on isotope ratios measured in urine collected before and until 36 h after isotope administration, true fractional calcium absorption was calculated. Calcium absorption during the treatments with the reference substance, 5 g and 10 g of lactulose was (mean +/- SD) 27.7 +/- 7.7, 30.0 +/- 7.6, and 32.2 +/- 7.0, respectively. A significant difference in calcium absorption was found between the highest dose of lactulose and the reference treatment (p0.01). A significant linear trend was found between the dose of lactulose and its positive effect on calcium absorption. In conclusion, in postmenopausal women a 9-day consumption of lactulose increases calcium absorption in a dose-response way. More research is warranted to explore how lactulose stimulates calcium absorption and whether it is able to improve calcium balance and/or to attenuate the rate of aging bone loss.

Sandra Drummond looks at the role of calcium in preventing osteoporosis

Concern has recently arisen about the potential adverse effects of excessive calcium intakes, i.e., calcium loading from supplements, on arterial calcification and risks of cardiovascular diseases (CVD) in older adults. Published reports that high calcium intakes in free-living adults have relatively little or no beneficial impact on bone mineral density (BMD) and fracture rates suggest that current recommendations of calcium for adults may be set too high. Because even healthy kidneys have limited capability of eliminating excessive calcium in the diet, the likelihood of soft-tissue calcification may increase in older adults who take calcium supplements, particularly in those with age or disease-related reduction in renal function. The maintenance of BMD and bone health continues to be an important goal of adequate dietary calcium consumption, but eliminating potential risks of CVDs from excessive calcium intakes needs to be factored into policy recommendations for calcium by adults.

The effect of dietary lentils on calcium balance was evaluated in nine healthy male subjects. The Control and Experimental (+ 130 g dry lentils) diets were each fed for three weeks in a cross-over design. Study diets were matched to subjects' usual calcium and energy intakes, and balanced for protein and phytate. Complete fecal collections were made for all weeks and 24-hour urine collections were made in Week 3 of each period. Calcium balance was maintained during both the Control (0.4 ± 0.8 mmol/day, mean ± SEM) and Experimental periods (− 0.6 ± 0.9 mmol/day); fecal calcium remained unchanged (28.5 ± 1.7 mmol/day, 29.7 ± 1.5 mmol/day, respectively). Urinary excretion, however, varied from Control to Experimental periods for the following: calcium decreased from 5.43 ± 0.44 to 4.53 ± 0.41 mmol/day (P

Bone acts as a major reservoir that is available for the maintenance of serum calcium levels. An adult loses about 200 mg of calcium per day through the faeces (100 mg), urine (100 mg), and a very small amount through the skin. In children, about 400 mg per day of calcium are deposited in bone and they will cease 1:o grow normally if not maintained in sufficiently positive calcium balance. After the cessation of linear growth, bone undergoes remodelling at a rate of about 10% per year. The overall exchange of calcium in this process of remodelling is 500 rag/day (18.4 kg/year !). In a normal individual, these calcium needs are supplied by gut absorption, and therefore with intestinal disease, maintenance of calcium homeostasis becomes a major problem.