RESUMEN

BACKGROUND: Patients with end-stage kidney disease on hemodialysis (HD) have an increased risk of death due to the high prevalence of cardiovascular disease. Vascular calcification (VC) is predictive of cardiovascular disease and mortality. We conducted a study to evaluate the prevalence and risk factors for VC in dialysis patients in Qatar. METHODS: This is a retrospective nationwide study including all chronic ambulatory dialysis patients in Qatar from 2020 to 2022. We used our national electronic medical record to track demographics, clinical characteristics, comorbidities, laboratory values, and diagnostic data for each patient. Calcifications were assessed by echocardiography (routinely done for all our dialysis population per national protocol), computed tomography, X-ray, and ultrasound. The study protocol was approved by the local medical research ethics committee (MRC-01-20-377). RESULTS: 842 HD patients were included in this study. Vascular calcifications (VC) were prevalent in 52.6% of patients. The main site of VC was Mitral valve calcifications in 55.5% of patients. Patients with VC were significantly older and had more prevalence of diabetes mellitus (p = 0.001 and p = 0.006, respectively). There was no statistically significant difference between patients with calcifications and patients without calcifications regarding serum calcium, phosphorus, and PTH level. In multivariate analysis, age and diabetes significantly increased the risk factor for calcification (95% CI 1.033-1.065, p < 0.0001, and 95% CI 1.128-2.272, p < 0001, respectively). Moreover, higher vitamin D levels and higher doses of IV Alfacalcidol were significant risk factors for calcifications (95% CI 1.005-1.030, p < 0.007, and 95% CI 1.092-1.270, p < 0.0001, respectively). CONCLUSION: Our study found that vascular calcification was widespread among our dialysis population in Qatar. Implementing the practice of echocardiography in dialysis patients was extremely helpful and the most productive in detecting vascular calcification. Diabetes mellitus almost doubles the risk for vascular calcifications in dialysis patients. These results are beneficial in identifying risk factors for vascular calcification, which can help stratify dialysis patients' risk of cardiovascular disease and optimize prevention efforts.

RESUMEN

PURPOSE: Successful pregnancy rates on dialysis are increasing with the advent of intensive hemodialysis and advances in medical management. SUMMARY: Data support the use of intensive hemodialysis in pregnant women with end-stage kidney disease (ESKD). This paper provides an overview of common pharmacotherapeutic changes in management when caring for a pregnant woman receiving intensive hemodialysis. Pregnant patients on peritoneal dialysis were excluded from this analysis due to insufficient data. Topics covered include those related to anemia (iron and erythropoietin stimulating agents), blood pressure agents, monitoring of phosphorus, as well as nutrition and anticoagulation. CONCLUSION: When patients on hemodialysis become pregnant, medication adjustments are needed regarding antihypertensives, anemia management, and mineral-bone disease management as many agents require dose adjustment, switching agents due to teratogenicity, or cessation due to fetal complications. There are minimal data in this population; however, successful and healthy infants have been delivered in this patient population with the medication changes discussed.

Asunto(s)

RESUMEN

Although reduced bone mineral density (BMD) is associated with a higher risk of fractures, morbidity, and mortality in kidney transplant patients (KTRs), there is no consensus on optimal treatment for the alterations of BMD in this population. This study aims at assessing the effect of cholecalciferol supplementation on BMD over a follow-up period of 2 years in a cohort of long-term KTRs. Patients with age ≥ 18 years were included and divided into two subgroups based on treatment with bisphosphonate and/or calcimimetics and/or active vitamin D sterols (KTRs-treated) or never treated with the above medications (KTRs-free). BMD was evaluated at lumbar vertebral bodies (LV) and right femoral neck (FN) with standard DEXA at the beginning and end of the study. According to World Health Organization (WHO) criteria, results were expressed as T-score and Z-score. Osteoporosis and osteopenia were defined as T score ≤ -2.5 SD and T score < -1 and >-2.5 SD, respectively. Cholecalciferol was supplemented at a dose of 25,000 IU/week over 12 weeks followed by 1500 IU/day. KTRs-free (n. 69) and KTRs-treated (n. 49) consecutive outpatients entered the study. KTRs-free were younger (p < 0.05), with a lower prevalence of diabetes (p < 0.05) and of osteopenia at FN (46.3 % vs. 61.2 %) compared to KTRs-treated. At the entry none of the study subjects had a sufficient level of cholecalciferol; Z-score and T-score at LV and FN were not different between groups. At the end of the study period, serum cholecalciferol concentration was significantly increased in both groups (p < 0.001); the KTRs-free group presented an improvement in both T-score and Z-score at LV (p < 0.05) as well as a lower prevalence of osteoporotic cases (21.7% vs. 15.9%); in contrast, no changes were recorded in KTR-treated individuals. In conclusion, supplementation with cholecalciferol ameliorated Z-score and T-score at LV in long-term KTRs who had been never treated with active or inactive vitamin D sterols, bisphosphonates, and calcimimetics. Future endeavours are needed to confirm these preliminary findings.

Asunto(s)

RESUMEN

BACKGROUND: Chronic kidney disease (CKD) has been a highly prevalent medical condition in all parts of the world affecting the haemostasis of the body in number of ways. Epidemiological data suggest that no region of the world has been spared from this condition and both developing and developed countries equally share the burden of this disease. Objective was to compare the vascular calcification and mineral bone disease in non-dialysis vs dialysis patients suffering from chronic kidney disease at a tertiary care hospital of Pakistan. It is a Comparative study, conducted at the Department of nephrology Pak Emirates Military Hospital Rawalpindi. Four months from November 2020 to February 2021. METHODS: A total of 310 cases were included in the study, which were diagnosed as chronic kidney disease in nephrology department by a consultant nephrologist on basis of National Kidney Foundation/Kidney Disease Outcome Quality Initiative (NKF/KDOQI) 2002. They were divided into two equal groups by block randomization. Group I had the patients who were not dependent on dialysis (CKD4/5ND) while group II had dialysis dependent patients. Abdominal aorta, mitral and tricuspid valves were assessed to look for vascular calcification. Calcium, phosphate and parathyroid hormone levels were done to assess the mineral bone profile. RESULTS: Out of 310 patients, 192 (61.9%) patients were males and 118 (38.1%) were females. Ninty-eight (31.6%) had evidence of vascular calcification while 212 (68.4%) did not have vascular calcification. 147 (47.4%) had hypocalcaemia, 167 (53.8%) had hyperphosphatemia while 98 (31.6%) patients had raised Parathyroid hormone levels. Regression analysis revealed that vascular calcification and abnormal mineral bone profile was significantly present more among patients who were dependent on dialysis (p-value<0.05). CONCLUSIONS: Bone mineral disease and vascular calcification were consistent findings among patients suffering from chronic kidney disease. Patients who were dependent on dialysis were more prone to develop these complications as compared to those who were not dependent on dialysis.

Asunto(s)

RESUMEN

BACKGROUND: Kidney transplant patients frequently suffer from Chronic Kidney Disease associated with Mineral Bone Disease (CKD-MBD), a complex condition that affects mainly kidney transplant patients. Post-transplantation bone disease is complex, especially in patients with pre-existing metabolic bone disorders that are further affected by immunosuppressive medications and changes in renal allograft function. Main biochemical abnormalities of mineral metabolism in kidney transplantation (KTx) include hypophosphatemia, hyperparathyroidism (HPTH), insufficiency or deficiency of vitamin D, and hypercalcemia. OBJECTIVE: This review aims to summarize the pathophysiology and main biomarkers of CKD-MBD in KTx. METHODS: A comprehensive and non-systematic search in PubMed was independently made, emphasizing biomarkers in mineral bone disease in KTx. RESULTS: CKD-MBD can be associated with numerous factors, including secondary HPTH, metabolic dysregulations before KTx, and glucocorticoid therapy in post-transplant subjects. Fibroblast growth factor 23 (FGF23) reaches normal levels after KTx with good allograft function, while calcium, vitamin D, and phosphorus, ultimately result in hypercalcemia, persistent vitamin D insufficiency, and hypophosphatemia, respectively. As for PTH levels, there is an initial tendency of a significant decrease, followed by a rise due to secondary or tertiary HPTH. In regard to sclerostin levels, there is no consensus in the literature. CONCLUSION: KTx patients should be continuously evaluated for mineral homeostasis and bone status, both in cases with successful kidney transplantation and those with reduced functionality. Additional research on CKD-MBD pathophysiology, diagnosis, and management is essential to guarantee long-term graft function, better prognosis, good quality of life, and reduced mortality for KTx patients.

Asunto(s)

RESUMEN

Vitamin D insufficiency has been associated with reduced bone mineral density (BMD) in kidney transplant patients (KTRs). However, the efficacy of vitamin D supplementation on BMD remains poorly defined, especially for long-term KTRs. We aimed to investigate the effect of native vitamin D supplementation on the BMD of KTRs during a 2-year follow-up. Demographic, clinical, and laboratory data were collected. BMD was evaluated with standard DEXA that was performed at baseline (before vitamin D supplementation) and at the end of study period. BMD was assessed at lumbar vertebral bodies (LV) and right femoral neck (FN) by a single operator. According to WHO criteria, results were expressed as the T-score (standard deviation (SD) relative to young healthy adults) and Z-score (SD relative to age-matched controls). Osteoporosis and osteopenia were defined as a T-score ≤ -2.5 SD and a T-score < -1 and a > -2.5 SD, respectively. Based on plasma levels, 25-OH-vitamin D (25-OH-D) was supplemented as recommended for the general population. Data from 100 KTRs were analyzed. The mean study period was 27.7 ± 3.4 months. At study inception, 25-OH-D insufficiency and deficiency were recorded in 65 and 35 patients. At the basal DEXA, the percentage of osteopenia and osteoporosis was 43.3% and 18.6% at LV and 54.1% and 12.2% at FN, respectively. At the end of the study, no differences in the Z-score and T-score gains were observed. During linear mixed model analysis, native vitamin D supplementation was found to have a negative nitration with Z-score changes at the right femoral neck in KTRs (p < 0.05). The mean dose of administered cholecalciferol was 13.396 ± 7.537 UI per week; increased 25-OH-D levels were found (p < 0.0001). Either low BMD or 25-OH-vitamin D concentration was observed in long-term KTRs. Prolonged supplementation with 25-OH-D did not modify BMD, Z-score, or T-score.

Asunto(s)

RESUMEN

Uraemic Cardiomyopathy (UC) is recognised as an intricate and multifactorial disease which portends a significant burden in patients with End-Stage Renal Disease (ESRD). The cardiovascular morbidity and mortality associated with UC is significant and can be associated with the development of arrythmias, cardiac failure and sudden cardiac death (SCD). The pathophysiology of UC involves a complex interplay of traditional implicative factors such as haemodynamic overload and circulating uraemic toxins as well as our evolving understanding of the Chronic Kidney Disease-Mineral Bone Disease pathway. There is an instrumental role for multi-modality imaging in the diagnostic process; including transthoracic echocardiography and cardiac magnetic resonance imaging in identifying the hallmarks of left ventricular hypertrophy and myocardial fibrosis that characterise UC. The appropriate utilisation of the aforementioned diagnostics in the ESRD population may help guide therapeutic approaches, such as pharmacotherapy including beta-blockers and aldosterone-antagonists as well as haemodialysis and renal transplantation. Despite this, there remains limitations in effective therapeutic interventions for UC and ongoing research on a cellular level is vital in establishing further therapies.

Asunto(s)

RESUMEN

Glucocorticoids are first-line therapy for children with idiopathic nephrotic syndrome (INS). These children are at risk of deranged bone metabolism and low bone mineral density (BMD). We studied 60 children with INS and divided them into two groups. Group 1 included 21 children (initial and infrequent relapsing) and group 2 included 39 children (frequent relapsing, steroid dependent and steroid resistant). Dual-energy X-ray absorptiometry of the lumbar spine was performed to assess BMD. Mean BMD Z-score was compared in both groups; this correlated significantly on univariate analysis with cumulative steroid dose, serum vitamin D levels and calcium supplementation. However, on multivariate analysis, serum vitamin D level was the only factor significantly predictive of low z-score.

Asunto(s)

RESUMEN

Studies on vitamin D deficiency status and its impact on bone health in a developing country are limited. We assessed the bone mineral density and vitamin D levels in healthy school-going children of Western India. Around 65% children had vitamin D deficiency and vitamin D levels had good correlation with bone mineral density. PURPOSE: Vitamin D is an important substrate in the metabolism of calcium homeostasis and skeletal metabolism. Epidemiological studies on vitamin D deficiency status and its impact on bone mineral metabolism in healthy children in a developing country are limited. We assessed the bone mineral density and vitamin D levels in healthy school-going children of Western India. METHODS: We measured serum levels of 25-hydroxy vitamin D (25(OH)D) in healthy school-going children, aged 60 to 120 months. Dual-energy X-ray absorptiometry scan was done to assess the bone mineral density (BMD). The BMD status was compared with the levels of 25(OH)D and serum parathormone hormone in all the children. RESULTS: A total of 100 school-going children were examined for evidence of vitamin D deficiency and 65% had deficiency (less than 50 nmol/L). The mean age was 90 months in males and 89 months in females. In the vitamin D-deficient group, the mean BMD (gm/cm2) measurements for the lumbar spine was 0.439 ± 0.098 (p < 0.001) and the mean BMD (gm/cm2) in the normal group was 0.606 ± 0.071 (p < 0.001). Pearson's and Spearman's rank correlation coefficients between vitamin D levels and BMD z score showed a significant positive correlation (r = 0.82, ρ = 0.924). CONCLUSIONS: We confirmed the high prevalence of vitamin D deficiency among healthy school-going children. The serum levels of vitamin 25(OH)D has a good correlation with bone mineral density.

Asunto(s)

RESUMEN

BACKGROUND AND AIMS: Since accelerated atherosclerosis has been reported in systemic lupus erythematosus (SLE), predictive biomarkers of cardiovascular disease (CVD) are needed. Among non-traditional risk factors, bone mineral density (BMD) has been related to CVD. However, its role in SLE remains controversial. This study aims to analyze the associations of subclinical atherosclerosis with traditional and non-traditional CV risk factors. METHODS AND RESULTS: In a cross-sectional study, atherosclerosis burden was compared between 112 female SLE patients and 31 controls. Plaque number and carotid intima-media wall thickness (cIMT) were assessed by ultrasonography. In a retrospective study, BMD determinations obtained 5-years before the ultrasonography assessment were analyzed in a subgroup of 62 patients. Plaque frequency was increased in SLE, even in patients without CV events or carotid wall thickening. cIMT was increased in patients with CVD, positively correlated with body mass index (BMI). Interestingly, a paradoxical effect of BMI on carotid parameters was observed. Whereas underweight patients (BMI < 20) showed increased prevalence of carotid plaques with low cIMT, those with BMI > 30 showed higher cIMT and plaque burden. Overweight patients (25 < BMI<30) exhibited both elevated cIMT and plaque number. BMI was an independent predictor of BMD. In our retrospective study, patients with either clinical or subclinical CVD exhibited lower BMD levels than their CV-free counterparts. A low lumbar spine BMD independently predicted CVD development after adjusting for confounders. CONCLUSION: SLE was associated with a higher subclinical atherosclerosis burden, a bimodal effect being observed for BMI. Decreased BMD can be a CV risk biomarker in SLE.

Asunto(s)

RESUMEN

BACKGROUND: Previous studies suggest normal mineral status in children receiving elemental formula. However, a recent multicenter survey described 51 children who developed hypophosphatemia and bone disease while receiving elemental formula. Our aim is to determine the prevalence of metabolic bone disease in children receiving extensively hydrolyzed or amino acid-based formula. METHODS: We established a retrospective cohort using an institutional database of tube-fed children. We defined a "confirmed case" as a child with biochemical and radiographic evidence of bone disease (rickets and/or low-trauma fractures). We defined a "suspected case" as a child who had biochemical evidence and/or radiographic evidence of bone disease but with incomplete data during the review period. RESULTS: A total of 102 tube-fed children receiving elemental or semi-elemental formula were identified. The four elemental and semi-elemental formulas evaluated were Neocate®, EleCare®, Pregestimil®, and Alimentum®. Not all children had complete monitoring data performed during the review period. Of the children receiving Neocate who had monitoring data (46%), 23% developed hypophosphatemia and radiographic abnormalities (fractures or rickets), which resolved with phosphorus supplementation and/or change in the formula brand. CONCLUSIONS: We estimate that at least 11% and up to 23% of all tube-fed children receiving Neocate develop metabolic bone disease. Based upon the estimated prevalence, we recommend cautious use of this formula with monitoring for evolving bone disease in this population.

Asunto(s)

RESUMEN

Soon after kidney transplant (KT), a decrease in parathormone and bone mineral density (BMD) occur, but little is known on the impact of KT on novel bone quality parameters including trabecular bone score (TBS) and bone material strength index (BMSi). We aimed to study BMD, TBS and BMSi in the first year after KT, in patients not treated with any bone therapy. A cohort including 36 patients underwent KT on a low-glucocorticoid-dose protocol (5 mg daily-prednisone from post-operative-day 42 onwards) and was observed for 12 months prospectively. At 3 months, phosphorus and parathormone decreased, while calcium increased. We also observed at 3 months a transient mild 2.9% bone loss at femoral neck (BMD change 0.752 ±â€¯0.15 vs 0.730 ±â€¯0.15; p = 0.004), but no change at either spine or total hip. Both TBS and BMSi remained stable. At 12 months, lumbar (but not total hip or femoral neck) BMD slightly decreased by 2.1% vs baseline (0.950 ±â€¯0.15 vs 0.930 ±â€¯0.5; p = 0.046), while TBS and BMSi remained unmodified. In KT patients on low-dose glucocorticoids and no bone therapy, there were small BMD decreases at femoral neck (at 3 months) and lumbar spine (at 12 months), but no change in either TBS or BMSi. Low-dose post-KT glucocorticoid treatment shows limited impact on bone, supporting steroid-restrictive protocols.

Asunto(s)

RESUMEN

Bone disease related to chronic kidney disease and, particularly, to kidney transplant patients is a common cause or morbidity and mortality, especially due to a higher risk of osteoporotic fractures. Despite the fact that this has been known for decades, to date, an appropriate diagnostic strategy has yet to be established. Apart from bone biopsy, which is invasive and scarcely used, no other technique is available to accurately establish the risk of fracture in kidney patients. Techniques applied to the general population, such as bone densitometry, have not been subjected to sufficient external validation and their use is not systematic. This means that the identification of patients at risk of fracture and therefore those who are candidates for preventive strategies is an unmet need. Bone strength, defined as the ability of the bone to resist fracture, is determined by bone mineral density (measured by bone densitometry), trabecular architecture and bone tissue quality. The trabecular bone score estimates bone microarchitecture, and low values have been described as an independent predictor of increased fracture risk. Bone microindentation is a minimally invasive technique that measures resistance of the bone to micro-cracks (microscopic separation of mineralised collagen fibres), and therefore bone tissue biomechanical properties. The superiority over bone densitometry of the correlation between the parameters measured by trabecular bone score and microindentation with the risk of fracture in diverse populations led us to test its feasibility in chronic kidney disease and kidney transplant patients.

Asunto(s)

RESUMEN

Background: Renal transplant recipients (RTRs) are often Vitamin D (VitD) depleted as a result of both chronic kidney disease and mandated sun avoidance behaviours. Repleting VitD may be warranted, but how, and for how long, is unknown, as is the impact of seasonality on the success of repletion. We investigated the impact of seasonality on VitD status following VitD repletion in a large cohort of stable, long-term RTRs. Methods: Serum 25-hydroxyvitamin D [25(OH)D] concentrations and bone biochemistry parameters were analysed from 102 VitD repletion courses in 98 RTRs that had undergone VitD repletion. Repletion was delivered over 6 months with either 240 000 IU colecalciferol if pre-repletion serum VitD was between 20 and 50 nmol/L, or with 360 000 IU if VitD was <20 nmol/L. Twelve months post-repletion 25(OH)D and parathyroid hormone (PTH) were available for 75 patients. Results: At baseline, 25(OH)D was 20.1 ± 1.0 nmol/L, increasing to 65.4 ± 1.8 nmol/L following repletion (+7.55 nmol/L/month, P < 0.0001). Twelve months post-repletion and after no further VitD administration, 25(OH)D fell to 35.4 ± 1.8 nmol/L (14.2 ± 0.7 ng/mL; -2.50 nmol/L/month, P < 0.0001). PTH followed the opposite trend with baseline, repletion-end and post-repletion values being 144.2 ± 12.0, 109.6 ± 7.5 and 129.2 ± 11.4 ng/L, respectively. VitD repletion during the summer was associated with significantly higher at repletion-end 25(OH)D compared with any other time of year [summer 80.9 ± 4.0, autumn 64.1 ± 3.0 (P = 0.002), winter 48.9 ± 3.0 (P <0.001), spring 63.8 ± 2.5 nmol/L (P <0.001)]. There was no hypercalcaemia during repletion and renal transplant function remained stable without any evidence of allograft rejection. Conclusions: VitD repletion can safely and effectively be achieved in the majority of chronic stable RTRs using a 6-month bolus intermediate-dose schedule. Winter repletion is associated with an inadequate response in 25(OH)D; however, all patients experience a post-repletion fall towards deficiency in the absence of maintenance supplementation, irrespective of the season of repletion.

RESUMEN

Bone health is assessed by bone mineral density (BMD). Other techniques such as trabecular bone score and microindentation could improve the risk of fracture's estimation. Our chronic kidney disease (CKD) patients presented worse bone health (density, microarchitecture, mechanical properties) than controls. More than BMD should be done to evaluate patients at risk of fracture. INTRODUCTION: BMD measured by dual-energy X-ray absorptiometry (DXA) is used to assess bone health in end-stage renal disease (ESRD) patients. Recently, trabecular bone score (TBS) and microindentation that can measure microarchitectural and mechanical properties of bone have demonstrated better correlation with fractures than DXA in different populations. We aimed to characterize bone health (BMD, TBS, and strength) and calcium/phosphate metabolism in a cohort of 53 ESRD patients undergoing kidney transplantation (KT) and 94 controls with normal renal function. METHODS: Laboratory workout, lumbar spine/hip BMD measurements (using DXA), lumbar spine TBS, and bone strength were carried out. The latter was assessed with an impact microindentation device, standardized as percentage of a reference value, and expressed as bone material strength index (BMSi) units. Multivariable linear regression was used to study differences between cases and controls adjusted by age, gender, and body mass index. RESULTS: Among cases, serum calcium was 9.6 ± 0.7 mg/dl, phosphorus 4.4 ± 1.2 mg/dl, and intact parathyroid hormone 214 pg/ml [102-390]. Fourteen patients (26.4%) had prevalent asymptomatic fractures in spinal X-ray. BMD was significantly lower among ESRD patients compared to controls: lumbar 0.966 ± 0.15 vs 0.982 ± 0.15 (adjusted p = 0.037), total hip 0.852 ± 0.15 vs 0.902 ± 0.13 (adjusted p < 0.001), and femoral neck 0.733 ± 0.15 vs 0.775 ± 0.12 (adjusted p < 0.001), as were TBS (1.20 [1.11-1.30] vs 1.31 [1.19-1.43] (adjusted p < 0.001)) and BMSi (79 [71.8-84.2] vs 82. [77.5-88.9] (adjusted p = 0.005)). CONCLUSIONS: ESRD patients undergoing transplant surgery have damaged bone health parameters (density, microarchitecture, and mechanical properties) despite acceptably controlled hyperparathyroidism. Detecting these abnormalities may assist in identifying patients at high risk of post-transplantation fractures.

Asunto(s)

RESUMEN

Background: Major acid-base variations during dialysis and the imbalances in serum calcium levels intensified by them play a role in cardiovascular damage of hemodialysis patients. Early vascular walls modifications can be objectified by determining the pulse wave velocity (PWV) - a marker of vascular stiffness that is associated with increased risk of cardiovascular events. Material and methods: This was a prospective study conducted on 63 chronic hemodialysis patients with diuresis above 500 mL/ 24 hours and predialysis blood pressure below 160 mmHg (treatment controlled) randomized in two groups for 12 months - the study group receiving interdialitic oral sodium bicarbonate doses and control group, without oral sodium bicarbonate supplementation, but receiving higher bicarbonate prescriptions in dialysis. All the patients were monthly evaluated by biochemical tests (serum calcium, phosphate, iPTH, bicarbonate), the assessment of prescribed doses of phosphate binders being undergone. Two PWV determinations and chest X-ray exams for coronary calcifications were done - at the beginning and end of the study for every patient. Results: In the study group (n = 29), the mean age was 56.48 ± 12.78 years and the average duration of dialysis was 55.51 ± 34.53 months, the mean dialysis bicarbonate was 29.81 ± 1.41 mEq/ L and 27 of them (subgroup 0) had alkaline reserve (AR) 20-22 mEq/ L. The control group (n = 34) had a mean age of 57.35 ± 15.32 years and the mean dialysis duration 59.67 ± 34.79 months, with an average level of dialysis bicarbonate of 33 ± 2.2 mEq/ L necessary to maintain AR within guidelines. Depending on the mean AR obtained, this group was divided into three subgroups (subgroup 1, subgroup 2, and subgroup 3). There were statistically significant differences regarding the necessary of dialysis bicarbonate (p < 0.001), average serum calcium levels (p < 0.001) and serum phosphorus (p < 0.001), as well as PWV mean values and the number of vascular calcifications (p = 0.036) between the study and the control group. The average dose of phosphate binders was significantly higher in the study group (p = 0.01). At the end of the study, the serum iPTH average levels were decreased in the study group (p < 0.001) and significantly increased in the control group (p < 0.001). Conclusions: Avoiding large variations in serum bicarbonate levels is an important step in hemodialysis patients' management because wide acidosis-alkalosis variation can increase cardiovascular risks in terms of altering the vessel walls elasticity and favoring their calcifications. Abbreviations: GFR = glomerular filtration rate,PWV = pulse wave velocity, iPTH = intact parathyroid hormone,AR = alkaline reserve, BP = blood pressure,mEq = milliequivalents,L = liter.

Asunto(s)

RESUMEN

Patients with chronic kidney disease (CKD) frequently have mineral and bone disorders (CKD-MBD) that are caused by several mechanisms. Recent research has suggested that uremic toxins from the gut such as p-cresyl sulfate (PCS) and indoxyl sulfate (IS) could also be involved in the development of bone disease in patients with CKD. IS and PCS are produced by microbiota in the gut, carried into the plasma bound to serum albumin, and are normally excreted into the urine. However, in patients with CKD, there is an accumulation of high levels of these uremic toxins. The exact mechanisms of action of uremic toxins in bone disease remain unclear. The purpose of this brief review is to discuss the link between uremic toxins (IS and PCS) and bone mineral disease in chronic kidney disease.

Asunto(s)

RESUMEN

Idiopathic hypercalciuria (IH) is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density (BMD), as described previously in pediatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs (gut, bone and kidney), which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins (i.e., fibroblast growth-factor-23). Usually, a primary defect in one organ induces compensatory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary to a primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular transport of this ion in intestines, kidneys and bones. Reduced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking at the end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.