D. Hernández, J. Alonso-Titos, A. Armas-Padrón, V. López, M. Cabello, E. Sola, L. Fuentes, E. Gutiérrez, T. Vázquez, T. Jiménez, P. Ruiz-Esteban, M. González‐Molina
Background: Chronic kidney disease (CKD) is an important independent risk factor for adverse cardiovascular events in patients waitlisted for kidney transplantation (KT). Although KT reduces cardiovascular risk, these patients still have a higher all-cause and cardiovascular mortality than the general population. This concerning situation is due to a high burden of traditional and nontraditional risk factors as well as uremia-related factors and transplant-specific factors, leading to 2 differentiated processes under the framework of CKD, atherosclerosis and arteriosclerosis. These can be initiated by insults to the vascular endothelial endothelium, leading to vascular calcification (VC) of the tunica media or the tunica intima, which may coexist. Several pathogenic mechanisms such as inflammation-related endothelial dysfunction, mineral metabolism disorders, activation of the renin-angiotensin system, reduction of nitric oxide, lipid disorders, and the fibroblast growth factor 23-klotho axis are involved in the pathogenesis of atherosclerosis and arteriosclerosis, including VC. Summary: This review focuses on the current understanding of atherosclerosis and arteriosclerosis, both in patients on the waiting list as well as in kidney transplant recipients, emphasizing the cardiovascular risk factors in both populations and the inflammation-related pathogenic mechanisms. Key Message: The importance of cardiovascular risk factors and the pathogenic mechanisms related to inflammation in patients waitlisted for KT and kidney transplant recipients.
{"title":"Waiting List and Kidney Transplant Vascular Risk: An Ongoing Unmet Concern","authors":"D. Hernández, J. Alonso-Titos, A. Armas-Padrón, V. López, M. Cabello, E. Sola, L. Fuentes, E. Gutiérrez, T. Vázquez, T. Jiménez, P. Ruiz-Esteban, M. González‐Molina","doi":"10.1159/000504546","DOIUrl":"https://doi.org/10.1159/000504546","url":null,"abstract":"Background: Chronic kidney disease (CKD) is an important independent risk factor for adverse cardiovascular events in patients waitlisted for kidney transplantation (KT). Although KT reduces cardiovascular risk, these patients still have a higher all-cause and cardiovascular mortality than the general population. This concerning situation is due to a high burden of traditional and nontraditional risk factors as well as uremia-related factors and transplant-specific factors, leading to 2 differentiated processes under the framework of CKD, atherosclerosis and arteriosclerosis. These can be initiated by insults to the vascular endothelial endothelium, leading to vascular calcification (VC) of the tunica media or the tunica intima, which may coexist. Several pathogenic mechanisms such as inflammation-related endothelial dysfunction, mineral metabolism disorders, activation of the renin-angiotensin system, reduction of nitric oxide, lipid disorders, and the fibroblast growth factor 23-klotho axis are involved in the pathogenesis of atherosclerosis and arteriosclerosis, including VC. Summary: This review focuses on the current understanding of atherosclerosis and arteriosclerosis, both in patients on the waiting list as well as in kidney transplant recipients, emphasizing the cardiovascular risk factors in both populations and the inflammation-related pathogenic mechanisms. Key Message: The importance of cardiovascular risk factors and the pathogenic mechanisms related to inflammation in patients waitlisted for KT and kidney transplant recipients.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90084860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and Objectives: This study was to characterize the association of cumulative exposure to increased high-sensitivity C-reactive protein (hs-CRP) with chronic kidney diseases (CKD). Methods: We included 35,194 participants with hs-CRP measured at three examinations in 2006, 2008, 2010. Participants were classified into nonexposed group (hs-CRP <3.0 mg/L in all 3 examinations), 1-exposed group (hs-CRP ≥3.0 mg/L in 1 of the 3 examinations), 2-exposed group (hs-CRP ≥3.0 mg/L in 2 of the 3 examinations), and 3-exposed group (hs-CRP ≥3.0 mg/L in 3 examinations). Cox proportional hazards models were used to assess the association of cumulative hs-CRP with incident CKD. CKD includes an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or urinary protein positive. Results: The study showed the risk of CKD as the number of years of exposure to hs-CRP increases. Participants in 3-exposed group had significantly increased CKD risk with hazard ratio (HR) (95% confidence interval, CI) of 1.70 (1.49–1.93), in comparison with 1.47 (1.34–1.62) for participants in the 2-exposed group, and 1.08 (1.00–1.16) for those in the 1-exposed group (p < 0.01); meanwhile, the similar and significant associations were also observed for eGFR <60 mL/min/1.73 m2, proteinuria positive, in participants of the 3-exposed group in comparison with the nonexposed group, with respective HRs (95% CI) of 1.27 (1.01–1.58) and 2.27 (1.87–2.76). Conclusions: Cumulative exposure to hs-CRP was associated with a subsequent increased risk of CKD and was of great value to risk prediction.
{"title":"The Cumulative Exposure to High-Sensitivity C-Reactive Protein Predicts the Risk of Chronic Kidney Diseases","authors":"Jingli Gao, Aitian Wang, Xiaolan Li, Junjuan Li, Hualing Zhao, Jianjun Zhang, Jingtao Liang, Shuohua Chen, Shouling Wu","doi":"10.1159/000504251","DOIUrl":"https://doi.org/10.1159/000504251","url":null,"abstract":"Background and Objectives: This study was to characterize the association of cumulative exposure to increased high-sensitivity C-reactive protein (hs-CRP) with chronic kidney diseases (CKD). Methods: We included 35,194 participants with hs-CRP measured at three examinations in 2006, 2008, 2010. Participants were classified into nonexposed group (hs-CRP <3.0 mg/L in all 3 examinations), 1-exposed group (hs-CRP ≥3.0 mg/L in 1 of the 3 examinations), 2-exposed group (hs-CRP ≥3.0 mg/L in 2 of the 3 examinations), and 3-exposed group (hs-CRP ≥3.0 mg/L in 3 examinations). Cox proportional hazards models were used to assess the association of cumulative hs-CRP with incident CKD. CKD includes an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or urinary protein positive. Results: The study showed the risk of CKD as the number of years of exposure to hs-CRP increases. Participants in 3-exposed group had significantly increased CKD risk with hazard ratio (HR) (95% confidence interval, CI) of 1.70 (1.49–1.93), in comparison with 1.47 (1.34–1.62) for participants in the 2-exposed group, and 1.08 (1.00–1.16) for those in the 1-exposed group (p < 0.01); meanwhile, the similar and significant associations were also observed for eGFR <60 mL/min/1.73 m2, proteinuria positive, in participants of the 3-exposed group in comparison with the nonexposed group, with respective HRs (95% CI) of 1.27 (1.01–1.58) and 2.27 (1.87–2.76). Conclusions: Cumulative exposure to hs-CRP was associated with a subsequent increased risk of CKD and was of great value to risk prediction.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84135320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Bunz, O. Tschritter, M. Haap, R. Riessen, N. Heyne, F. Artunc
Background: In patients with renal failure, gadolinium-based contrast agents (GBCA) can be removed by intermittent hemodialysis (iHD) to prevent possible toxic effects. There is no data on the efficacy of GBCA removal via sustained low efficiency daily dialysis (SLEDD) which is mainly used in intensive care unit (ICU) patients. Methods: We compared the elimination of the GBCA gadobutrol in 6 ICU patients treated with SLEDD (6–12 h, 90 L dialysate) with 7 normal ward inpatients treated with iHD (4 h, dialysate flow 500 mL/min). Both groups received 3 dialysis sessions on 3 consecutive days starting after the application of gadobutrol. Blood samples were drawn before and after each session and total dialysate, as well as urine was collected. Gadolinium (Gd) concentrations were measured using mass spectrometry and eliminated Gd was calculated from dialysate and urine. Results: The initial mean plasma Gd concentration was 385 ± 183 µM for the iHD and 270 ± 97 µM for the SLEDD group, respectively (p > 0.05). The Gd-reduction rate after the first dialysis session was 83 ± 9 and 67 ± 9% for the iHD and the SLEDD groups, respectively (p = 0.0083). The Gd-reduction rate after the second and third dialysis was 94–98 and 89–96% for the iHD and the SLEDD groups (p > 0.05). The total eliminated Gd was 89 ± 14 and 91 ± 4% of the dose in the iHD and the SLEDD groups, respectively (p > 0.05). Gd dialyzer clearance was 95 ± 22 mL/min and 79 ± 19 mL/min for iHD and SLEDD, respectively (p > 0.05). Conclusions: Gd-elimination with SLEDD is equally effective as iHD and can be safely used to remove GBCA in ICU patients.
{"title":"Elimination of Contrast Agent Gadobutrol with Sustained Low Efficiency Daily Dialysis Compared to Intermittent Hemodialysis","authors":"H. Bunz, O. Tschritter, M. Haap, R. Riessen, N. Heyne, F. Artunc","doi":"10.1159/000502960","DOIUrl":"https://doi.org/10.1159/000502960","url":null,"abstract":"Background: In patients with renal failure, gadolinium-based contrast agents (GBCA) can be removed by intermittent hemodialysis (iHD) to prevent possible toxic effects. There is no data on the efficacy of GBCA removal via sustained low efficiency daily dialysis (SLEDD) which is mainly used in intensive care unit (ICU) patients. Methods: We compared the elimination of the GBCA gadobutrol in 6 ICU patients treated with SLEDD (6–12 h, 90 L dialysate) with 7 normal ward inpatients treated with iHD (4 h, dialysate flow 500 mL/min). Both groups received 3 dialysis sessions on 3 consecutive days starting after the application of gadobutrol. Blood samples were drawn before and after each session and total dialysate, as well as urine was collected. Gadolinium (Gd) concentrations were measured using mass spectrometry and eliminated Gd was calculated from dialysate and urine. Results: The initial mean plasma Gd concentration was 385 ± 183 µM for the iHD and 270 ± 97 µM for the SLEDD group, respectively (p > 0.05). The Gd-reduction rate after the first dialysis session was 83 ± 9 and 67 ± 9% for the iHD and the SLEDD groups, respectively (p = 0.0083). The Gd-reduction rate after the second and third dialysis was 94–98 and 89–96% for the iHD and the SLEDD groups (p > 0.05). The total eliminated Gd was 89 ± 14 and 91 ± 4% of the dose in the iHD and the SLEDD groups, respectively (p > 0.05). Gd dialyzer clearance was 95 ± 22 mL/min and 79 ± 19 mL/min for iHD and SLEDD, respectively (p > 0.05). Conclusions: Gd-elimination with SLEDD is equally effective as iHD and can be safely used to remove GBCA in ICU patients.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78958360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yuan Zu, Xiangxue Lu, Jinghong Song, Ling Yu, Han Li, Shixiang Wang
Objective: To assess the long-term effects including all-cause mortality, cardiovascular mortality, and fracture incidence, of cinacalcet on secondary hyperparathyroidism (SHPT) in patients on dialysis. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials were searched from their inception to October 2018. Randomized controlled trials (RCTs) and cohort design prospective observational studies assessing cinacalcet for the treatment of SHPT in dialysis patients were included. Data extraction was independently completed by 2 authors who determined the methodological quality of the studies and extracted data in duplicate. Study-specific risk estimates were tested by using a fixed effects model. Results: A total of 14 articles with 38,219 participants were included, of which 10 RCTs with 7,471 participants and 4 prospective observational studies with 30,748 participants fulfilled the eligibility criteria. Compared with no cinacalcet, cinacalcet administration reduced all-cause mortality (relative risk [RR] 0.91, 95% CI 0.89–0.94, p < 0.001) and cardiovascular mortality (RR 0.92, 95% CI 0.89–0.95, p < 0.001), but it did not significantly reduce the incidence of fractures (RR 0.93, 95% CI 0.87–1.00, p = 0.05). Conclusions: The results of this meta-analysis indicated that the treatment of SHPT with cinacalcet may in fact reduce all-cause mortality and cardiovascular mortality among patients receiving maintenance dialysis.
目的:评估cinacalcet对透析患者继发性甲状旁腺功能亢进症(SHPT)的长期影响，包括全因死亡率、心血管死亡率和骨折发生率。方法:检索PubMed、Embase和Cochrane中央对照试验注册库从成立到2018年10月的资料。随机对照试验(rct)和队列设计前瞻性观察研究评估了cinacalcet治疗透析患者SHPT的效果。数据提取由两位作者独立完成，他们确定了研究的方法学质量，并重复提取数据。使用固定效应模型检验特定研究的风险估计。结果:共纳入14篇文章38,219名受试者，其中10项rct纳入7,471名受试者，4项前瞻性观察性研究纳入30,748名受试者，符合入选标准。与未使用cinacalcet组相比，cinacalcet组降低了全因死亡率(相对危险度[RR] 0.91, 95% CI 0.89-0.94, p < 0.001)和心血管死亡率(RR 0.92, 95% CI 0.89-0.95, p < 0.001)，但未显著降低骨折发生率(RR 0.93, 95% CI 0.87-1.00, p = 0.05)。结论:本荟萃分析的结果表明，cinacalcet治疗SHPT实际上可以降低接受维持性透析患者的全因死亡率和心血管死亡率。
{"title":"Cinacalcet Treatment Significantly Improves All-Cause and Cardiovascular Survival in Dialysis Patients: Results from a Meta-Analysis","authors":"Yuan Zu, Xiangxue Lu, Jinghong Song, Ling Yu, Han Li, Shixiang Wang","doi":"10.1159/000504139","DOIUrl":"https://doi.org/10.1159/000504139","url":null,"abstract":"Objective: To assess the long-term effects including all-cause mortality, cardiovascular mortality, and fracture incidence, of cinacalcet on secondary hyperparathyroidism (SHPT) in patients on dialysis. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials were searched from their inception to October 2018. Randomized controlled trials (RCTs) and cohort design prospective observational studies assessing cinacalcet for the treatment of SHPT in dialysis patients were included. Data extraction was independently completed by 2 authors who determined the methodological quality of the studies and extracted data in duplicate. Study-specific risk estimates were tested by using a fixed effects model. Results: A total of 14 articles with 38,219 participants were included, of which 10 RCTs with 7,471 participants and 4 prospective observational studies with 30,748 participants fulfilled the eligibility criteria. Compared with no cinacalcet, cinacalcet administration reduced all-cause mortality (relative risk [RR] 0.91, 95% CI 0.89–0.94, p < 0.001) and cardiovascular mortality (RR 0.92, 95% CI 0.89–0.95, p < 0.001), but it did not significantly reduce the incidence of fractures (RR 0.93, 95% CI 0.87–1.00, p = 0.05). Conclusions: The results of this meta-analysis indicated that the treatment of SHPT with cinacalcet may in fact reduce all-cause mortality and cardiovascular mortality among patients receiving maintenance dialysis.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78625294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Tanabe, Y. Ogura, Mikie Nakabayashi, Y. Nagai, Shiika Watanabe, T. Sugaya, Keiichi Ohata, Daisuke Ichikawa, Kazuho Inoue, Seiko Hoshino, K. Kimura, Y. Shibagaki, Y. Ono, A. Kamijo-Ikemori
Background: Renal hypoxia is an aggravating factor for tubulointerstitial damage, which is strongly associated with renal prognosis in diabetic kidney disease (DKD). Therefore, urinary markers that can detect renal hypoxia are useful for monitoring DKD. Objective: To determine the correlation between urinary liver-type fatty acid-binding protein (L-FABP) and renal hypoxia using a novel animal model of type 2 diabetes. Methods: Male spontaneously diabetic Torii (SDT) fatty rats (n = 6) were used as an animal model of type 2 diabetes. Age- and sex-matched Sprague-Dawley (SD) rats (n = 8) were used as controls. Body weight, systolic blood pressure, and blood glucose levels were measured at 8, 12, 16, and 24 weeks of age. Urine samples and serum and kidney tissues were collected at 24 weeks of age. Microvascular blood flow index (BFI) was measured using diffuse correlation spectroscopy before sampling both the serum and kidneys for the evaluation of renal microcirculation at the corticomedullary junction. Results: Obesity, hyperglycemia, and hypertension were observed in the SDT fatty rats. Focal glomerular sclerosis, moderate interstitial inflammation, and fibrosis were significantly more frequent in SDT fatty rats than in SD rats. While the frequency of peritubular endothelial cells and phosphoendothelial nitric oxide synthase levels were similar in both types of rats, the degree of renal hypoxia-inducible factor-1α (HIF-1α) expression was significantly higher (and with no change in renal vascular endothelial growth factor expression levels) in the SDT fatty rats. Urinary L-FABP levels were significantly higher and renal microvascular BFI was significantly lower in the SDT fatty rats than in the SD rats. Urinary L-FABP levels exhibited a significant positive correlation with renal HIF-1α expression and a significant negative correlation with renal microvascular BFI. Conclusions: Urinary L-FABP levels reflect the degree of renal hypoxia in DKD in a type 2 diabetic animal model. Urinary L-FABP may thus prove useful as a renal hypoxia marker for monitoring DKD in patients with type 2 diabetes in clinical practice.
{"title":"The Possibility of Urinary Liver-Type Fatty Acid-Binding Protein as a Biomarker of Renal Hypoxia in Spontaneously Diabetic Torii Fatty Rats","authors":"J. Tanabe, Y. Ogura, Mikie Nakabayashi, Y. Nagai, Shiika Watanabe, T. Sugaya, Keiichi Ohata, Daisuke Ichikawa, Kazuho Inoue, Seiko Hoshino, K. Kimura, Y. Shibagaki, Y. Ono, A. Kamijo-Ikemori","doi":"10.1159/000503926","DOIUrl":"https://doi.org/10.1159/000503926","url":null,"abstract":"Background: Renal hypoxia is an aggravating factor for tubulointerstitial damage, which is strongly associated with renal prognosis in diabetic kidney disease (DKD). Therefore, urinary markers that can detect renal hypoxia are useful for monitoring DKD. Objective: To determine the correlation between urinary liver-type fatty acid-binding protein (L-FABP) and renal hypoxia using a novel animal model of type 2 diabetes. Methods: Male spontaneously diabetic Torii (SDT) fatty rats (n = 6) were used as an animal model of type 2 diabetes. Age- and sex-matched Sprague-Dawley (SD) rats (n = 8) were used as controls. Body weight, systolic blood pressure, and blood glucose levels were measured at 8, 12, 16, and 24 weeks of age. Urine samples and serum and kidney tissues were collected at 24 weeks of age. Microvascular blood flow index (BFI) was measured using diffuse correlation spectroscopy before sampling both the serum and kidneys for the evaluation of renal microcirculation at the corticomedullary junction. Results: Obesity, hyperglycemia, and hypertension were observed in the SDT fatty rats. Focal glomerular sclerosis, moderate interstitial inflammation, and fibrosis were significantly more frequent in SDT fatty rats than in SD rats. While the frequency of peritubular endothelial cells and phosphoendothelial nitric oxide synthase levels were similar in both types of rats, the degree of renal hypoxia-inducible factor-1α (HIF-1α) expression was significantly higher (and with no change in renal vascular endothelial growth factor expression levels) in the SDT fatty rats. Urinary L-FABP levels were significantly higher and renal microvascular BFI was significantly lower in the SDT fatty rats than in the SD rats. Urinary L-FABP levels exhibited a significant positive correlation with renal HIF-1α expression and a significant negative correlation with renal microvascular BFI. Conclusions: Urinary L-FABP levels reflect the degree of renal hypoxia in DKD in a type 2 diabetic animal model. Urinary L-FABP may thus prove useful as a renal hypoxia marker for monitoring DKD in patients with type 2 diabetes in clinical practice.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77688263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Miao Lin, Huibin Huang, Jin Yao, Ji-xing Liang, Lian-tao Li, Wei Lin, Li-xiang Lin, F. Hong, Jieli Lu, Y. Bi, Weiqing Wang, J. Wen, Gang Chen
Background: Depression is prevalent in patients with all stages of CKD and is associated with adverse outcome. Abnormally elevated GFR, or hyperfiltration, may play a crucial role in the initiation and progression of CKD. However, the association between depression and hyperfiltration is not known. The aim of this study is to investigate the relationship between depression and hyperfiltration. Methods: This was an observational cross-sectional study. A total of 3,716 volunteers (1,303 males and 2,413 females) aged 40–75 years without CKD from a community in China were included for the study. Depressive symptoms and the presence of a minor or major depressive episode were assessed with the 9-item Patient Health Questionnaire (PHQ-9) and Diagnostic and Statistical Manual of Mental Disorders (4th edition)-based structured interview, respectively. Results: The mean age of the participants in the present study was 53.8 ± 9.0 years. 115 participants had clinically relevant depression, and 122 participants had a minor or major depressive episode. In a multivariable logistic regression analysis adjusted for potential confounders, the association between clinically relevant depression and renal hyperfiltration remained significant in men but not in women. As compared with men without depression (PHQ <5) or depressive episodes, those with clinically relevant depression (PHQ ≥10) had a significantly higher risk of renal hyperfiltration. The fully adjusted OR (95% CI) was 4.81 (1.62–14.30, p = 0.005), those with a major depressive episode had a higher risk of renal hyperfiltration (OR 7.45; 95% CI 2.04–27.21, p = 0.002). Conclusion: Depressive symptoms and major depressive episodes are associated with renal hyperfiltration in middle-aged and elderly Chinese men without CKD. Future studies are needed to verify and clarify the role of depression in the development of abnormally high eGFR and CKD.
背景:抑郁症在CKD各阶段患者中普遍存在，并与不良预后相关。异常升高的GFR或超滤过可能在CKD的发生和发展中起着至关重要的作用。然而，抑郁症和超滤过之间的关系尚不清楚。本研究旨在探讨抑郁症与高滤过症之间的关系。方法:这是一项观察性横断面研究。共有3716名志愿者(1303名男性和2413名女性)来自中国的一个社区，年龄在40-75岁之间，没有慢性肾病。采用9项患者健康问卷(PHQ-9)和基于结构化访谈的《精神障碍诊断与统计手册》(第四版)分别对抑郁症状和轻度或重度抑郁发作进行评估。结果:本研究参与者的平均年龄为53.8±9.0岁。115名参与者有临床相关的抑郁症，122名参与者有轻微或严重的抑郁发作。在一项针对潜在混杂因素进行调整的多变量logistic回归分析中，临床相关的抑郁症和肾高滤过之间的相关性在男性中仍然显著，但在女性中没有。与没有抑郁症(PHQ <5)或抑郁发作的男性相比，有临床相关性抑郁症(PHQ≥10)的男性发生肾高滤过的风险明显更高。完全调整后的OR (95% CI)为4.81 (1.62-14.30,p = 0.005)，重度抑郁发作的患者发生肾高滤过的风险更高(OR 7.45;95% CI 2.04 ~ 27.21, p = 0.002)。结论:中国中老年无CKD男性的抑郁症状和重度抑郁发作与肾高滤过有关。未来的研究需要验证和阐明抑郁症在异常高eGFR和CKD发展中的作用。
{"title":"Association between Depression and Renal Hyperfiltration in a General Chinese Population","authors":"Miao Lin, Huibin Huang, Jin Yao, Ji-xing Liang, Lian-tao Li, Wei Lin, Li-xiang Lin, F. Hong, Jieli Lu, Y. Bi, Weiqing Wang, J. Wen, Gang Chen","doi":"10.1159/000503922","DOIUrl":"https://doi.org/10.1159/000503922","url":null,"abstract":"Background: Depression is prevalent in patients with all stages of CKD and is associated with adverse outcome. Abnormally elevated GFR, or hyperfiltration, may play a crucial role in the initiation and progression of CKD. However, the association between depression and hyperfiltration is not known. The aim of this study is to investigate the relationship between depression and hyperfiltration. Methods: This was an observational cross-sectional study. A total of 3,716 volunteers (1,303 males and 2,413 females) aged 40–75 years without CKD from a community in China were included for the study. Depressive symptoms and the presence of a minor or major depressive episode were assessed with the 9-item Patient Health Questionnaire (PHQ-9) and Diagnostic and Statistical Manual of Mental Disorders (4th edition)-based structured interview, respectively. Results: The mean age of the participants in the present study was 53.8 ± 9.0 years. 115 participants had clinically relevant depression, and 122 participants had a minor or major depressive episode. In a multivariable logistic regression analysis adjusted for potential confounders, the association between clinically relevant depression and renal hyperfiltration remained significant in men but not in women. As compared with men without depression (PHQ <5) or depressive episodes, those with clinically relevant depression (PHQ ≥10) had a significantly higher risk of renal hyperfiltration. The fully adjusted OR (95% CI) was 4.81 (1.62–14.30, p = 0.005), those with a major depressive episode had a higher risk of renal hyperfiltration (OR 7.45; 95% CI 2.04–27.21, p = 0.002). Conclusion: Depressive symptoms and major depressive episodes are associated with renal hyperfiltration in middle-aged and elderly Chinese men without CKD. Future studies are needed to verify and clarify the role of depression in the development of abnormally high eGFR and CKD.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78486034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Acute kidney injury (AKI) is a clinical syndrome characterized by significant morbidity and a high death rate. Interleukin (IL)-27 is a newly described member of the IL-6/IL-12 heterodimeric cytokine family and displays anti-inflammatory and antiapoptotic properties. Objectives: To determine the effect and mechanism of IL-27 in AKI. Method: We used a mouse model of renal ischemia/reperfusion (I/R) injury to investigate whether IL-27 has a therapeutic potential for the treatment of AKI. For the IL-27 administration group, IL-27 protein was injected 1 h before ischemia. Human proximal tubular epithelial cells were exposed to ischemia for 2 h and followed by 2 h of reperfusion (I2h+R2h treatment) used as an in vitro model to investigate the effect of IL-27. Results: Two IL-27 subunits, Epstein-Barr virus gene 3 and p28, were upregulated in kidneys 24 h after I/R. Renal expression of IL-27 receptor subunits (gp130 and WSX-1) was also increased. Treatment with IL-27 reduced structural/functional damages, ameliorated renal inflammation, inhibited the cleaved caspase-3 expression, upregulated antiapoptotic protein Bcl-2 and downregulated proapoptotic protein Bax in the kidneys of mice subjected to I/R. Meanwhile, the level of IL-27 receptor on renal tubular epithelial cells was increased after I2h+R2h treatment, and IL-27 administration suppressed I2h+R2h-induced epithelial cell apoptosis. Furthermore, IL-27 treatment led to activation of signal transducer and activator of transcription 3 (STAT3) both in vivo and in vitro, and IL-27-mediated protection against I2h+R2h injury was abolished by STAT3 inhibition. Conclusions: IL-27 protects against renal I/R injury by activating STAT3, suggesting that IL-27 may represent a novel strategy for the treatment of AKI.
{"title":"Interleukin-27 Ameliorates Renal Ischemia-Reperfusion Injury through Signal Transducers and Activators of Transcription 3 Signaling Pathway","authors":"Peihui Zhou, Bo Deng, Ming Wu, F. Ding, Li Wang","doi":"10.1159/000503923","DOIUrl":"https://doi.org/10.1159/000503923","url":null,"abstract":"Background: Acute kidney injury (AKI) is a clinical syndrome characterized by significant morbidity and a high death rate. Interleukin (IL)-27 is a newly described member of the IL-6/IL-12 heterodimeric cytokine family and displays anti-inflammatory and antiapoptotic properties. Objectives: To determine the effect and mechanism of IL-27 in AKI. Method: We used a mouse model of renal ischemia/reperfusion (I/R) injury to investigate whether IL-27 has a therapeutic potential for the treatment of AKI. For the IL-27 administration group, IL-27 protein was injected 1 h before ischemia. Human proximal tubular epithelial cells were exposed to ischemia for 2 h and followed by 2 h of reperfusion (I2h+R2h treatment) used as an in vitro model to investigate the effect of IL-27. Results: Two IL-27 subunits, Epstein-Barr virus gene 3 and p28, were upregulated in kidneys 24 h after I/R. Renal expression of IL-27 receptor subunits (gp130 and WSX-1) was also increased. Treatment with IL-27 reduced structural/functional damages, ameliorated renal inflammation, inhibited the cleaved caspase-3 expression, upregulated antiapoptotic protein Bcl-2 and downregulated proapoptotic protein Bax in the kidneys of mice subjected to I/R. Meanwhile, the level of IL-27 receptor on renal tubular epithelial cells was increased after I2h+R2h treatment, and IL-27 administration suppressed I2h+R2h-induced epithelial cell apoptosis. Furthermore, IL-27 treatment led to activation of signal transducer and activator of transcription 3 (STAT3) both in vivo and in vitro, and IL-27-mediated protection against I2h+R2h injury was abolished by STAT3 inhibition. Conclusions: IL-27 protects against renal I/R injury by activating STAT3, suggesting that IL-27 may represent a novel strategy for the treatment of AKI.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84191520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Cardiac death is increased in peritoneal dialysis (PD) patients. Pulse wave velocity (PWV) is a measurement of arterial stiffness, and previous reports linked PWV to increased extracellular water (ECW). As cyclers and icodextrin are increasingly used, we wished to determine whether this association between PWV and ECW remains. Methods: We measured aortic PWV (aPWV) and bioimpedance (InBody, Seoul, South Korea) in consecutive PD patients attending for peritoneal membrane testing. Results: 189 patients were included, 62.4% male, mean age 63.1 ± 15.2 years, 45.3% diabetic, median dialysis duration 12.3 (6.5–25.1) months, 71.4% using cyclers, weight 73.0 ± 16.1 kg, systolic blood pressure 142 ± 21 mm Hg, aPWV 10.4 ± 5.1 m/s. aPWV was associated with pulse pressure (r = 0.26, p = 0.001), Davies comorbidity score (r = 0.18, p = 0.013), and N-terminal pro-brain-type natriuretic peptide (NTproBNP; r = 0.18, p = 0.011). Patients with aPWV ≥10 m/s were older (65.9 ± 13.6 vs. 60.1 ± 16.3 years, p < 0.01) with a higher ECW-to-total body water ratio (0.400 ± 0.012 vs. 0.396 ± 0.013, p < 0.05), but ECW/height was not different (8.52 ± 2.32 vs. 8.75 ± 1.78 L/m), as was NTproBNP (2,472 [788–5,422] vs. 1,234 [410–6,230] ng/L). On multivariable testing, aPWV was positively associated with β-blocker prescription (standardised β coefficient [Stβ] 0.3, 95% confidence limits [95% CL] 0.7–2.6, p = 0.001) and negatively with icodextrin prescription (Stβ 0.19, 95% CL –0.2 to –2.1, p = 0.04). Conclusions: Compared to previous studies, we did not find an independent association between aPWV and ECW and estimates of ECW excess, using the InBody bioimpedance device, suggesting that vascular stiffness in PD patients is more complex than simple ECW volume expansion in PD patients.
背景:腹膜透析(PD)患者心脏死亡增加。脉搏波速度(PWV)是动脉硬度的测量指标，以前的报道将PWV与细胞外水(ECW)的增加联系起来。随着循环剂和碘糊精的使用越来越多，我们希望确定PWV和ECW之间的这种关联是否仍然存在。方法:我们测量了连续参加腹膜检测的PD患者的主动脉PWV (aPWV)和生物阻抗(InBody, Seoul, South Korea)。结果:纳入189例患者，男性占62.4%，平均年龄63.1±15.2岁，糖尿病患者占45.3%，中位透析持续时间12.3(6.5-25.1)个月，71.4%使用循环器，体重73.0±16.1 kg，收缩压142±21 mm Hg, aPWV 10.4±5.1 m/s。aPWV与脉压(r = 0.26, p = 0.001)、Davies合并症评分(r = 0.18, p = 0.013)、n端脑型前利钠肽(NTproBNP;R = 0.18, p = 0.011)。aPWV≥10 m/s的患者年龄较大(65.9±13.6岁比60.1±16.3岁，p < 0.01)， ECW与全身水分比较高(0.400±0.012比0.396±0.013,p < 0.05)，但ECW/身高差异无统计学意义(8.52±2.32比8.75±1.78 L/m)， NTproBNP差异无统计学意义(2,472[788-5,422]比1,234 [10 - 6,230]ng/L)。在多变量检验中，aPWV与β受体阻滞剂处方呈正相关(标准化β系数[Stβ] 0.3, 95%置信限[95% CL] 0.7 ~ 2.6, p = 0.001)，与icodextrin处方呈负相关(Stβ 0.19, 95% CL -0.2 ~ -2.1, p = 0.04)。结论:与以往的研究相比，我们没有发现aPWV和ECW以及使用InBody生物阻抗装置估计ECW过量之间的独立关联，这表明PD患者的血管僵硬比PD患者简单的ECW体积扩张更复杂。
{"title":"Aortic Pulse Wave Velocity in Peritoneal Dialysis Patients Is Not Simply Associated with Extracellular Water Expansion","authors":"K. Tangvoraphonkchai, A. Davenport","doi":"10.1159/000503424","DOIUrl":"https://doi.org/10.1159/000503424","url":null,"abstract":"Background: Cardiac death is increased in peritoneal dialysis (PD) patients. Pulse wave velocity (PWV) is a measurement of arterial stiffness, and previous reports linked PWV to increased extracellular water (ECW). As cyclers and icodextrin are increasingly used, we wished to determine whether this association between PWV and ECW remains. Methods: We measured aortic PWV (aPWV) and bioimpedance (InBody, Seoul, South Korea) in consecutive PD patients attending for peritoneal membrane testing. Results: 189 patients were included, 62.4% male, mean age 63.1 ± 15.2 years, 45.3% diabetic, median dialysis duration 12.3 (6.5–25.1) months, 71.4% using cyclers, weight 73.0 ± 16.1 kg, systolic blood pressure 142 ± 21 mm Hg, aPWV 10.4 ± 5.1 m/s. aPWV was associated with pulse pressure (r = 0.26, p = 0.001), Davies comorbidity score (r = 0.18, p = 0.013), and N-terminal pro-brain-type natriuretic peptide (NTproBNP; r = 0.18, p = 0.011). Patients with aPWV ≥10 m/s were older (65.9 ± 13.6 vs. 60.1 ± 16.3 years, p < 0.01) with a higher ECW-to-total body water ratio (0.400 ± 0.012 vs. 0.396 ± 0.013, p < 0.05), but ECW/height was not different (8.52 ± 2.32 vs. 8.75 ± 1.78 L/m), as was NTproBNP (2,472 [788–5,422] vs. 1,234 [410–6,230] ng/L). On multivariable testing, aPWV was positively associated with β-blocker prescription (standardised β coefficient [Stβ] 0.3, 95% confidence limits [95% CL] 0.7–2.6, p = 0.001) and negatively with icodextrin prescription (Stβ 0.19, 95% CL –0.2 to –2.1, p = 0.04). Conclusions: Compared to previous studies, we did not find an independent association between aPWV and ECW and estimates of ECW excess, using the InBody bioimpedance device, suggesting that vascular stiffness in PD patients is more complex than simple ECW volume expansion in PD patients.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91371019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Magda Fliszkiewicz, M. Niemczyk, Andrzej Kulesza, A. Łabuś, L. Pączek
Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent monogenic renal disease with a prevalence of 1:1,000 births and it is the 4th most common cause of dialysis-dependent end-stage renal disease (ESDR). Recent reports suggest an association between APDKD and metabolic derangements, particularly impaired glucose metabolism. Methods: In this cross-sectional study we analyzed data obtained from case records of 189 patients with ADPKD, including kidney transplant recipients, managed in an outpatient department. Results: The mean BMI was 25.4 ± 3.9; 25.25 before and 27.7 after transplantation. A fasting glucose level above 100 mg/dL (5.6 mmol/L) was observed in 60 patients (29%) – 27% without transplantation and 41% kidney transplant recipients. Diabetes mellitus was diagnosed in 17 patients (8.9%), including 3 (2.3%) without a history of transplantation and 14 (24.1%) after kidney transplantation (p < 0.01). We observed dyslipidemia in 30% and hyperuricemia in 53% of patients. Conclusion: Demonstrated metabolic abnormalities should be considered in maintenance of ADPKD patients, including kidney transplant recipients.
{"title":"Glucose and Lipid Metabolism Abnormalities among Patients with Autosomal Dominant Polycystic Kidney Disease","authors":"Magda Fliszkiewicz, M. Niemczyk, Andrzej Kulesza, A. Łabuś, L. Pączek","doi":"10.1159/000503423","DOIUrl":"https://doi.org/10.1159/000503423","url":null,"abstract":"Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent monogenic renal disease with a prevalence of 1:1,000 births and it is the 4th most common cause of dialysis-dependent end-stage renal disease (ESDR). Recent reports suggest an association between APDKD and metabolic derangements, particularly impaired glucose metabolism. Methods: In this cross-sectional study we analyzed data obtained from case records of 189 patients with ADPKD, including kidney transplant recipients, managed in an outpatient department. Results: The mean BMI was 25.4 ± 3.9; 25.25 before and 27.7 after transplantation. A fasting glucose level above 100 mg/dL (5.6 mmol/L) was observed in 60 patients (29%) – 27% without transplantation and 41% kidney transplant recipients. Diabetes mellitus was diagnosed in 17 patients (8.9%), including 3 (2.3%) without a history of transplantation and 14 (24.1%) after kidney transplantation (p < 0.01). We observed dyslipidemia in 30% and hyperuricemia in 53% of patients. Conclusion: Demonstrated metabolic abnormalities should be considered in maintenance of ADPKD patients, including kidney transplant recipients.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86619308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alejandra García-García, P. Demelo-Rodríguez, L. Ordieres-Ortega, E. Cervilla-Muñoz, Irene García-Fernández-Bravo, M. Pulfer, Ana López-Aparicio, F. Galeano-Valle, J. del Toro-Cervera
Background: There is limited evidence on the etiology and outcomes of renal infarction. A provoking factor is identified only in one- to two-thirds of patients. Methods: This is a retrospective observational study. The clinical characteristics and outcomes of patients with acute renal infarction were studied; the sample was divided into two groups according to the presence of at least one provoking factor at the time of diagnosis (atrial fibrillation, flutter, major thrombophilia, or renal artery malformations). Results: The study comprised 59 patients with a mean age of 63 (±16.7) years and a follow-up period of 3.1 (±2.8) years. An identifiable provoking factor was found for 59.3% of the renal infarctions at the time of diagnosis, and atrial fibrillation was the most frequent one (in 49.2% of all patients). Renal impairment was found in 49.2% of the patients at diagnosis and in 50.8% of the patients 6 months after the event (p = 0.525). When compared with the idiopathic group, the patients with provoked infarction were older (69.8 vs. 57.9 years, p = 0.014) and had a higher rate of recurrence of arterial thrombosis during follow-up (18.8 vs. 0%, p = 0.028), but there were no differences in the rest of the baseline characteristics or in mortality rates. Six patients (10.2%) in the idiopathic group were diagnosed with atrial fibrillation during follow-up. Conclusions: Atrial fibrillation, both at diagnosis and at follow-up, is the most common identifiable cause of renal infarction; however, a significant number of patients are idiopathic, and these are younger, but they have a similar burden of cardiovascular disease and a lower risk of arterial recurrence.
{"title":"Idiopathic versus Provoked Renal Infarction: Characteristics and Long-Term Follow-Up of a Cohort of Patients in a Tertiary Hospital","authors":"Alejandra García-García, P. Demelo-Rodríguez, L. Ordieres-Ortega, E. Cervilla-Muñoz, Irene García-Fernández-Bravo, M. Pulfer, Ana López-Aparicio, F. Galeano-Valle, J. del Toro-Cervera","doi":"10.1159/000503425","DOIUrl":"https://doi.org/10.1159/000503425","url":null,"abstract":"Background: There is limited evidence on the etiology and outcomes of renal infarction. A provoking factor is identified only in one- to two-thirds of patients. Methods: This is a retrospective observational study. The clinical characteristics and outcomes of patients with acute renal infarction were studied; the sample was divided into two groups according to the presence of at least one provoking factor at the time of diagnosis (atrial fibrillation, flutter, major thrombophilia, or renal artery malformations). Results: The study comprised 59 patients with a mean age of 63 (±16.7) years and a follow-up period of 3.1 (±2.8) years. An identifiable provoking factor was found for 59.3% of the renal infarctions at the time of diagnosis, and atrial fibrillation was the most frequent one (in 49.2% of all patients). Renal impairment was found in 49.2% of the patients at diagnosis and in 50.8% of the patients 6 months after the event (p = 0.525). When compared with the idiopathic group, the patients with provoked infarction were older (69.8 vs. 57.9 years, p = 0.014) and had a higher rate of recurrence of arterial thrombosis during follow-up (18.8 vs. 0%, p = 0.028), but there were no differences in the rest of the baseline characteristics or in mortality rates. Six patients (10.2%) in the idiopathic group were diagnosed with atrial fibrillation during follow-up. Conclusions: Atrial fibrillation, both at diagnosis and at follow-up, is the most common identifiable cause of renal infarction; however, a significant number of patients are idiopathic, and these are younger, but they have a similar burden of cardiovascular disease and a lower risk of arterial recurrence.","PeriodicalId":17810,"journal":{"name":"Kidney and Blood Pressure Research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81611493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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