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

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.

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang

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.


Author(s):  
Shahida Akhter ◽  
A. S. M. Rizwan

Background: Hyperuricaemia is a metabolic marker of decreased renal function in chronic kidney disease (CKD). It increases cardiovascular, cerebrovascular and mortality risk in patients with CKD. Objectives: To estimate serum uric acid level in different stages of CKD. Methods: The present study was a cross sectional analytical study and was conducted in the Department of Physiology, Dhaka Medical College, Dhaka from July 2012 to June 2013 on 300 participants. They were divided into group A (150 control healthy participants) and group B (150 diagnosed cases of CKD). Serum creatinine and serum uric acid levels were measured by auto analyzer in Department of Pathology, Dhaka Medical College. Estimated glomerular filtration rate (eGFR) was calculated from serum creatinine level by Modification of Diet in Renal Disease (MDRD) equation. For statistical analysis unpaired Student “t” test, one way ANOVA test, Bonferroni test, Pearson’s correlation coefficient (r) test and Linear regression were performed using SPSS for windows version 20. Result: In this study, serum uric acid level was significantly (p<0.05) higher and eGFR were significantly lower in study groups than that of control group. There was gradual rise of serum uric acid level in CKD subjects from stage I to V. A significant inverse correlation was observed between serum uric acid level and eGFR. Serum uric acid level increased 0.048 mg/dl for each ml/min/1.73m2 decrease of eGFR. Conclusion: This study concludes that serum uric acid level increases gradually in accordance with the higher stages of CKD. There is a negative correlation of serum uric acid with eGFR in all stages of CKD which was statistically significant (p<0.05). Screening of serum uric acid level in different stages of CKD may be beneficial for assessing renal damage as well as prediction of co-morbidities associated with it.


2011 ◽  
Vol 33 (4) ◽  
pp. 298-304 ◽  
Author(s):  
Mehmet Kanbay ◽  
Mahmut Ilker Yilmaz ◽  
Alper Sonmez ◽  
Faruk Turgut ◽  
Mutlu Saglam ◽  
...  

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
JIWON RYU ◽  
Chung Sik Lee ◽  
Sejoong Kim ◽  
Ran-Hui Cha ◽  
Hajeong Lee, ◽  
...  

Abstract Background and Aims Serum uric acid (UA) is associated with renal disease. Hyperuricemia can be a risk of hypertension, intrarenal vascular disease and renal injury. We investigate the serum UA has an association with renal disease progression in patients with chronic kidney disease (CKD) with hypertension. Method We recruited 270 CKD patients with hypertension from 4 centers in Korea through the APrODiTe study and followed for 1 year. Serum UA was evaluated as a continuous value and groups divided by quartiles. The renal outcomes were an increase in random urine protein/creatinine ratio (PCR) than baseline value or estimated glomerular filtration rate (eGFR) deterioration which means a decrease in eGFR ≥ 5 (ml/min/1.73m2). Results Baseline serum UA was 6.58 ± 1.73 mg/dl and 6.52 ± 3.59 mg/dl after 1 year. For proteinuria progression, a 1 mg/dl higher serum UA has independent correlation in multivariate regression (odds ratio (OR): 1.272; 95% confidence interval (CI): 1.031-1.568; P = 0.024). The higher quartile of serum UA showed a correlation with the odd ratio than lower quartile (OR: 2.243; 95% CI: 0.862-5.837; P = 0.098, OR:3.417; 95% CI: 1.275-9.152; P= 0.015, OR: 2.754; 95% CI: 1.013-7.488; P &lt; 0.047). In subgroup analysis, the patients with late CKD stage (3-5) showed serum UA has a positive correlation with proteinuria progression (OR: 1.311; 95% CI: 1.022-1.682; P= 0.033) and the top quartile group was correlated with the increased odds ratio compared to lower quartile (OR: 3.811; 95% CI: 1.153-12.59; P = 0.028). For eGFR deterioration, the higher quartile of UA was positively correlated with the odd ratio in only univariate analysis. Conclusion Serum UA level has an independent correlation with proteinuria progression in especially late CKD patient with hypertension. Whereas for eGFR deterioration, serum UA did not show a significant correlation.


2017 ◽  
Vol 266 ◽  
pp. 121-127 ◽  
Author(s):  
Yuta Matsukuma ◽  
Kosuke Masutani ◽  
Shigeru Tanaka ◽  
Akihiro Tsuchimoto ◽  
Naoki Haruyama ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Vigil ◽  
Emilia Condés ◽  
Luis Vigil ◽  
Paloma Gallar ◽  
Aniana Oliet ◽  
...  

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.


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