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Chronic kidney disease (CKD) and cardiovascular disease (CVD) are highly prevalent conditions, each significantly contributing to the global burden of morbidity and mortality. CVD and CKD share a great number of common risk factors, such as hypertension, diabetes, obesity, and smoking, among others. Their relationship extends beyond these factors, encompassing intricate interplay between the two systems. Within this complex network of pathophysiological processes, vitamin D has emerged as a potential linchpin, exerting influence over diverse physiological pathways implicated in both CKD and CVD. In recent years, scientific exploration has unveiled a close connection between these two prevalent conditions and vitamin D, a crucial hormone traditionally recognized for its role in bone health. This article aims to provide an extensive review of vitamin D's multifaceted and expanding actions concerning its involvement in CKD and CVD. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) stands as a prevalent global health concern, and mineral and bone disease are among the most impactful consequences. A severe complication arising from mineral and bone disease is the occurrence of fragility fractures, which disproportionately affect individuals with CKD compared to the general population. The prevalence of these fractures impacts both survival rates and quality of life. The aims of this study are analyzing and identifying (i) patient-related risk factors and (ii) CKD-related risk factors to contribute to the development of preventive measures for fragility fractures for this population. Methods: A retrospective, single-center observational study was conducted, encompassing patient data from the years 2021 to 2023. Registry data were recorded, including patient-related and CKD-related data. Patients were interviewed about traumatological history, and their answers were recorded. Logistic regression analysis was employed to investigate the association between independent variables and dependent variables. Results: Eighty-four patients, with a mean age of 64.3 ± 15.2 years and a male percentage of 58.3%, were included in this study. Among them, 19.5% exhibited smoking habits. The mean Charlson Comorbidity Index was 3.06 ± 1.21. All patients were diagnosed with end-stage chronic kidney disease, with mean durations of 208 months from the diagnosis and 84.5 months from the beginning of dialysis. The logistic regression analysis, adjusted for age, sex, and CCI, revealed that smoking habits play a significant role as a risk factor for fragility fractures in lower limbs (p: 0.011 *). The incidence of fragility fractures increases directly proportionally to the time since diagnosis (p-value: 0.021 *) and the beginning of dialysis treatment (p-value: 0.001 *). Conclusions: Among patient-related factors, smoking habits seem to significantly affect lower-limb fracture rates (p < 0.05), whereas among CKD-related factors, time since CKD diagnosis and time since the beginning of dialysis treatment are directly related to higher risks of fragility fractures. No relevant correlations emerged in the studied treatments, except for a reduction in proximal femur fracture occurrence when patients underwent a combined treatment of a calcimimetic and a vitamin D analog. [ABSTRACT FROM AUTHOR]

In patients treated with peritoneal dialysis (PD), lowering the calcium level in PD fluids results in lower serum calcium levels and higher parathyroid hormone (PTH) levels. It is hypothesized that this effect is attenuated when patients are using icodextrin 7.5% for the once-daily long dwell (containing high calcium concentration). In this case series, we included 8 stable PD patients (mean age 68 ± 13 years, 7 male), all using icodextrin 7.5% (containing 1.75 mmol/L calcium) for the once-daily long dwell. The calcium content of the PD fluids for the remaining dwells was lowered from 1.75 mmol/L to 1.25 mmol/L. Bone mineral parameters and phosphate prescription at baseline, 6 weeks after this change, and after 6 months were compared. After lowering calcium concentration of the PD fluids – except for the icodextrin 7.5% – from 1.75 mmol/L to 1.25 mmol/L, calcium levels changed from 2.32 ± 0.11 to 2.29 ± 0.12 (p = NS); intact PTH (iPTH) from 39.6 ± 28.3 to 64.9 ± 34.5 pmol/L (p = 0.045); and alkaline phosphatase from 104.13 ± 48.75 to 101.38 ± 32.39 (p = NS). After 6 months, all bone mineral parameters were similar to baseline levels; however, slightly higher calcium-based phosphate binders were prescribed. Lowering calcium content from 1.75 mmol/L to 1.25 mmol/L in PD fluids in patients on icodextrin resulted in stable calcium values, a temporal increase in iPTH and a modest increase in calcium-based phosphate binder prescription. Using icodextrin for the long once-daily dwell appears to attenuate the effects on bone mineral parameters when lowering the calcium concentration of the short dwells.

Modern intravenous iron compounds (e.g., ferric carboxymaltose [FCM] and ferric derisomaltose [FDI]) are utilized in the treatment of iron deficiency anemia in non-dialysis-dependent chronic kidney disease (ND-CKD). Product-specific alterations in the metabolism of fibroblast growth factor 23 (FGF-23) leading to hypophosphatemia have been described for certain intravenous iron compounds, such as FCM, with potential effects on bone and cardiovascular health and quality of life. No prior head-to-head comparison between FCM and FDI exists in ND-CKD. This single-center exploratory double-blind randomized controlled trial primarily aimed to investigate the differential impact of FCM and FDI on FGF-23 and phosphate in patients with iron deficiency +/− anemia and ND-CKD (stages 3a–5 – serum ferritin

Mineral and bone disease in the posttransplantation patient is common and requires thorough evaluation for appropriate management. This includes secondary renal osteodystrophy, rickets, osteomalacia, osteoporosis, and osteonecrosis. Biochemical markers along with imaging and bone biopsy help to establish the diagnosis and treatment planning. Lack of appropriate management plan can lead to chronic pains, fractures, and osteonecrosis affecting long-term bone health. Tailoring immunosuppressants with appropriate medical therapy, nutritional supplements, and anti-resorptive agents is the mainstay of treatment. Here, we discuss the current management strategies with illustrative cases.

Mineral and bone disease in the posttransplantation patient is common and requires thorough evaluation for appropriate management. This includes secondary renal osteodystrophy, rickets, osteomalacia, osteoporosis, and osteonecrosis. Biochemical markers along with imaging and bone biopsy help to establish the diagnosis and treatment planning. Lack of appropriate management plan can lead to chronic pains, fractures, and osteonecrosis affecting long-term bone health. Tailoring immunosuppressants with appropriate medical therapy, nutritional supplements, and anti-resorptive agents is the mainstay of treatment. Here, we discuss the current management strategies with illustrative cases. [ABSTRACT FROM AUTHOR]

Background: The description of the clinical presentation of celiac disease (CeD) has usually come from studies at referral centers. Data about CeD presentation in the community are sparse. Aims: We aim to describe the clinical presentation of patients with biopsy-proven CeD at a community-based adult gastroenterology practice and compare it to a referral center. Methods: We performed a retrospective study of two cohorts of patients diagnosed with CeD between 2000–2007 (n = 117) and 2013–2016 (n = 91) in a community practice, and a third cohort (n = 188) diagnosed between 2000 and 2007 in a tertiary referral center. The clinical presentation, body mass index, tissue-transglutaminase levels, DEXA scan, vitamin D levels, and vaccine recommendations were assessed. Results: Celiac disease presentation changed over time in the two community cohorts. Recently, fewer patients presented with diarrhea and anemia, but constipation and neurologic symptoms were more common. The most recent cohort had a higher proportion of patients who were overweight or obese than the first cohort. However, the body mass index in both community cohorts was higher than in the tertiary referral center. The frequency of osteopenia and osteoporosis was high in both community cohorts. The tertiary referral center patients were younger, presented with a higher proportion of diarrhea and a lower body mass index. Conclusions: The clinical presentation of CeD differs between the community setting and a tertiary referral center. Patients with CeD presenting to the community setting tended to be older, overweight, and to have a high proportion of mineral bone disease. [ABSTRACT FROM AUTHOR]

Abstract Background Hyperphosphatemia occurs frequently in end-stage renal disease patients on hemodialysis and is associated with increased mortality. Hyperphosphatemia contributes to vascular calcification in these patients, but there is emerging evidence that it is also associated with endothelial cell dysfunction. Methods We conducted a cross-sectional study in hypertensive hemodialysis patients. We obtained pre-hemodialysis measurements of total peripheral resistance index (TPRI, non-invasive cardiac output monitor) and plasma levels of endothelin-1 (ET-1) and asymmetric dimethylarginine (ADMA). We ascertained the routine peridialytic blood pressure (BP) measurements from that treatment and the most recent pre-hemodialysis serum phosphate levels. We used generalized linear regression analyses to determine independent associations between serum phosphate with BP, TPRI, ET-1, and ADMA while controlling for demographic variables, parathyroid hormone (PTH), and interdialytic weight gain. Results There were 54 patients analyzed. Mean pre-HD supine and seated systolic and diastolic BP were 164 (27), 158 (21), 91.5 (17), and 86.1 (16) mmHg. Mean serum phosphate was 5.89 (1.8) mg/dL. There were significant correlations between phosphate with all pre-hemodialysis BP measurements (r = 0.3, p = .04; r = 0.4, p = .002; r = 0.5, p

Modern intravenous iron compounds (e.g., ferric carboxymaltose [FCM] and ferric derisomaltose [FDI]) are utilized in the treatment of iron deficiency anemia in non-dialysis-dependent chronic kidney disease (ND-CKD). Product-specific alterations in the metabolism of fibroblast growth factor 23 (FGF-23) leading to hypophosphatemia have been described for certain intravenous iron compounds, such as FCM, with potential effects on bone and cardiovascular health and quality of life. No prior head-to-head comparison between FCM and FDI exists in ND-CKD. This single-center exploratory double-blind randomized controlled trial primarily aimed to investigate the differential impact of FCM and FDI on FGF-23 and phosphate in patients with iron deficiency +/− anemia and ND-CKD (stages 3a–5 – serum ferritin <200 μg/L or serum ferritin 200–299 μg/L and transferrin saturation <20%). Patients were randomized (1:1) to receive either FCM or FDI over two infusions (1 month apart). Follow-up was 3 months. Measurements of serum intact FGF-23, phosphate, vitamin D metabolites, parathyroid hormone, other bone metabolism, cardiovascular, and quality of life markers were monitored. 168 patients were prescreened. Thirty-five patients were screened; 26 patients were randomized. The mean (standard deviation) age was 67.9 (12.4) years and 17 participants were male. Most participants had stage 4 CKD (median [interquartile range] estimated glomerular filtration rate [eGFR]: 18.0 [11.3] mL/min/1.73 m2). A higher than normal median (interquartile range) level of intact FGF-23 (212.1 [116.4] pg/mL) was noted. Serum phosphate was within normal range, while parathyroid hormone was higher and 1,25 (OH)2 vitamin D lower than the normal range. The "Iron and Phosphaturia – ExplorIRON-CKD" trial will provide important information regarding the differential effect of intravenous iron products in terms of FGF-23, phosphate, and other markers of bone and cardiovascular metabolism, alongside patient-reported outcome measures in patients with ND-CKD. [ABSTRACT FROM AUTHOR]

In patients treated with peritoneal dialysis (PD), lowering the calcium level in PD fluids results in lower serum calcium levels and higher parathyroid hormone (PTH) levels. It is hypothesized that this effect is attenuated when patients are using icodextrin 7.5% for the once-daily long dwell (containing high calcium concentration). In this case series, we included 8 stable PD patients (mean age 68 ± 13 years, 7 male), all using icodextrin 7.5% (containing 1.75 mmol/L calcium) for the once-daily long dwell. The calcium content of the PD fluids for the remaining dwells was lowered from 1.75 mmol/L to 1.25 mmol/L. Bone mineral parameters and phosphate prescription at baseline, 6 weeks after this change, and after 6 months were compared. After lowering calcium concentration of the PD fluids – except for the icodextrin 7.5% – from 1.75 mmol/L to 1.25 mmol/L, calcium levels changed from 2.32 ± 0.11 to 2.29 ± 0.12 (p = NS); intact PTH (iPTH) from 39.6 ± 28.3 to 64.9 ± 34.5 pmol/L (p = 0.045); and alkaline phosphatase from 104.13 ± 48.75 to 101.38 ± 32.39 (p = NS). After 6 months, all bone mineral parameters were similar to baseline levels; however, slightly higher calcium-based phosphate binders were prescribed. Lowering calcium content from 1.75 mmol/L to 1.25 mmol/L in PD fluids in patients on icodextrin resulted in stable calcium values, a temporal increase in iPTH and a modest increase in calcium-based phosphate binder prescription. Using icodextrin for the long once-daily dwell appears to attenuate the effects on bone mineral parameters when lowering the calcium concentration of the short dwells. [ABSTRACT FROM AUTHOR]

BackgroundMineral bone disorders (MBD) are common in sickle cell anemia (SCA). Frequent vaso-occlusive crises (VOC) further impact MBD in children with SCA. We evaluated the prevalence of markers of SCA-related MBD (sMBD) in hospitalized children and assessed the relationship between sMBD and individual mineral abnormalities with kidney disease.MethodsWe prospectively recruited 185 children with SCA hospitalized with a VOC. Serum measures of mineral bone metabolism (calcium, phosphate, parathyroid hormone, 25-hydroxy vitamin D, FGF23, osteopontin) were measured at enrollment. The primary outcome was markers of sMBD defined as a composite of hypocalcemia, hyperphosphatemia, hyperparathyroidism, or deficiency in 25-OH vitamin D. Secondary outcomes included individual abnormalities in mineral metabolism. The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines were used to define SCA-associated acute kidney injury (AKI). AKI was further assessed using urine NGAL as a marker of tubular injury. Acute kidney disease (AKD) was defined as a composite of AKI, an eGFR

Background: Hyperphosphatemia occurs frequently in end-stage renal disease patients on hemodialysis and is associated with increased mortality. Hyperphosphatemia contributes to vascular calcification in these patients, but there is emerging evidence that it is also associated with endothelial cell dysfunction.Methods: We conducted a cross-sectional study in hypertensive hemodialysis patients. We obtained pre-hemodialysis measurements of total peripheral resistance index (TPRI, non-invasive cardiac output monitor) and plasma levels of endothelin-1 (ET-1) and asymmetric dimethylarginine (ADMA). We ascertained the routine peridialytic blood pressure (BP) measurements from that treatment and the most recent pre-hemodialysis serum phosphate levels. We used generalized linear regression analyses to determine independent associations between serum phosphate with BP, TPRI, ET-1, and ADMA while controlling for demographic variables, parathyroid hormone (PTH), and interdialytic weight gain.Results: There were 54 patients analyzed. Mean pre-HD supine and seated systolic and diastolic BP were 164 (27), 158 (21), 91.5 (17), and 86.1 (16) mmHg. Mean serum phosphate was 5.89 (1.8) mg/dL. There were significant correlations between phosphate with all pre-hemodialysis BP measurements (r = 0.3, p = .04; r = 0.4, p = .002; r = 0.5, p < .0001; and r = 0.5, p = .0003.) The correlations with phosphate and TPRI, ET-1, and ADMA were 0.3 (p = .01), 0.4 (p = .007), and 0.3 (p = .04). In our final linear regression analyses controlling for baseline characteristics, PTH, and interdialytic weight gain, independent associations between phosphate with pre-hemodialysis diastolic BP, TPRI, and ET-1 were retained (β = 4.33, p = .0002; log transformed β = 0.05, p = .005; reciprocal transformed β = -0.03, p = .047).Conclusions: Serum phosphate concentration is independently associated with higher pre-HD BP, vasoconstriction, and markers of endothelial cell dysfunction. These findings demonstrate an additional negative impact of hyperphosphatemia on cardiovascular health beyond vascular calcification.Trial Registration: The study was part of a registered clinical trial, NCT01862497 (May 24, 2013). [ABSTRACT FROM AUTHOR]

Background: Albumin‐adjusted calcium remains widely used in clinical practice with guidelines for chronic kidney disease (CKD) mineral bone disorder recommending the use of serum calcium for monitoring. This is despite ionized calcium being the biologically active fraction. This study aimed to investigate the ability of total calcium and albumin‐adjusted calcium to correctly assign calcium status in stage 5/5D CKD across non‐dialysis, haemodialysis and peritoneal dialysis patients. Methods: Over a 6‐months, 352 paired serum and ionized calcium samples were collected from stage 5 (n = 58) and 5D (n = 294, 196 haemodialysis, 98 peritoneal dialysis) CKD patients in a tertiary‐hospital setting. Albumin‐adjusted calcium was calculated using the modified‐Payne formula. Ionized calcium was the reference standard. The agreement between the two methods in assigning calcium status was assessed using Cohen's weighted kappa (κ) statistic. Results: Albumin‐adjusted calcium was a poor predictor of calcium status compared to ionized calcium in stage 5/5D CKD (observed agreement 0.42, weighted κ 0.20, 95% CI 0.15–0.26). Dialysis dependence was associated with worse agreement (observed agreement 0.38, weighted κ 0.14, 95% CI 0.09–0.19). Total calcium was more reliable, however, remained inaccurate. Calcium status was not more accurately classified in those with higher albumin levels ≥30 g/L (observed agreement 0.47, weighted κ 0.23, 95% CI 0.10–0.36). Conclusion: Total calcium provides better approximation of calcium status than albumin‐adjusted calcium in stage 5/5D CKD. Albumin‐adjusted calcium tends to 'overcorrect' serum calcium upward. Clinicians should use ionized calcium where accurate measure of calcium is indicated, with total calcium used as the next best option where resources are limited. SUMMARY AT A GLANCE: Total serum calcium provided a better approximation of calcium status than albumin‐adjusted calcium across 58 CKD and 294 dialysis‐dependent CKD (HD:PD = 196:98) paired calcium samples. Albumin‐adjusted calcium 'over‐corrected' calcium levels upwards. It was suggested that clinicians should use ionised calcium where accurate measure of calcium is indicated, with total calcium used as the next best option where resources are limited. [ABSTRACT FROM AUTHOR]

Introduction: The prevalence of intracranial arterial calcification (ICAC) in maintenance hemodialysis (MHD) patients is about 90%, and its severity is correlated with age, hemodialysis vintage, and mineral bone disease. Elevated concentrations of calcium and phosphorus are not sufficient for medial calcification because of inhibition by pyrophosphate. Alkaline phosphatase (ALP) promotes calcification by hydrolyzing extracellular pyrophosphate. Epigenetic mechanisms involving ALP inhibition by apabetalone were investigated as a potential target for preventing vascular calcifications (VCs). This study assessed the combined impact of VCs and elevated serum ALP on mortality among chronic HD patients. Methods: VCs represented by ICAC were measured simultaneously with mineral bone disease parameters including serum ALP of MHD patients who underwent noncontrast brain computed tomography from 2015 to 2018 in our institution. Results: This retrospective study included 150 MHD patients (mean age 71.3 ± 12.1 years, 60.1% male). Of the total cohort, 12 (7.8%) had no brain calcifications and 69 (45.1%) had multiple intracranial calcifications. Considering the patients with normal ALP and no calcification as the reference group yielded adjusted odds ratios for all-cause mortality of 4.6 (95% CI: 1.7–12.7) among patients with brain calcifications and normal ALP (p = 0.003) and odds ratios for all-cause mortality of 6.1 (95% CI: 2.1–17.7) among patients with brain calcifications and elevated ALP (p= 0.001). Conclusion: We found an independent association between ICAC and the risk of death among MHD patients. The combined effect of ICAC and elevated ALP was associated with a higher odds ratio for all-cause mortality in MHD patients and may contribute to the risk stratification of these patients. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is a term that encompasses all degrees of decreased renal function, from damaged-at risk through mild, moderate, and severe chronic kidney failure. CKD is now a public health problem affecting an estimated 10-13% of the world population. The Kidney disease: Improving global outcomes (KDIGO) define CKD as either structural or functional kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least 3 months. CKDmineral and bone disorder (CKD-MBD) is a broader, newly defined term to define the mineral, bone, hormonal, and calcific cardiovascular abnormalities occurring in CKD. Ours study aims to evaluate the prevalence CKD-MBD in CKD stages 3, 4 and 5. Material And Methods: Ours is a retrospective observational study involving Patients >18 years known cases of CKD as per KDIGO guidelines with a minimum follow up duration of 3 or more months. Result: Our study population had a mean age of 52.8 years with male preponderance (72%). All of the patients had some form of MBD present. Conclusion: Our study was able to demonstrate a very high prevalence of CKD-MBD in patients of CKD indicating a need for better understanding the factors behind MBD in Indian patients and the need to emphasize on preventing and treating MBD in patients. [ABSTRACT FROM AUTHOR]

Introduction: Mineral bone disease is an important complication of chronic kidney disease ends up in increased cardiovascular morbidity and mortality in these patients. The aim of present study was to determine the pattern, prevalence and the clinical, biochemical and radiological profile of mineral bone disease in predialysis and dialysis (stage 5D) patients of chronic kidney disease.Methods: Patients of stage 3, 4, 5 and 5D of chronic kidney disease admitted to the department of nephrology were enrolled in this study.Results: 200 patients of chronic kidney disease (19, 29, 43 and 109 cases of stage 3, 4, 5 and 5D respectively) with mean age of 52.4 ± 16.7 years and male to female ratio of 2.4:1 were enrolled. Diabetic nephropathy (45%), hypertensive nephropathy (33%), and chronic glomerulonephritis (14.5%) were the most common etiologies of chronic kidney disease. Proximal muscle weakness (91.5%) bone pain (59.5%) and pruritus (25.5%) were the common symptoms. Biochemical parameters showed hypercalcemia (19%), hypocalcaemia (55%), hyperphosphatemia (75.5%) and vitamin D deficiency in 84.5% of cases. High turnover bone disease was present in all predialysis and only 7% of dialysis patients. Adynamic bone disease was observed in 92.7% of dialysis patients. On univariate analysis i-PTH was significantly associated with sex, eGFR, serum calcium, and 25(OH) vit-D level and no association was found with age and FGF-23 levels.Conclusion: Adynamic bone disease has emerged as the most common form of CKD-MBD in dialysis patients and secondary hyperparathyroidism being common in the predialysis patients of chronic kidney disease. Hyperphosphatemia and vitamin D deficiency were the most common reported biochemical abnormalities. [ABSTRACT FROM AUTHOR]

Purpose: Cardiovascular (CV) disease remains the leading cause of mortality among end-stage kidney disease (ESKD) patients. Cathepsin-K (CatK), a small cysteine protease involved in bone and extracellular matrix remodeling, has recently emerged as a key-factor in the pathogenesis of various conditions predisposing to CV disease, including atherosclerosis, obesity, diabetes, and vascular calcification. In this pilot prospective study, we aimed at evaluating the clinical significance and the predictive power of CatK in a small cohort of hemodialysis (HD) patients. Methods: Cathepsin-K was measured in 54 prevalent HD patients and in 30 controls together with routine parameters. Patients were then followed up to 26 months and the time of cardiovascular death (endpoint of the study prospective phase) recorded. Results: CatK levels were increased in the HD cohort as compared with controls (p < 0.001). In HD patients, CatK was also independently correlated to PTH (β = 0.368; p = 0.001), alkaline phosphatase (β = 0.383; p < 0.001), C-reactive protein (β = 0.260; p = 0.01), and white cell count (β = − 0.219; p = 0.02). After baseline assessment, patients were followed for CV death (mean follow-up 24.8 ± 3.1 months). Kaplan–Meier analysis showed a worsen survival (log-rank p = 0.04) in HD patients with CatK levels > 440 pg/mL (best ROC-derived cut-off with 69.6% sensitivity and 79.8% specificity) with a crude HR (Mantel–Haenszel) of CV death of 3.46 (95% CI 1.89–13.44). Conclusions: In prevalent HD patients, altered CatK levels may reflect mineral dysmetabolism and inflammation, and predict CV death in the mid-term. These preliminary findings prompt the rationale for further investigations on larger cohorts to validate CatK as a biomarker for improving CV risk stratification in ESKD. [ABSTRACT FROM AUTHOR]

Background Serial assessment of phosphorus is currently recommended by the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, but its additional value versus a single measurement is uncertain. Methods We studied data from 17 414 HD patients in the Dialysis Outcomes and Practice Patterns Study, a prospective cohort study, and calculated the area under the curve (AUC) by multiplying the time spent with serum phosphorus >4.5 mg/dL over a 6-month run-in period by the extent to which this threshold was exceeded. We estimated the association between the monthly average AUC and cardiovascular (CV) mortality using Cox regression. We formally assessed whether AUC was a better predictor of CV mortality than other measures of phosphorus control according to the Akaike information criterion. Results Compared with the reference group of AUC = 0, the adjusted hazard ratio (HR) of CV mortality was 1.12 [95% confidence interval (CI) 0.90–1.40] for AUC > 0–0.5, 1.26 (95% CI 0.99–1.62) for AUC > 0.5–1, 1.44 (95% CI 1.11–1.86) for AUC > 1–2 and 2.03 (95% CI 1.53–2.69) for AUC > 2. The AUC was predictive of CV mortality within strata of the most recent phosphorus level and had a better model fit than other serial measures of phosphorus control (mean phosphorus, months out of target). Conclusions We conclude that worse phosphorus control over a 6-month period was strongly associated with CV mortality. The more phosphorus values do not exceed 4.5 mg/dL the better is survival. Phosphorus AUC is a better predictor of CV death than the single most recent phosphorus level, supporting with real-world data KDIGO's recommendation of serial assessment of phosphorus to guide clinical decisions. [ABSTRACT FROM AUTHOR]

Introduction: There is little evidence on the ideal frequency of routine blood work in maintenance dialysis patients to manage complications, including anemia, mineral bone disease (MBD), and hyperkalemia. Recent quality improvement studies from Ontario showed no negative impacts when decreasing the frequency from monthly to every 6 weeks in conventional in-center hemodialysis (ICHD) patients. In December 2020, Alberta Kidney Care-South (AKC-S) reduced the frequency of routine blood work from every 6 weeks to every 8 weeks for ICHD patients., Objective: We aimed to assess the impact of reducing blood work frequency on patient outcomes., Methods: We compared prevalent AKC-S ICHD patients in 2 cohorts: (1) retrospective control (October 31, 2019-October 31, 2020) and (2) prospective intervention (December 1, 2020-December 1, 2021). Primary outcomes were true frequency of routine blood work, odds of patients being within target for anemia and MBD, and proportion of lab values of hyperkalemia. Furthermore, we compared hospitalizations and mortality., Results: A total of 972 patients in Calgary's ICHD program were included, 787 in each period (with 602 patients overlapping both cohorts). The frequency of routine blood work decreased from every 39.5 days in the control period to every 54.2 days in the intervention period ( P < .01). There was a reduction in the odds of phosphate values in targets ( P = .02), and an increase in the odds of labs with hyperkalemia (>6.0 mmol/L) during the intervention period ( P = .01). There was no significant change in the odds of being within the accepted targets during the intervention period compared with the control period for hemoglobin, Tsat, calcium, or parathyroid hormone (PTH). Fewer patients were hospitalized during the intervention period and the risk of death decreased as well, although additional factors such as the COVID-19 pandemic may have affected this. A cost-savings of $32 962 occurred from the reduced anemia and MBD blood work during the intervention period., Conclusions: When ICHD units in Calgary reduced routine blood work frequency from every 6 weeks to 8 weeks, there were no negative impacts on hospitalizations or deaths. A slightly lower proportion of phosphate values were within target, and a 0.7% increase in potassium values greater than 6 mmol/L was demonstrated. Our study suggests that blood work frequency in ICHD dialysis patients may be further reduced to every 8 weeks safely. Ultimately, additional pragmatic trials are needed to identify the optimal frequency of routine blood work., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2024.)

Background Hyperphosphatemia is a common consequence in end stage renal disease. It is associated with increased cardiovascular risk and mortality, also development of hyperparathyroidism and mineral bone disease. A patient educational program involving physician, pharmacist and dietician was developed to manage hyperphosphatemia among hemodialysis patients. Objective To investigate the efficacy of the program in optimal phosphate control among hemodialysis patients. Setting Kuala Lipis Hospital, Malaysia. Method This was a non-randomized, single-arm community trial running for a period of 6 months. The program consisted of a small group seminar and individual counseling sessions. Two individual counseling sessions were conducted for each patient, focusing on diet and medication adherence, by an accredited dietician and pharmacist respectively. The group seminar was delivered by a multidisciplinary team involving a physician, pharmacist and dietician. Topics included basic knowledge of hyperphosphatemia, phosphate binder and dietary phosphate control. Eligible and consented patients had knowledge and medication adherence assessment, measurement of pre-dialysis serum calcium, albumin, phosphate, haemoglobin and alkaline phosphatase before and after the educational program. Main outcome measure Phosphate level, knowledge and medication adherence assessment. Results Fifty-seven patients completed the program and were included into final data analysis. The median (IQR) phosphate level (mmol/L) was 1.86 (1.45-2.24) before and decreased to 1.47 (1.21-1.91) and 1.49 (1.28-1.81) 3 months and 6 months after PEP (p < 0.001). The percentage of patients with uncontrolled phosphate level was reduced from 59.3 to 35.6% and 42.1% after the PEP (p = 0.003). The mean knowledge score almost doubled after the intervention, with a mean pre-score of 8.61 (95% CI 7.85-9.37) to mean post-score of 15.31 (95% CI 14.85-15.76). The adherence to phosphate binder also improved from 17.2 to 41.4% after PEP (p = 0.007). Conclusion A multidisciplinary patient education program is an effective approach to manage hyperphosphatemia among hemodialysis patients in Malaysia. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is characterized by manifestations and symptoms involving systemic organs and apparatus, associated with elevated cardiovascular morbidity and mortality, bone disease, and other tissue involvement. Arterial hypertension (AH), diabetes mellitus (DM), and dyslipidemia, with glomerular or congenital diseases, are the traditional risk factors recognized as the main causes of progressive kidney dysfunction evolving into uremia. Acute kidney injury (AKI) has recently been considered an additional risk factor for the worsening of CKD or the development of CKD de novo. Evidence underlies the role of systemic inflammation as a linking factor between AKI and CKD, recognizing the role of inflammation in AKI evolution to CKD. Moreover, abnormal increases in oxidative stress (OS) and inflammatory status in CKD seem to exert an important pathogenetic role, with significant involvement in the clinical management of this condition. With our revision, we want to focus on and update the inflammatory mechanisms responsible for the pathologic conditions associated with CKD, with particular attention on the development of AKI and AKI-CKD de novo, the alteration of calcium-phosphorus metabolism with bone disease and CKD-MBD syndrome, the status of malnutrition and malnutrition–inflammation complex syndrome (MICS) and protein-energy wasting (PEW), uremic sarcopenia, the status of OS, and the different inflammatory pathways, highlighting a new approach to CKD. The depth comprehension of the mechanisms underlying the development of inflammation in CKD may present new possible therapeutic approaches in CKD and hopefully improve the management of correlated morbidities and provide a reduction in associated mortality.

R Scarpioni, M Ricardi, V Albertazzi, S De Amicis, F Rastelli, L Zerbini Department of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital “Guglielmo da Saliceto”, Piacenza, Italy Abstract: Amyloidosis refers to the extracellular tissue deposition of fibrils composed of low-molecular-weight subunits of a variety of proteins. These deposits may result in a wide range of clinical manifestations depending upon their type, location, and the amount of deposition. Dialysis-related amyloidosis is a serious complication of long-term dialysis therapy and is characterized by the deposition of amyloid fibrils, principally composed of β2 microglobulins (β2M), in the osteoarticular structures and viscera. Most of the β2M is eliminated through glomerular filtration and subsequent reabsorption and catabolism by the proximal tubules. As a consequence, the serum levels of β2M are inversely related to the glomerular filtration rate; therefore, in end-stage renal disease patients, β2M levels increase up to 60-fold. Serum levels of β2M are also elevated in several pathological conditions such as chronic inflammation, liver disease, and above all, in renal dysfunction. Retention of amyloidogenic protein has been attributed to several factors including type of dialysis membrane, prolonged uremic state and/or decreased diuresis, advanced glycation end products, elevated levels of cytokines and dialysate. Dialysis treatment per se has been considered to be an inflammatory stimulus, inducing cytokine production (such as interleukin-1, tumor necrosis factor-α, interleukin-6) and complement activation. The released cytokines are thought to stimulate the synthesis and release of β2M by the macrophages and/or augment the expression of human leukocyte antigens (class I), increasing β2M expression. Residual renal function is probably the best determinant of β2M levels. Therefore, it has to be maintained as long as possible. In this article, we will focus our attention on the etiology of dialysis-related amyloidosis, its prevention, therapy, and future solutions. Keywords: chronic inflammation, long-term dialysis, β2 microglobulin, high-flux dialysis membrane, mineral bone disease

The overwhelming majority of patients with chronic kidney disease (CKD) die prematurely before reaching end-stage renal disease, mainly due to cardiovascular causes, of which heart failure is the predominant clinical presentation. We hypothesized that CKD-induced increases of plasma FGF23 impair cardiac diastolic and systolic function. To test this, mice were subjected to 5/6 nephrectomy (5/6Nx) or were injected with FGF23 for seven consecutive days. Six weeks after surgery, plasma FGF23 was higher in 5/6Nx mice compared to sham mice (720 ± 31 vs. 256 ± 3 pg/mL, respectively, P = 0.034). In cardiomyocytes isolated from both 5/6Nx and FGF23 injected animals the rise of cytosolic calcium during systole was slowed (-13% and -19%, respectively) as was the decay of cytosolic calcium during diastole (-15% and -21%, respectively) compared to controls. Furthermore, both groups had similarly decreased peak cytosolic calcium content during systole. Despite lower cytosolic calcium contents in CKD or FGF23 pretreated animals, no changes were observed in contractile parameters of cardiomyocytes between the groups. Expression of calcium handling proteins and cardiac troponin I phosphorylation were similar between groups. Blood pressure, the heart weight:tibia length ratio, α-MHC/β-MHC ratio and ANF mRNA expression, and systolic and diastolic function as measured by MRI did not differ between groups. In conclusion, the rapid, CKD-induced rise in plasma FGF23 and the similar decrease in cardiomyocyte calcium transients in modeled kidney disease and following 1-week treatment with FGF23 indicate that FGF23 partly mediates cardiomyocyte dysfunction in CKD. [ABSTRACT FROM AUTHOR]

Background: Previously, we reported that hydrochlorothiazide (HCTZ)-based regimen aggravated arterial calcification and stiffness in a rat model of chronic kidney disease (CKD) with mineral and bone disorder (MBD). In this study, we investigated if all diureticbased treatments aggravate of arterial stiffness and calcification in CKD-MBD rats. Methods: In rats with renal mass ablation-induced CKD, MBD was generated by a Ca/P-rich diet and calcitriol. The animals were divided into four groups; (1) CKD-MBD control; (2) CKD-MBD + HCTZ (thiazide diuretic, 5 mg/kg/d); (3) CKD-MBD + Chlorthalidone (thiazide-like diuretic, 5 mg/kg/d), and; (4) CKD-MBD + Furosemide (loop diuretics, 10 mg/kg/d). At week 6, systolic and mean blood pressure (SBP and MBP), pulse pressure (PP) and pulse wave velocity (PWV) were determined invaisively. Thoracic aorta calcification was assessed by von Kossa staining. Results: SBP was reduced by all types of diuretics. Contrary to chlortalidone and furosemide, HCTZ treatment led to a reduction of MBP, but an increase in PP and PWV in CKD-MBD rats (p < 0.05). As expected from these hemodynamic changes, medial calcification in the thoracic aorta was significantly greater in CKD-MBD rats treated with HCTZ as compared to all the other groups of rats (p < 0.05). Conclusions: In rats with CKD-MBD, HCTZ, but not other types of diuretic, exacerbated arterial stiffness and vascular calcification despite a reduction in SBP. The deleterious effect of HCTZ in CKDMBD rats may have major clinical impact as this diuretic is widely use in patients with CKD that often develop MBD. [ABSTRACT FROM AUTHOR]

Background: Mineral bone disease (MBD) is a systemic disorder of mineral and bone metabolism due to chronic kidney disease (CKD). Bone disease in CKD is due to secondary hyperparathyroidism. Serum intact parathyroid hormone (iPTH) level estimation is a potential noninvasive method for the diagnosis of MBD at early stage. Aim: Treating renal bone disease should be one of the primary aims of therapy for CKD. Evaluation of the biochemical parameters of CKD-MBD (primarily phosphorus, calcium, parathyroid hormone, and Vitamin D levels) as early as CKD stage 3, and an assessment of bone status (by the best means available), should be used to guide treatment decisions. The adverse effects of high phosphorus intake relative to renal clearance (including stimulation of hyperparathyroidism) precede hyperphosphatemia, which presents late in CKD. Early reduction of phosphorus load may ameliorate these adverse effects. Evidence that calcium load may influence progression of vascular calcification with effects on mortality, should also be considered when choosing the type and dose of phosphate binder to be used. MBD in CKD has high morbidity and mortality and hence it is important to detect it at an early stage. iPTH levels can be highly sensitive and it is one of the useful noninvasive biochemical parameters to detect MBD in CKD. Materials and Methods: This was an observational study carried out in a tertiary care teaching hospital. The study involved 60 patients of CKD. Detailed history, physical examination, and biochemical parameters were assessed in all of them. Results: There was a significant association between hypertension, diabetes with nephropathy, and highly significant association between serum iPTH and raised blood urea levels in MBD group, however there was no significant association between duration of CKD, hemoglobin, creatinine, uric acid, phosphorous, calcium, and alkaline phosphatase with MBD. Conclusions: MBD in CKD can be detected at early stage by the use of noninvasive methods of estimation of serum iPTH levels.

Background: In the past few years, a distinct and multifactorial clinical entity called chronic kidney disease-mineral and bone disorder (CKD-MBD) that leads to decreased bone density and osteoporosis has been identified. The aim of this study was to assess the levels of the matrix metalloproteinase-1 and -2 (MMP-1 and MMP-2) in chronic kidney disease (CKD) patients of various disease stages in correlation to other bone turnover markers (BTM). This study is an initial investigative approach to a possible role of matrix metalloproteinases (MMPs) in the evaluation of bone disease in uremic patients. Methods: We enrolled 60 patients at different stages of pre-dialysis CKD, 20 patients on hemodialysis (HD), and 20 age-matched healthy controls. Serum intact parathyroid hormone (iPTH), osteocalcin (OC), N-terminal propeptide of type I collagen (P1NP), and beta-C-terminal telopeptide of type I collagen (ß-CTX), were measured by electrochemiluminescence on automatic analyzers. Serum MMP-1 and MMP-2 levels were estimated using a commercial enzymelinked immunosorbent assay (ELISA). Serum levels of urea, creatinine, calcium, phosphorus, and alkaline phosphatase were estimated. Creatinine clearance (ClCr) was calculated using the traditional clearance formula based on a 24-hour urine collection. Results: Serum iPTH, OC, P1NP, ß-CTX concentrations were significantly higher (p <0.0001) while ClCr was significantly lower (p <0.0001) in CKD patients, as compared with those of healthy controls. A positive correlation was established between serum MMP-1 and OC levels (r =0.245, p =0.014), as well as with serum ß-CTX levels (r =0.197, p =0.048), and a negative correlation between MMP-2 and OC (r =-0.222, p =0.025). Conclusions: In CKD patients MMP-1 serum levels may reflect increased bone turnover rates. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the outcome of bone metabolism and bone mineral density (BMD) in haemodialysis patients after parathyroidectomy (PTX).Methods: A total of 31 haemodialysis patients with secondary hyperparathyroidism (SHPT) were treated with PTX. BMD of lumbar spine (LS) and femoral neck (FN) was determined by dual energy X-ray absorptiometry.Results: Parathyroidectomy ledds to significant decrease of serum β-crosslaps (β-CTX), osteocalcin (OC) and procollagen type I amino-terminal propeptide (PINP) while serum sclerostin (SOST) increased after surgery. BMD was markedly improved in both LS and FN after PTX. Z-scores analysis further confirmed that PTX significantly benefited bone metabolism in haemodialysis patients, which well correlated with the improvement of serum iPTH and OC.Conclusions: Parathyroidectomy leads to significant improvement of serum OC, PINP, β-CTX and SOST, which may beneficially modify calcium-phosphorus metabolism and BMD in haemodialysis patients with SHPT. [ABSTRACT FROM AUTHOR]

Introduction: Studies suggest that hemodialysis (HD) patients are less likely to adhere to phosphate dietary restriction than to potassium, sodium, or fluid restriction. It is particularly important that dietary education is provided appropriately, consistently, and reinforced regularly to encourage compliance with diet and phosphate-binder regimens. Patient awareness of the consequences of a chronically raised phosphate and its treatment is associated with lower serum phosphate levels. Objective: The aim of this study was to assess the impact of a structured educational program on patient knowledge and control of serum phosphate in a maintenance HD population. Methods: Thirty-six patients with a phosphate level >1.7 mmol/L for the previous 3 months were assessed. A phosphate knowledge questionnaire was devised by the authors and completed by the patient group. This focused on patient knowledge of dietary sources of phosphate and complications of high phosphate levels. The education program was divided into three modules and was based around diet, phosphate additives, and complications of hyperphosphatemia. Visual aids, oral, and written information were provided to each patient throughout the sessions. Seventeen patients completed the education sessions. The knowledge and food frequency questionnaire were repeated at the end of the modules to assess change. Results: Phosphate levels dropped from an average of 2.12-1.73 mmol/L over the education period with a significance level of P = 0.000481 (significant if P < 0.001). This average falls in line with recommended guidelines. Knowledge questionnaire results improved overall. Conclusion: This education program displayed excellent outcomes with an overall reduction in phosphate levels and an improved phosphate knowledge among our sampled HD population. This education program shows that discovering novel ways of education is crucial to enhancing dietetic practice with renal dietitians best placed to deliver patient specific phosphate education. [ABSTRACT FROM AUTHOR]

Background: Vitamin D analogs have generally been recommended for treatment of mineral bone disease in chronic kidney disease (CKD). However, the association between this treatment and CKD progression has not yet been established. Methods: We designed a post hoc propensity score-matched cohort analysis derived from 3-year follow-up data of a prospective cohort. Adult participants with pre-dialysis CKD stages 4-5 who had newly been prescribed active vitamin D analogs during the observation period were eligible as matched cases. Then, matched controls were extracted from participants who had never been prescribed active vitamin D analogs. The primary outcome was a composite of end-stage renal disease or a 50 % reduction in estimated glomerular filtration rate (eGFR). A Cox proportional hazards model evaluated the association between the use of vitamin D analogs and the primary outcome. Results: We enrolled 240 patients (males, 65 %). The number of matched cases and controls was 30 and 210, respectively. The primary outcome was observed in 94 patients, whereas 25 patients died. The mean ± standard deviation age and eGFR were 69 ± 12 years and 17 ± 5.7 ml/min/1.73 m, respectively. In a Cox proportional hazard model, the use of vitamin D analogs was independently associated with a lower risk of the primary outcome (crude hazard ratio 0.41; 95 % confidence interval 0.19, 0.89; adjusted hazard ratio 0.38; 95 % confidence interval 0.17, 0.88). Conclusion: The use of vitamin D analogs is independently associated with the preservation of renal function in patients with pre-dialysis CKD stages 4-5. [ABSTRACT FROM AUTHOR]

Introduction Chronic kidney disease-related mineral and bone disorder (CKD-MBD), characterized by abnormalities in calcium, phosphate, and parathyroid hormone metabolism, with impaired bone turnover and extravascular calcification is a known complication of advanced chronic kidney disease (CKD). Secondary hyperparathyroidism (SHPT) develops early in the disease and its prevalence gradually increases with the disease progression, becoming almost universal in patients with end-stage renal disease (ESRD). The treatment for SHPT includes synthetic vitamin D analogs, calcitriol or calcimimetics. Recently, intravenous etelcalcetide was introduced as a second-generation calcimimetic. This article provides the real-world experience of using etelcalcetide in multiethnic Asian patients receiving hemodialysis at community-based hemodialysis centers in Singapore. Methods This study was real-world evidence, generated by a retrospective clinical audit of routine clinical care of hemodialysis patients in community-based centers in Singapore who received etelcalcetide for treating SHPT. The information on the starting and maximum dose of etelcalcetide, duration of treatment on hemodialysis, parathyroid hormone (PTH) levels, dialysate calcium, concomitant medications, and reasons for discontinuation were collected from the medical records. PTH levels were collected at four-, eight-, and twelve-month intervals. Results A total of 148 patients received etelcalcetide during the study period. Ten patients died and twenty discontinued their treatment, with 118 patients remaining on treatment. Demographically, the patients included Chinese, Malay, Indians, and those belonging to other racial groups. The starting dose of etelcalcetide ranged from 2.5 mg once per week to 7.5 mg three times a week. There was a 16.8% reduction (p=<0.001) in intact-PTH after four months of therapy. Target intact-PTH level of less than 60 pmol/L, was reported as 1.4% at baseline, with 22.3% at four months (p<0.001) and 25.9% at eight months (p=0.028). Calcium and phosphate levels were also tracked as part of the safety and efficacy measures of using etelcalcetide. No symptomatic hypocalcemia was noted and phosphate levels were noted to decline significantly. Overall, the calcium-phosphate product reduced at four months (13.2%, p=<0.001) and eight months (12.7%, p<0.05). An analysis of concomitant medication usage, dialysate calcium utilized, and the side effects of etelcalcetide were also recorded. Finally, a brief descriptive analysis of the patient's subjective feedback regarding etelcalcetide was also reported, especially regarding the reduction in pill burden and overall compliance to medications. Conclusion Etelcalcetide is safe and effective for treating SHPT in multi-ethnic Asian hemodialysis patients and can be considered an alternative to oral cinacalcet. Our study showed no side effects, which was one of the key reasons for non-compliance to traditional calcimimetics. A favorable compliance profile with reduced pill burden was noted by using this intravenous calcimimetic., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Khan et al.)

Background: Mineral bone disease (MBD) is a systemic disorder of mineral and bone metabolism due to chronic kidney disease (CKD). Bone disease in CKD is due to secondary hyperparathyroidism. Serum intact parathyroid hormone (iPTH) level estimation is a potential noninvasive method for the diagnosis of MBD at early stage. Aim: Treating renal bone disease should be one of the primary aims of therapy for CKD. Evaluation of the biochemical parameters of CKDMBD (primarily phosphorus, calcium, parathyroid hormone, and Vitamin D levels) as early as CKD stage 3, and an assessment of bone status (by the best means available), should be used to guide treatment decisions. The adverse effects of high phosphorus intake relative to renal clearance (including stimulation of hyperparathyroidism) precede hyperphosphatemia, which presents late in CKD. Early reduction of phosphorus load may ameliorate these adverse effects. Evidence that calcium load may influence progression of vascular calcification with effects on mortality, should also be considered when choosing the type and dose of phosphate binder to be used. MBD in CKD has high morbidity and mortality and hence it is important to detect it at an early stage. iPTH levels can be highly sensitive and it is one of the useful noninvasive biochemical parameters to detect MBD in CKD. Materials and Methods: This was an observational study carried out in a tertiary care teaching hospital. The study involved 60 patients of CKD. Detailed history, physical examination, and biochemical parameters were assessed in all of them. Results: There was a significant association between hypertension, diabetes with nephropathy, and highly significant association between serum iPTH and raised blood urea levels in MBD group, however there was no significant association between duration of CKD, hemoglobin, creatinine, uric acid, phosphorous, calcium, and alkaline phosphatase with MBD. Conclusions: MBD in CKD can be detected at early stage by the use of noninvasive methods of estimation of serum iPTH levels. [ABSTRACT FROM AUTHOR]

Purpose Cinacalcet is indicated for treatment of secondary hyperparathyroidism in patients receiving hemodialysis. Cinacalcet reduces serum calcium concentrations by decreasing parathyroid hormone secretion, but the frequency and degree of calcium reduction following cinacalcet initiation, subsequent physician response, and ultimate calcium recovery in clinical practice are not well described. Methods Patients receiving hemodialysis at a large dialysis organization who enrolled in the organization's prescription benefits service and initiated cinacalcet at serum calcium ≥8.4 mg/dL were studied ( N = 13 723). Patients were categorized by whether they experienced a reduction in calcium to <8.4 mg/dL and to what level (<7.5, 7.5-7.9, and 8.0-8.3 mg/dL). Baseline characteristics, frequency of subsequent intervention, and calcium recovery were compared. Results Of those who experienced a reduction in calcium to <8.4 mg/dL ( n = 6437 [46.9%]), 6.6% had calcium <7.5 mg/dL and 24.5% had calcium 7.5-7.9 mg/dL, while the majority (68.9%) had a level of 8-8.3 mg/dL. Higher baseline parathyroid hormone and alkaline phosphatase were associated with lower resultant calcium. Among patients with calcium reductions, 45.6-63.5% received one or more directed clinical therapeutic responses, including 15.6-28.4% for whom cinacalcet was discontinued; the majority of patients recovered to calcium ≥8.4 mg/dL within 90 days of first detection. Only modest differences in recovery were noted between patients who did and did not receive any therapeutic response and patients who did and did not discontinue cinacalcet. Conclusion Serum calcium reductions following cinacalcet initiation were common; declines <7.5 mg/dL were infrequent. Calcium recovery occurred in the majority of patients, with or without therapeutic intervention. Copyright © 2015 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Purpose of Review: Magnesium is an essential mineral for bone metabolism, but little is known about how magnesium intake alters fracture risk. We conducted a narrative review to better understand how magnesium intake, through supplementation, diet, or altering the concentration of dialysate magnesium, affects mineral bone disease and the risk of fracture in individuals across the spectrum of kidney disease., Sources of Information: Peer-reviewed clinical trials and observational studies., Methods: We searched for relevant articles in MEDLINE and EMBASE databases. The methodologic quality of clinical trials was assessed using a modified version of the Downs and Black criteria checklist., Key Findings: The role of magnesium intake in fracture prevention is unclear in both the general population and in patients receiving maintenance dialysis. In those with normal kidney function, 2 meta-analyses showed higher bone mineral density in those with higher dietary magnesium, whereas 1 systematic review showed no effect on fracture risk. In patients receiving maintenance hemodialysis or peritoneal dialysis, a higher concentration of dialysate magnesium is associated with a lower concentration of parathyroid hormone, but little is known about other bone-related outcomes. In 2 observational studies of patients receiving hemodialysis, a higher concentration of serum magnesium was associated with a lower risk of hip fracture., Limitations: This narrative review included only articles written in English. Observed effects of magnesium intake in the general population may not be applicable to those with chronic kidney disease particularly in those receiving dialysis., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2023.)