scholarly journals Impaired Retinal Vessel Dilation Predicts Mortality in End-Stage Renal Disease

2019 ◽  
Vol 124 (12) ◽  
pp. 1796-1807 ◽  
Author(s):  
Roman Günthner ◽  
Henner Hanssen ◽  
Christine Hauser ◽  
Susanne Angermann ◽  
Georg Lorenz ◽  
...  

Rationale : Patients with end-stage renal disease are characterized by increased cardiovascular and all-cause mortality because of advanced remodeling of the macrovascular and microvascular beds. Objective : The aim of this study was to determine whether retinal microvascular function can predict all-cause and cardiovascular mortality in patients with end-stage renal disease. Methods and Results : In the multicenter prospective observational ISAR study (Risk Stratification in End-Stage Renal Disease), data on dynamic retinal vessel analysis were available in a subcohort of 214 dialysis patients (mean age, 62.6±15.0; 32% women). Microvascular dysfunction was quantified by measuring maximum arteriolar dilation and maximum venular dilation (vMax) of retinal vessels in response to flicker light stimulation. During a mean follow-up of 44 months, 55 patients died, including 25 cardiovascular and 30 noncardiovascular fatal events. vMax emerged as a strong independent predictor for all-cause mortality. In the Kaplan-Meier analysis, individuals within the lowest tertile of vMax showed significantly shorter 3-year survival rates than those within the highest tertile (66.9±5.8% versus 92.4±3.3%). Univariate and multivariate hazard ratios for all-cause mortality per SD increase of vMax were 0.62 (0.47–0.82) and 0.65 (0.47–0.91), respectively. Maximum arteriolar dilation and vMax were able to significantly predict nonfatal and fatal cardiovascular events (hazard ratio, 0.74 [0.57–0.97] and 0.78 [0.61–0.99], respectively). Conclusions : Our results provide the first evidence that impaired retinal venular dilation is a strong and independent predictor of all-cause mortality in hemodialyzed end-stage renal disease patients. Dynamic retinal vessel analysis provides added value for prediction of all-cause mortality and may be a novel diagnostic tool to optimize cardiovascular risk stratification in end-stage renal disease and other high-risk cardiovascular cohorts. Clinical Trial Registration : URL: http://www.clinicaltrials.gov . Unique identifier: NCT01152892.

2012 ◽  
Vol 101 (2) ◽  
pp. 138-143 ◽  
Author(s):  
F. Biancari ◽  
E. Arvela ◽  
M. Korhonen ◽  
M. Söderström ◽  
K. Halmesmäki ◽  
...  

Objectives: This study was planned to evaluate the prognostic impact of end-stage renal disease (ESRD) in patients with critical leg ischemia (CLI) undergoing infrainguinal revascularization. Materials and Methods: 1425 patients who underwent infrainguinal revascularization for CLI were the subjects of the present analysis. Ninety-five patients had ESRD (eGFR < 15 ml/min/m2), and of them 66 (70%) underwent percutaneous transluminal angioplasty and 29 (30%) underwent bypass surgery. Results: ESRD patients had significantly lower overall survival (at 3-year, 27.1% vs. 59.7%, p < 0.0001), leg salvage (at 3-year, 57.7% vs. 83.0%, p<0.0001), and amputation free survival (at 3-year, 16.2% vs. 52.9%, p < 0.0001) than patients with no or less severe renal failure. The difference in survival was even greater between 86 one-to-one propensity matched pairs (at 3-year, 23.1% vs. 67.3%, p < 0.0001). ESRD was an independent predictor of all-cause mortality (RR 2.46, 95%CI 1.85–3.26). Logistic regression showed that age ≥ 75 years was the only independent predictor of 1-year all-cause mortality (OR 4.92, 95%CI 1.32–18.36). Classification and regression tree analysis showed that age ≥ 75 years and, among younger patients, bypass surgery for leg ulcer and gangrene were associated with significantly higher 1-year mortality. Conclusions: Lower limb revascularization in patients with CLI and end-stage renal failure is associated with favourable leg salvage. However, these patients have a very poor survival and this may jeopardize any attempt of revascularization. Further studies are needed to identify ESRD patients with acceptable life expectancy and who may benefit from lower limb revascularization.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hung-Chieh Yeh ◽  
I.-Wen Ting ◽  
Han-Chun Huang ◽  
Hsiu-Yin Chiang ◽  
Chin-Chi Kuo

AbstractCurrent acute kidney injury (AKI) diagnostic criteria are restricted to the inpatient setting. We proposed a new AKI diagnostic algorithm for the outpatient setting and evaluate whether outpatient AKI (AKIOPT) modifies the disease course among patients with chronic kidney disease (CKD) enrolled in the national predialysis registry. AKIOPT was detected when a 50% increase in serum creatinine level or 35% decline in eGFR was observed in the 180-day period prior to enrollment in the predialysis care program. Outcomes were progression to end-stage renal disease (ESRD) and all-cause mortality. Association analyses were performed using multiple Cox regression and coarsened exact matching (CEM) analysis. Among 6,046 patients, 31.5% (1,905 patients) had developed AKIOPT within the 180-day period before enrollment. The adjusted hazard ratios of the 1-year and overall risk of ESRD among patients with preceding AKIOPT compared with those without AKIOPT were 2.61 (95% CI: 2.15–3.18) and 1.97 (1.72–2.26), respectively. For 1-year and overall risk of all-cause mortality, patients with AKIOPT had respectively a 141% (95% CI: 89–209%) and 84% (56–117%) higher risk than those without AKIOPT. This statistical inference remained robust in CEM analysis. We also discovered a complete reversal in the eGFR slope before and after the AKIOPT from −10.61 ± 0.32 to 0.25 ± 0.30 mL/min/1.73 m2 per year; however, the loss of kidney function is not recovered. The new AKIOPT diagnostic algorithm provides prognostic insight in patients with CKD.


Diabetes Care ◽  
2015 ◽  
Vol 38 (5) ◽  
pp. 883-890 ◽  
Author(s):  
Nicolae M. Panduru ◽  
Markku Saraheimo ◽  
Carol Forsblom ◽  
Lena M. Thorn ◽  
Daniel Gordin ◽  
...  

2015 ◽  
Vol 88 (5) ◽  
pp. 1178-1186 ◽  
Author(s):  
Cécile G. Couchoud ◽  
Jean-Baptiste R. Beuscart ◽  
Jean-Claude Aldigier ◽  
Philippe J. Brunet ◽  
Olivier P. Moranne

Medicine ◽  
2015 ◽  
Vol 94 (47) ◽  
pp. e2113 ◽  
Author(s):  
Yueh-Han Hsu ◽  
Peir-Haur Hung ◽  
Chih-Hsin Muo ◽  
Wen-Chen Tsai ◽  
Chih-Cheng Hsu ◽  
...  

2021 ◽  
Author(s):  
Susana Rocha ◽  
Maria João Valente ◽  
Susana Coimbra ◽  
Cristina Catarino ◽  
Petronila Rocha-Pereira ◽  
...  

Abstract Chronic inflammation plays an important role in the progression and outcome of chronic kidney disease (CKD). The inflammatory biomarkers interleukin-6 (IL6) and pentraxin 3 (PTX3) are enhanced in CKD patients and associated with progression of the disease and higher risk for cardiovascular events, the major cause of death in these patients. Our aim was to study how the polymorphisms of their encoding genes affect the inflammatory response and outcome of end-stage renal disease (ESRD) patients on dialysis. We analyzed two single nucleotide polymorphisms (SNP), the IL6 (rs1800795) polymorphism in the promoter region (-174G/C), and the PTX3 polymorphism in the intron 1 (+ 281A/G), in ESRD patients on dialysis and in heathy individuals. The allelic frequencies, genotype distribution and their association with the circulating levels of the inflammatory markers high sensitivity C-reactive protein (hsCRP), interleukin (IL6), growth differentiation factor 15 (GDF15) and PTX3, were determined in ESRD patients; events of death were recorded along one year to evaluate all-cause mortality and the association between inflammation and the studied polymorphisms. The allelic frequencies and genotyping distribution for IL6 and PTX3 in controls and ESRD patients were similar and in agreement with European reports. For the IL6 polymorphism, we found an association of the GG and CC genotype with higher IL6 levels; the CC genotype showed also high PTX3, hsCRP and GDF15 levels. For the PTX3 polymorphism, the AA genotype was linked to the highest values of hsCRP and IL6. The mortality rate after 1-year follow-up was 10.4%. The CC genotype (IL6 polymorphism), in deceased patients, was associated to increased levels of hsCRP, IL6 and PTX3, with low levels of GDF15 and with a highest mortality risk. The AA genotype for PTX3 polymorphism, in spite of the enhancement in inflammation, showed no significant impact on mortality. Our results show that the CC genotype of the IL6 polymorphism was associated with an enhanced inflammatory state and a poorer survival rate. Both IL6 and PTX3 polymorphisms seem to modulate the inflammatory response and, therefore, disease progression and outcome. Our data also highlights the importance of research on genetic variants that, although less frequent, may have significant biological value.


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