scholarly journals GENOTYPE-GUIDED P2Y12 INHIBITION FOLLOWING PCI BENEFITS CYP2C19 LOSS OF FUNCTION PATIENTS WITH NORMAL RENAL FUNCTION COMPARED TO THOSE WITH CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 77 (18) ◽  
pp. 30
Author(s):  
Roy Mathew ◽  
Mandeep Sidhu ◽  
Michael Farkouh ◽  
Charanjit Rihal ◽  
Ryan Lennon ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cheng-Kai Hsu ◽  
Tai-Shuan Lai ◽  
Yih-Ting Chen ◽  
Yi-Ju Tseng ◽  
Chin-Chan Lee ◽  
...  

AbstractAssociations between hepatitis C virus (HCV) and chronic kidney disease (CKD) have been reported; however, differences of renal progression between general and CKD population remain to be elucidated in prospective studies. A total of 1179 participants, who have tested for anti-HCV antibody, were enrolled and prospectively followed for 3 years. The risks associated with HCV infection, in terms of incidence of CKD, annual estimated glomerular filtration rate (eGFR) changes and 50% decline of eGFR at 3-year from baseline, were compared between normal renal function subjects and CKD patients. Overall, 111 of 233 (47.6%) CKD patients and 167 of 946 (17.7%) non-CKD subjects had HCV infection. The crude incidence rates of CKD were 226.9 per 1000 person-years and 14.8 per 1000 person-years in in HCV and non-HCV infected patients, respectively. The adjusted hazard ratio of HCV infection for incident CKD was 7.9 (95% CI 5–12.7). The HCV-infected normal renal function subjects were independently associated with increased risks of eGFR decline in the 1-year, 2-year and 3-year, respectively. The risk associations remained significant in 50% decline of eGFR at 3 years models and in different subgroup analyses. The increases of risks of eGFR decline were also notorious among overall HCV-infected CKD patients. However, the risk associations were less prominent in subgroup analyses (elderly, women and diabetic patients). The findings highlighted the importance of viral diagnosis with not only prognostic but also public health implications for preserving kidney function.


2018 ◽  
Vol 8 (3) ◽  
pp. 228-236 ◽  
Author(s):  
Ik Jun Choi ◽  
Sungmin Lim ◽  
Eun-Ho Choo ◽  
Jin-Jin Kim ◽  
Byung-Hee Hwang ◽  
...  

Aim: The aim of this study was to assess the combined effects of chronic kidney disease (CKD) and diabetes on the extent and developmental pattern of coronary artery disease (CAD). Methods: A total of 3,017 self-referred asymptomatic individuals without known CAD who underwent 64-channel dual-source coronary computed tomography angiography between 2006 and 2010 were enrolled. The patients were divided into six groups based on their diabetes status (nondiabetic or diabetic) and estimated glomerular filtration rate (eGFR) (eGFR > 90 mL/min/1.73 m2, normal renal function; eGFR 60–89, mild CKD; or eGFR 30–59, moderate CKD). We compared the coronary artery calcium score (CACS), segment stenosis score (SSS), and ≥50% obstructive CAD among the groups. Results: In nondiabetics, whereas SSS and ≥50% obstructive CAD were not different as renal function deteriorated, after adjusting for cardiovascular risk factors, CACS showed a unique developmental pattern: no CACS increase until mild CKD, but abrupt increase from the stage of moderate CKD (moderate vs. normal renal function, adjusted OR 5.118, 95% CI 1.293–20.262, p = 0.020). In diabetics, patients from the stage of mild CKD were more likely to have ≥50% obstructive CAD (p = 0.004), higher CACS (p = 0.020), and SSS (p = 0.001) in multivariable analysis. Conclusions: The presence of CKD did not have a significant impact on the development of coronary atherosclerosis, but affected the progression of coronary calcification more markedly from the stage of moderate CKD in nondiabetics. However, in diabetics, the deterioration of renal function was significantly associated with the development of coronary atherosclerosis and calcification from the stage of mild CKD.


2021 ◽  
pp. 1-9
Author(s):  
Hyo-Sun You ◽  
Sang-Jun Shin ◽  
Joungyoun Kim ◽  
Hee-Taik Kang

<b><i>Introduction:</i></b> Dyslipidemia is a known risk factor for chronic kidney disease (CKD). The effects of statins on CKD have already been studied in patients with CKD; however, data on the general population are limited. This study aimed to determine the relationship between statin use and the incidence of CKD in patients with hypercholesterolemia having normal renal function. <b><i>Methods:</i></b> A total of 7,856 participants aged 40–79 years at baseline (2009–2010) were included in the final analyses. The participants were divided into statin users (<i>n</i> = 4,168) and statin nonusers (<i>n</i> = 3,668), according to the statin usage. The Cox proportional hazard regression model was used to evaluate the adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for CKD. <b><i>Results:</i></b> The median follow-up duration was 5.8 years. A total of 543 cases of CKD (285 cases in males and 258 cases in females) occurred during the study period. The estimated cumulative incidence of CKD was significantly different between male statin nonusers and users (<i>p</i> &#x3c; 0.001), while it was not statistically significant between female statin nonusers and users (<i>p</i> = 0.126). Compared with statin nonusers, the fully adjusted HRs (95% CIs) for CKD in statin users were 1.014 (0.773–1.330) in males and 1.117 (0.843–1.481) in females. <b><i>Conclusion:</i></b> Dyslipidemia is an obvious risk factor for CKD; however, statin use in patients with hypercholesterolemia having normal renal function does not demonstrate a clear relationship with the incidence of CKD.


2018 ◽  
Vol 93 (4) ◽  
pp. 921-931 ◽  
Author(s):  
Chang-Yun Yoon ◽  
Juhwan Noh ◽  
Jinae Lee ◽  
Youn Kyung Kee ◽  
Changhwan Seo ◽  
...  

2010 ◽  
Vol 212 (1) ◽  
pp. 345-350 ◽  
Author(s):  
Hirofumi Tomiyama ◽  
Hirofumi Tanaka ◽  
Hideki Hashimoto ◽  
Chisa Matsumoto ◽  
Mari Odaira ◽  
...  

2018 ◽  
Vol 115 (21) ◽  
pp. E4910-E4919 ◽  
Author(s):  
Juanjuan Zhao ◽  
Katherine Lupino ◽  
Benjamin J. Wilkins ◽  
Chengxiang Qiu ◽  
Jian Liu ◽  
...  

Mitochondrial dysfunction is increasingly recognized as a critical determinant of both hereditary and acquired kidney diseases. However, it remains poorly understood how mitochondrial metabolism is regulated to support normal kidney function and how its dysregulation contributes to kidney disease. Here, we show that the nuclear receptor estrogen-related receptor gamma (ERRγ) and hepatocyte nuclear factor 1 beta (HNF1β) link renal mitochondrial and reabsorptive functions through coordinated epigenomic programs. ERRγ directly regulates mitochondrial metabolism but cooperatively controls renal reabsorption via convergent binding with HNF1β. Deletion of ERRγ in renal epithelial cells (RECs), in which it is highly and specifically expressed, results in severe renal energetic and reabsorptive dysfunction and progressive renal failure that recapitulates phenotypes of animals and patients with HNF1β loss-of-function gene mutations. Moreover, ERRγ expression positively correlates with renal function and is decreased in patients with chronic kidney disease (CKD). REC-ERRγ KO mice share highly overlapping renal transcriptional signatures with human patients with CKD. Together these findings reveal a role for ERRγ in directing independent and HNF1β-integrated programs for energy production and use essential for normal renal function and the prevention of kidney disease.


2009 ◽  
Vol 296 (6) ◽  
pp. F1477-F1483 ◽  
Author(s):  
Neeraj Dhaun ◽  
Pajaree Lilitkarntakul ◽  
Iain M. MacIntyre ◽  
Eline Muilwijk ◽  
Neil R. Johnston ◽  
...  

Chronic inflammation contributes to the development and progression of chronic kidney disease (CKD). Identifying renal inflammation early is important. There are currently no specific markers of renal inflammation. Endothelin-1 (ET-1) is implicated in the pathogenesis of CKD. Thus, we investigated the impact of progressive renal dysfunction and renal inflammation on plasma and urinary ET-1 concentrations. In a prospective study, plasma and urinary ET-1 were measured in 132 subjects with CKD stages 1 to 5, and fractional excretion of ET-1 (FeET-1) was calculated. FeET-1, serum C-reactive protein (CRP), urinary ET-1:creatinine ratio, and urinary albumin:creatinine ratio were also measured in 29 healthy volunteers, 85 subjects with different degrees of inflammatory renal disease but normal renal function, and in 10 subjects with rheumatoid arthritis without renal involvement (RA). In subjects with nephritis associated with systemic lupus erythematosus (SLE), measurements were done before and after 6 mo of treatment. In subjects with CKD, plasma ET-1 increased linearly as renal function declined, whereas FeET-1 rose exponentially. In subjects with normal renal function, FeET-1 and urinary ET-1:creatinine ratio were higher in SLE subjects than in other groups (7.7 ± 2.7%, 10.0 ± 3.0 pg/μmol, both P < 0.001), and correlated with CRP, and significantly higher than in RA subjects (both P < 0.01) with similar CRP concentrations. In SLE patients, following treatment, FeET-1 fell to 3.6 ± 1.4% ( P < 0.01). Renal ET-1 production increases as renal function declines. In subjects with SLE, urinary ET-1 may be a useful measure of renal inflammatory disease activity while measured renal function is still normal.


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