Approximately 30%-50% of people are recognized to have low levels of vitamin D,and insufficiency and deficiency of vitamin D are recognized as global health problems worldwide.Although the presence of hypovitamin D in...Approximately 30%-50% of people are recognized to have low levels of vitamin D,and insufficiency and deficiency of vitamin D are recognized as global health problems worldwide.Although the presence of hypovitamin D increases the risk of rickets and fractures,low vitamin D levels are also associated with hypertension,cancer,and cardiovascular disease.In addition,diabetes mellitus(DM) and chronic kidney disease(CKD) are also related to vitamin D levels.Vitamin D deficiency has been linked to onset and progression of DM.Although in patients with DM the relationship between vitamin D and insulin secretion,insulin resistance,and β-cell dysfunction are pointed out,evidence regarding vitamin D levels and DM is contradictory,and well controlled studies are needed.In addition,vitamin D influences the renin-angiotensin system,inflammation,and mineral bone disease,which may be associated with the cause and progression CKD.There is increasing evidence that vitamin D deficiency may be a risk factor for DM and CKD;however,it remains uncertain whether vitamin D deficiency also predisposes to death from DM and CKD.Although at this time,supplementation with vitamin D has not been shown to improve glycemic control or prevent incident DM,clinical trials with sufficient sample size,study periods,and optimal doses of vitamin D supplementation are still needed.This review focuses on the mechanism of vitamin D insufficiency and deficiency in DM or CKD,and discusses the current evidence regarding supplementation with vitamin D in patients with these diseases.展开更多
AIM To evaluate the prevalence of vitamin D deficiency and its relation to diabetes and kidney disease in Veterans residing in the North East United States(VISN 2). METHODS In this retrospective study, we used data fr...AIM To evaluate the prevalence of vitamin D deficiency and its relation to diabetes and kidney disease in Veterans residing in the North East United States(VISN 2). METHODS In this retrospective study, we used data from the computerized patient record system at Stratton Veterans Administration Medical Center at Albany, NY(VHA) for those patients who had 25-hydroxyvitamin D levels and 1,25(OH) vitamin D levels measured between 2007 and 2010. We collected demographic information including age, sex, body mass index and race; clinical data including diabetes, hypertension and CAD; and laboratory data including calcium, creatinine and parathyroid hormone(PTH)(intact). Vitamin D deficiency is defined as a serum 25-hydroxyvitamin D level of less than 20 ng/mL(50 nmol/L), and insufficiency is defined as a serum 25-hydroxyvitamin D level of 20 to 30 ng/mL(50 to 75 nmol/L). RESULTS Data was available for approximately 68000 subjects. We identified 64144 subjects for analysis after exclusion of duplicates. Among them, 27098 had diabetes. Themean age of subjects with diabetes was 68 ± 11 with a mean body mass index(BMI) of 32 ± 7 and duration of diabetes of 5.6 ± 3.2 years. The mean 25(OH) vitamin D level among subjects with diabetes was 27 ± 11.6. There was no significant difference in 25(OH) vitamin D levels between subjects with diabetes and glomerular filtration rate(e-GFR) < 60 compared to those with e-GFR ≥ 60. As expected, subjects with e-GFR < 60 had significantly lower 1,25(OH) vitamin D levels and significantly elevated PTH-intact. Of the 64144 subjects, 580 had end-stage renal disease. Of those, 407 had diabetes and 173 did not. Vitamin D levels in both groups were in the insufficiency range and there was no significant difference irrespective of presence or absence of diabetes. Subjects with vitamin D levels less than 20 ng/mL had a higher BMI and elevated PTH, and higher HbA 1C levels compared to those with vitamin D levels more than 20 ng/mL. CONCLUSION We conclude that we need to keep a close eye on vitamin D levels in subjects with mild chronic kidney disease as well as those with moderate control of diabetes.展开更多
AIM To evaluate thresholds for serum 25(OH)D concentrations in relation to death, kidney progression and hospitalization in non-dialysis chronic kidney disease(CKD) population.METHODS Four hundred and seventy non-dial...AIM To evaluate thresholds for serum 25(OH)D concentrations in relation to death, kidney progression and hospitalization in non-dialysis chronic kidney disease(CKD) population.METHODS Four hundred and seventy non-dialysis 3-5 stage CKD patients participating in OSERCE-2 study, a prospective, multicenter, cohort study, were prospectively evaluated and categorized into 3 groups according to 25(OH)D levels at enrollment(less than 20 ng/mL, between 20 and 29 ng/mL, and at or above 30 ng/mL), considering 25(OH)D between 20 and 29 ng/mL as reference group. Association between 25(OH)D levels and death(primary outcome), and time to first hospitalization and renal progression(secondary outcomes) over a 3-year followup, were assessed by Kaplan-Meier survival curves and Cox-proportional hazard models. To identify 25(OH)D levels at highest risk for outcomes, receiver operating characteristic(ROC) curves were performed.RESULTS Over 29 ± 12 mo of follow-up, 46(10%) patients dead, 156(33%) showed kidney progression, and 126(27%) were hospitalized. After multivariate adjustment, 25(OH)D < 20 ng/mL was an independent predictor of all-cause mortality(HR = 2.33; 95%CI: 1.10-4.91; P = 0.027) and kidney progression(HR = 2.46; 95%CI: 1.63-3.71; P < 0.001), whereas the group with 25(OH)D at or above 30 ng/mL did not have a different hazard for outcomes from the reference group. Hospitalization outcomes were predicted by 25(OH) levels(HR = 0.98; 95%CI: 0.96-1.00; P = 0.027) in the unadjusted Cox proportional hazards model, but not after multivariate adjusting. ROC curves identified 25(OH)D levels at highest risk for death, kidney progression, and hospitalization, at 17.4 ng/mL [area under the curve(AUC) = 0.60; 95%CI: 0.685-0.69; P = 0.027], 18.6 ng/mL(AUC = 0.65; 95%CI: 0.60-0.71; P < 0.001), and 19.0 ng/m L(AUC = 0.56; 95%CI: 0.50-0.62; P = 0.048), respectively.CONCLUSION25(OH)D < 20 ng/mL was an independent predictor of death and progression in patients with stage 3-5 CKD, with no additional benefits when patients reached the levels at or above 30 ng/m L suggested as optimal by CKD guidelines.展开更多
Deficient sleep quality (SQ) has been linked with a higher hospitalization rate and mortality in dialysis patients, however the prevalence of sleep disorders and their influence on prognosis in non-dialysis chronic ki...Deficient sleep quality (SQ) has been linked with a higher hospitalization rate and mortality in dialysis patients, however the prevalence of sleep disorders and their influence on prognosis in non-dialysis chronic kidney disease (CKD) has been poorly investigated. The aim of this study was to assess factors related with SQ in CKD patients (stages I-IV) followed in a nephrology outpatient clinic as well as the long-term impact of SQ on patient’s outcome. Between January and May 2008, Pittsburgh Sleep Quality Index (PSQI) was self-administered by 122 patients (68 males and 54 females) with a mean age of 65 years. Patients were classified as “good” (global PSQI < 6) and “poor” sleepers (global PSQI ≥ 6). We identified 66 (54%) poor sleepers (PS), characterized by an older age (66 ± 14.2 vs 57 ± 17.0, p < 0.01), female predominance (59% vs 26%, p < 0.01) and worse renal function (49 ± 19.1 vs 57 ± 23.2 ml/min, p < 0.05). There was a significant correlation between phosphate and PSQI score (r = 0.234, p = 0.01), however no correlation with calcium or PTH. Vitamin D was also lower in PS (17 ± 7.2 vs 23 ± 15.1 ng/ml, p < 0.05). Until June 2015, hospitalization rate was higher among PS (64% vs 44%, p < 0.05). In this period, there was also a trend towards higher mortality for PS (18% vs 16%). In summary, over 50% of CKD patients have poor SQ, which was associated with older age, female gender, worse renal function, lower vitamin D and higher phosphate levels. Deficient sleep was associated with a greater probability of hospitalization and might be a prognostic marker in CKD.展开更多
活性维生素D在临床上应用广泛。对于肝、肾功能逐渐衰退,伴有肌少症和/或神经功能损害的老年骨质疏松症(osteoporosis,OP)患者,妊娠/哺乳相关的OP及骨密度(bone mineral density,BMD)下降患者,均可适当补充。活性维生素D联合钙剂是甲状...活性维生素D在临床上应用广泛。对于肝、肾功能逐渐衰退,伴有肌少症和/或神经功能损害的老年骨质疏松症(osteoporosis,OP)患者,妊娠/哺乳相关的OP及骨密度(bone mineral density,BMD)下降患者,均可适当补充。活性维生素D联合钙剂是甲状旁腺功能减退症和骨软化症的首选治疗方案,同时也是慢性肾脏病-矿物质和骨异常患者预防和治疗继发性甲状旁腺功能亢进症的主要措施之一。活性维生素D治疗窗相对狭窄,用药期间需要定期监测安全性指标,如血钙磷、尿钙磷及全段甲状旁腺素等。展开更多
矿物质和骨异常(mineral and bone disorder,MBD)是慢性肾脏病(chronic kidney disease,CKD)的常见并发症之一,是CKD患者致残和致死的重要原因之一。维生素D缺乏是CKD-MBD发生、发展的重要原因。合理应用活性维生素D(包括骨化三醇或其...矿物质和骨异常(mineral and bone disorder,MBD)是慢性肾脏病(chronic kidney disease,CKD)的常见并发症之一,是CKD患者致残和致死的重要原因之一。维生素D缺乏是CKD-MBD发生、发展的重要原因。合理应用活性维生素D(包括骨化三醇或其他维生素D类似物),使血钙、磷和全段甲状旁腺素(intact parathyroid hormone,iPTH)维持在理想范围,可有效防治继发性甲状旁腺功能亢进症、血管钙化、肾性骨营养不良和骨质疏松等,改善CKD患者的生存质量,降低发病率和病死率。展开更多
慢性肾脏病-矿物质和骨代谢异常(chronic kidney disease-mineral and bone disorder,CKDMBD)是慢性肾脏病(chronic kidney disease,CKD)患者主要的并发症之一,目前CKD-MBD治疗手段主要包括:磷结合剂、活性维生素D及其类似物、拟钙剂等...慢性肾脏病-矿物质和骨代谢异常(chronic kidney disease-mineral and bone disorder,CKDMBD)是慢性肾脏病(chronic kidney disease,CKD)患者主要的并发症之一,目前CKD-MBD治疗手段主要包括:磷结合剂、活性维生素D及其类似物、拟钙剂等药物治疗以及甲状旁腺手术治疗。其中,活性维生素D及其类似物是最为常见的治疗药物,可以降低甲状旁腺激素(parathyroid hormone,PTH),改善骨质疏松和高转运骨病的骨损害,在临床上应用广泛,但使用不当也会导致高钙、高磷血症及加重血管钙化发展,为了更合理的使用该类药物,本文结合2017年KDIGO的CKD-MBD指南更新并就活性维生素D及其类似物在CKD-MBD的治疗进展进行介绍。展开更多
目的探讨活性维生素D用于慢性肾脏疾病的治疗效果。方法检索Ovide Medline、CINAHL、Embase、Cochrane Central Register of Controlled Trials、中国学术期刊全文数据库(CNKI)、中国生物医学文献数据库(CBM)、万方数据库(Wangfang)和...目的探讨活性维生素D用于慢性肾脏疾病的治疗效果。方法检索Ovide Medline、CINAHL、Embase、Cochrane Central Register of Controlled Trials、中国学术期刊全文数据库(CNKI)、中国生物医学文献数据库(CBM)、万方数据库(Wangfang)和维普中文科技期刊数据库(VIP)等数据库,收集活性维生素D用于慢性肾脏疾病治疗的临床随机对照研究(RCT),检索年限均为2005年1月-2018年6月。采用Revman 5.3软件进行数据分析。结果共纳入18个RCTs,Jadad量表评分均≥2分。治疗后试验组超敏C-反应蛋白(hs-CRP)[MD=-1.10,95%CI(-1.72,-0.49),P<0.05]、白介素6 (IL-6)[MD=-23.77, 95%CI (-38.32,-9.22), P<0.05]与肿瘤坏死因子-α(TNF-α)[MD=-120.28,95%CI (-177.02,-63.54),P<0.05]降低幅度均高于对照组,两组比较差异显著(P<0.05),试验组血肌酐(SCr)、24h尿蛋白定量与血尿素氮(BUN)降低幅度均高于对照组(P<0.05)。试验组血清甲状旁腺激素水平[MD=-10.87,95%CI(-13.44,8.30),P<0.05]降低幅度高于对照组。结论活性维生素D可降低CKD患者微炎症,改善患者肾功能,预防继发性甲状旁腺功能亢进。展开更多
文摘Approximately 30%-50% of people are recognized to have low levels of vitamin D,and insufficiency and deficiency of vitamin D are recognized as global health problems worldwide.Although the presence of hypovitamin D increases the risk of rickets and fractures,low vitamin D levels are also associated with hypertension,cancer,and cardiovascular disease.In addition,diabetes mellitus(DM) and chronic kidney disease(CKD) are also related to vitamin D levels.Vitamin D deficiency has been linked to onset and progression of DM.Although in patients with DM the relationship between vitamin D and insulin secretion,insulin resistance,and β-cell dysfunction are pointed out,evidence regarding vitamin D levels and DM is contradictory,and well controlled studies are needed.In addition,vitamin D influences the renin-angiotensin system,inflammation,and mineral bone disease,which may be associated with the cause and progression CKD.There is increasing evidence that vitamin D deficiency may be a risk factor for DM and CKD;however,it remains uncertain whether vitamin D deficiency also predisposes to death from DM and CKD.Although at this time,supplementation with vitamin D has not been shown to improve glycemic control or prevent incident DM,clinical trials with sufficient sample size,study periods,and optimal doses of vitamin D supplementation are still needed.This review focuses on the mechanism of vitamin D insufficiency and deficiency in DM or CKD,and discusses the current evidence regarding supplementation with vitamin D in patients with these diseases.
基金salary support from Veterans Health Administration
文摘AIM To evaluate the prevalence of vitamin D deficiency and its relation to diabetes and kidney disease in Veterans residing in the North East United States(VISN 2). METHODS In this retrospective study, we used data from the computerized patient record system at Stratton Veterans Administration Medical Center at Albany, NY(VHA) for those patients who had 25-hydroxyvitamin D levels and 1,25(OH) vitamin D levels measured between 2007 and 2010. We collected demographic information including age, sex, body mass index and race; clinical data including diabetes, hypertension and CAD; and laboratory data including calcium, creatinine and parathyroid hormone(PTH)(intact). Vitamin D deficiency is defined as a serum 25-hydroxyvitamin D level of less than 20 ng/mL(50 nmol/L), and insufficiency is defined as a serum 25-hydroxyvitamin D level of 20 to 30 ng/mL(50 to 75 nmol/L). RESULTS Data was available for approximately 68000 subjects. We identified 64144 subjects for analysis after exclusion of duplicates. Among them, 27098 had diabetes. Themean age of subjects with diabetes was 68 ± 11 with a mean body mass index(BMI) of 32 ± 7 and duration of diabetes of 5.6 ± 3.2 years. The mean 25(OH) vitamin D level among subjects with diabetes was 27 ± 11.6. There was no significant difference in 25(OH) vitamin D levels between subjects with diabetes and glomerular filtration rate(e-GFR) < 60 compared to those with e-GFR ≥ 60. As expected, subjects with e-GFR < 60 had significantly lower 1,25(OH) vitamin D levels and significantly elevated PTH-intact. Of the 64144 subjects, 580 had end-stage renal disease. Of those, 407 had diabetes and 173 did not. Vitamin D levels in both groups were in the insufficiency range and there was no significant difference irrespective of presence or absence of diabetes. Subjects with vitamin D levels less than 20 ng/mL had a higher BMI and elevated PTH, and higher HbA 1C levels compared to those with vitamin D levels more than 20 ng/mL. CONCLUSION We conclude that we need to keep a close eye on vitamin D levels in subjects with mild chronic kidney disease as well as those with moderate control of diabetes.
基金Supported by Abbott and the Spanish Society of Nephrology
文摘AIM To evaluate thresholds for serum 25(OH)D concentrations in relation to death, kidney progression and hospitalization in non-dialysis chronic kidney disease(CKD) population.METHODS Four hundred and seventy non-dialysis 3-5 stage CKD patients participating in OSERCE-2 study, a prospective, multicenter, cohort study, were prospectively evaluated and categorized into 3 groups according to 25(OH)D levels at enrollment(less than 20 ng/mL, between 20 and 29 ng/mL, and at or above 30 ng/mL), considering 25(OH)D between 20 and 29 ng/mL as reference group. Association between 25(OH)D levels and death(primary outcome), and time to first hospitalization and renal progression(secondary outcomes) over a 3-year followup, were assessed by Kaplan-Meier survival curves and Cox-proportional hazard models. To identify 25(OH)D levels at highest risk for outcomes, receiver operating characteristic(ROC) curves were performed.RESULTS Over 29 ± 12 mo of follow-up, 46(10%) patients dead, 156(33%) showed kidney progression, and 126(27%) were hospitalized. After multivariate adjustment, 25(OH)D < 20 ng/mL was an independent predictor of all-cause mortality(HR = 2.33; 95%CI: 1.10-4.91; P = 0.027) and kidney progression(HR = 2.46; 95%CI: 1.63-3.71; P < 0.001), whereas the group with 25(OH)D at or above 30 ng/mL did not have a different hazard for outcomes from the reference group. Hospitalization outcomes were predicted by 25(OH) levels(HR = 0.98; 95%CI: 0.96-1.00; P = 0.027) in the unadjusted Cox proportional hazards model, but not after multivariate adjusting. ROC curves identified 25(OH)D levels at highest risk for death, kidney progression, and hospitalization, at 17.4 ng/mL [area under the curve(AUC) = 0.60; 95%CI: 0.685-0.69; P = 0.027], 18.6 ng/mL(AUC = 0.65; 95%CI: 0.60-0.71; P < 0.001), and 19.0 ng/m L(AUC = 0.56; 95%CI: 0.50-0.62; P = 0.048), respectively.CONCLUSION25(OH)D < 20 ng/mL was an independent predictor of death and progression in patients with stage 3-5 CKD, with no additional benefits when patients reached the levels at or above 30 ng/m L suggested as optimal by CKD guidelines.
文摘Deficient sleep quality (SQ) has been linked with a higher hospitalization rate and mortality in dialysis patients, however the prevalence of sleep disorders and their influence on prognosis in non-dialysis chronic kidney disease (CKD) has been poorly investigated. The aim of this study was to assess factors related with SQ in CKD patients (stages I-IV) followed in a nephrology outpatient clinic as well as the long-term impact of SQ on patient’s outcome. Between January and May 2008, Pittsburgh Sleep Quality Index (PSQI) was self-administered by 122 patients (68 males and 54 females) with a mean age of 65 years. Patients were classified as “good” (global PSQI < 6) and “poor” sleepers (global PSQI ≥ 6). We identified 66 (54%) poor sleepers (PS), characterized by an older age (66 ± 14.2 vs 57 ± 17.0, p < 0.01), female predominance (59% vs 26%, p < 0.01) and worse renal function (49 ± 19.1 vs 57 ± 23.2 ml/min, p < 0.05). There was a significant correlation between phosphate and PSQI score (r = 0.234, p = 0.01), however no correlation with calcium or PTH. Vitamin D was also lower in PS (17 ± 7.2 vs 23 ± 15.1 ng/ml, p < 0.05). Until June 2015, hospitalization rate was higher among PS (64% vs 44%, p < 0.05). In this period, there was also a trend towards higher mortality for PS (18% vs 16%). In summary, over 50% of CKD patients have poor SQ, which was associated with older age, female gender, worse renal function, lower vitamin D and higher phosphate levels. Deficient sleep was associated with a greater probability of hospitalization and might be a prognostic marker in CKD.
文摘活性维生素D在临床上应用广泛。对于肝、肾功能逐渐衰退,伴有肌少症和/或神经功能损害的老年骨质疏松症(osteoporosis,OP)患者,妊娠/哺乳相关的OP及骨密度(bone mineral density,BMD)下降患者,均可适当补充。活性维生素D联合钙剂是甲状旁腺功能减退症和骨软化症的首选治疗方案,同时也是慢性肾脏病-矿物质和骨异常患者预防和治疗继发性甲状旁腺功能亢进症的主要措施之一。活性维生素D治疗窗相对狭窄,用药期间需要定期监测安全性指标,如血钙磷、尿钙磷及全段甲状旁腺素等。
文摘矿物质和骨异常(mineral and bone disorder,MBD)是慢性肾脏病(chronic kidney disease,CKD)的常见并发症之一,是CKD患者致残和致死的重要原因之一。维生素D缺乏是CKD-MBD发生、发展的重要原因。合理应用活性维生素D(包括骨化三醇或其他维生素D类似物),使血钙、磷和全段甲状旁腺素(intact parathyroid hormone,iPTH)维持在理想范围,可有效防治继发性甲状旁腺功能亢进症、血管钙化、肾性骨营养不良和骨质疏松等,改善CKD患者的生存质量,降低发病率和病死率。
文摘慢性肾脏病-矿物质和骨代谢异常(chronic kidney disease-mineral and bone disorder,CKDMBD)是慢性肾脏病(chronic kidney disease,CKD)患者主要的并发症之一,目前CKD-MBD治疗手段主要包括:磷结合剂、活性维生素D及其类似物、拟钙剂等药物治疗以及甲状旁腺手术治疗。其中,活性维生素D及其类似物是最为常见的治疗药物,可以降低甲状旁腺激素(parathyroid hormone,PTH),改善骨质疏松和高转运骨病的骨损害,在临床上应用广泛,但使用不当也会导致高钙、高磷血症及加重血管钙化发展,为了更合理的使用该类药物,本文结合2017年KDIGO的CKD-MBD指南更新并就活性维生素D及其类似物在CKD-MBD的治疗进展进行介绍。