Aspirin for Primary Prevention of Cardiovascular Disease and Renal Disease Progression in Chronic Kidney Disease Patients: a Multicenter Randomized Clinical Trial (AASER Study)

2018 ◽  
Vol 32 (3) ◽  
pp. 255-263 ◽  
Author(s):  
Marian Goicoechea ◽  
Soledad García de Vinuesa ◽  
Borja Quiroga ◽  
Eduardo Verde ◽  
Carmen Bernis ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Trial ◽  
Chronic Kidney Disease ◽  
Primary Prevention ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Randomized Clinical Trial ◽  
Renal Disease Progression ◽  
Prevention Of Cardiovascular Disease

scholarly journals Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Reciprocal Relationship ◽  
Current Evidence ◽  
Renal Disease Progression ◽  
Lowering Therapy ◽  
The Relationship

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

Effect of Urate Lowering Therapy on Renal Disease Progression in Hyperuricemic Patients with Chronic Kidney Disease

2015 ◽  
Vol 42 (11) ◽  
pp. 2143-2148 ◽  
Author(s):  
Yoonjin Kim ◽  
Sungjoon Shin ◽  
Kyungsoo Kim ◽  
Sangtae Choi ◽  
Kwanghoon Lee
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Serum Uric Acid ◽  
Serum Uric Acid Level ◽  
Renal Disease Progression ◽  
Time Curve ◽  
Lowering Therapy

Objective.To determine whether urate lowering therapy (ULT) could delay renal disease progression in hyperuricemic patients with chronic kidney disease (CKD).Methods.We performed a retrospective review of hyperuricemic patients with stage 3 CKD followed from September 2005 to July 2014 in Dongguk University Ilsan Hospital, Goyang, Korea. A total of 158 eligible patients were identified and 65 of them were treated with ULT in addition to the usual CKD management. We divided the patients according to the use of ULT and compared the estimated glomerular filtration rate (eGFR) change from baseline value and the proportion of renal disease progression (decline of eGFR > 30% of the baseline value, initiation of dialysis or eGFR < 15 ml/min/1.73m2) at the time of last followup. Risk factors for renal disease progression were identified by logistic regression analysis.Results.After a median followup of 118.5 weeks (minimum 25, maximum 465), the ULT group showed better outcomes compared to the non-ULT group in terms of eGFR change from baseline (−1.19 ± 12.07 vs −7.37 ± 11.17 ml/min/1.73 m2, p = 0.001) and the proportion of renal disease progression (12.3% vs 27.9%, p = 0.01). Goal-directed ULT showed better clinical outcomes compared to maintaining the initial ULT dose. Actual (area under the SUA-time curve adjusted by total observation time period) serum uric acid was significantly associated with the risk of renal disease progression (p for trend = 0.04) and actual serum uric acid level < 7 mg/dl reduced the risk of renal disease progression by 69.4%.Conclusion.ULT significantly delayed renal disease progression in hyperuricemic patients with CKD. Goal-directed ULT seems to be better than continuing the initial ULT prescription.

scholarly journals Cystatin C as a Predictor of Mortality and Cardiovascular Events in a Population with Chronic Kidney Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Vigil ◽  
Emilia Condés ◽  
Luis Vigil ◽  
Paloma Gallar ◽  
Aniana Oliet ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Cystatin C ◽  
Cardiovascular Events ◽  
Interquartile Range ◽  
Renal Disease Progression ◽  
The Third ◽  
Overall Mortality

Background. We examine whether cystatin C, a surrogate marker of renal function, could identify patients with chronic kidney disease (CKD) with an increased risk of renal disease progression, death, or cardiovascular events.Methods. Data were obtained for 180 patients, with a diagnosis of chronic renal failure based on serum creatinine estimated glomerular filtration rate (eGFRcreat) <90 mL/min/1.73 m2. This population was grouped in tertiles according to cystatin C and creatinine values at baseline. Cardiovascular events and overall mortality were estimated for each tertile. Predictors of overall mortality and for the development of renal disease progression were analyzed.Results. The median age was 75 years (interquartile range 69–82) and the median eGFRcreat38 mL/min m2(interquartile range 33–49). Overall mortality was lower on the first and on the second tertiles of cystatin C than on the third one (HR = 0.060; 95% CI: 0.008–0.447 and HR = 0.094; 95% CI: 0.022–0.406, resp.). Deaths related to the creatinine tertiles followed the same pattern, but differences were not as large. Cardiovascular mortality was lower on the second than on the third cystatin C tertile (HR = 0.198; 95% CI: 0.040–0.987), but it did not show differences on the first and the second creatinine tertiles compared with the third one (HR = 0.126; 95% CI: 0.013–1.265 and HR = 0.403; 95% CI: 0.093–1.740). The only independent predictors of mortality during followup were baseline cystatin C (OR = 0.100; 95% CI: 0.021–0.463) and baseline uric acid (OR = 1.377; 95% CI: 1.070–1.773).Conclusion. Cystatin C may be an alternative to creatinine for detecting a high risk of death and cardiovascular events in a population with CKD.

Aspirin in the primary prevention of cardiovascular disease in individuals with chronic kidney disease: a systematic review and meta-analysis

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
S Pallikadavath ◽  
L Ashton ◽  
J Burton ◽  
N Brunskill ◽  
L Gray ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Primary Prevention ◽  
Kidney Disease ◽  
Meta Analysis ◽  
Minor Bleeding ◽  
Bleeding Events ◽  
All Cause Mortality ◽  
Randomised Controlled ◽  
Prevention Of Cardiovascular Disease

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Cardiovascular disease (CVD) is a major cause of morbidity and mortality in individuals with chronic kidney disease (CKD). Aspirin is widely used in secondary prevention of cardiovascular disease. Its use in primary prevention, particularly in CKD, is less clear. Previous reviews have offered inconclusive findings for the benefit of aspirin in CKD. Recent trials have been completed that may help provide more conclusive answers in CKD. Purpose This study aimed to assess the role of aspirin in the primary prevention of CVD and its associated adverse events in individuals with CKD. Methods A pre-defined protocol registered with PROSPERO (CRD42014008860) was used. The OVID Medline and EMBASE databases were searched for studies from 1996 to the 15th September 2020. Abstracts and full-texts were screened independently by two reviewers. Randomised controlled trials that compared aspirin to placebo in individuals with non-endstage CKD without CVD nor primary renal disease were included. The primary outcomes of interests were: CVD, major and minor bleeding events. Secondary outcomes of interest were: all-cause mortality, coronary artery disease and stroke. A meta-analysis was conducted using a random-effects model to calculate a pooled relative risk (RR). Results Five trials were included with 434 CVD events in 7,825 individuals with CKD. Aspirin offered no statistically significant benefit in reduction of CVD events (RR = 0.79, 95%CI: 0.57, 1.09) but significantly increased both minor (RR = 2.62, 95%CI: 1.64, 4.20) and major bleeding (RR= 1.51, 95%CI: 1.13, 2.02) events compared to placebo. Aspirin conferred no benefit for all-cause mortality (RR= 0.89, 95%CI: 0.64, 1.22), coronary heart disease (RR= 0.66, 95%CI: 0.27, 1.63) and stroke (RR= 0.94, 95%CI: 0.55, 1.58). Conclusion Aspirin cannot be recommended for the primary prevention of CVD in individuals with CKD as it offers no conclusive benefit and increases the risk of bleeding. Other strategies to optimise CVD primary prevention in individuals with CKD should be prioritised.

scholarly journals The Severity of Diabetic Retinopathy Is an Independent Factor for the Progression of Diabetic Nephropathy

2020 ◽  
Vol 10 (1) ◽  
pp. 3
Author(s):  
Shi-Chue Hsing ◽  
Chia-Cheng Lee ◽  
Chin Lin ◽  
Jiann-Torng Chen ◽  
Yi-Hao Chen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Retinopathy ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Renal Disease Progression ◽  
Hazard Ratios ◽  
Stage Renal Disease ◽  
End Stage

(1) Background: It has rarely been studied whether the severity of diabetic retinopathy (DR) could influence renal disease progression in end-stage renal disease (ESRD) and chronic kidney disease (CKD) in patients with type 2 diabetes. The aim of this study was to evaluate renal disease progression in ESRD and CKD according to DR severity in patients with type 2 diabetes. (2) Methods: We included 1329 patients and divided the cohort into two end-points. The first was to trace the incidence of ESRD in all enrolled participants and the other was to follow their progression to CKD. (3) Results: Significantly higher crude hazard ratios (HRs) of ESRD incidence in all enrolled participants were noted, and this ratio increased in a stepwise fashion. However, after adjustment, DR severity was not associated with ESRD events. Therefore, a subgroup of 841 patients without CKD was enrolled to track their progression to CKD. Compared with no diabetic retinopathy, the progression of CKD increased in a stepwise fashion, from mild nonproliferative diabetic retinopathy (NPDR) to moderate NPDR, to severe NPDR and to proliferative diabetic retinopathy (PDR), both in the crude and adjusted models. (4) Conclusions: The severity of retinopathy appeared to be associated with renal lesions and the development of CKD. Our findings suggest that the severity of DR is a risk factor for progression to CKD. Therefore, diabetic retinopathy is useful for prognosticating the clinical course of diabetic kidney disease.

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