Proaterogenic Metabolic Disorders in Patients With Chronic Kidney Disease Nondiabetic Origin: Possibility of Statin Therapy

Kardiologiia ◽  
2014 ◽  
Vol 6_2014 ◽  
pp. 40-43
Author(s):  
T. Solomenchyk Solomenchyk ◽  
Kh. Semegen-Bodak Semegen-Bodak ◽  
N. Slaba Slaba ◽  
G. Tshngryan Tshngryan ◽  
O. Klymkovich Klymkovich ◽  
...  
2019 ◽  
Vol 49 (4) ◽  
pp. 297-306 ◽  
Author(s):  
Manuel Rivera ◽  
Leonardo Tamariz ◽  
Maritza Suarez ◽  
Gabriel Contreras

Background: Management of chronic kidney disease (CKD) patients includes efforts directed toward modifying traditional cardiovascular risk factors. Such efforts include optimal management of hypertension together with the initiation of statin therapy. Methods: In this observational study, we determine the modifying effect of statins on the relationship of systolic blood pressure (SBP) goal with mortality and other outcomes in patients with CKD participating in a clinical trial. At baseline, 2,646 CKD patients (estimated glomerular filtration rate < 60 mL/min/1.73 m2) were randomized to an intensive SBP goal < 120 mm Hg or standard SBP goal <140 mm Hg. One thousand two hundred and seventy-three were not on statin, 1,354 were on a statin, and in 19 the use of statin was unknown. The 2 primary outcomes were all-cause mortality and cardiovascular disease (CVD) mortality. Results: The relationships of SBP goal with all-cause mortality (interaction p = 0.009) and cardiovascular (CV) mortality (interaction p = 0.021) were modified by the use of statin after adjusting for age, gender, race, CVD history, smoking, aspirin use, and blood pressure at baseline. In the statin group, targeting SBP to < 120 mm Hg compared to SBP < 140 mm Hg significantly reduced the risk of all-cause mortality (adjusted hazard ratio [aHR] 0.44 [0.28–0.71]; event rates 1.16 vs. 2.5 per 100 patient-years) and CV mortality (aHR 0.29 [0.12–0.74]; event rates 0.28 vs. 0.92 per 100 patient-years) after a median follow-up of 3.26 years. In the non-statin group, the risk of all-cause mortality (aHR 1.07 [0.69–1.66]; event rates 2.01 vs. 1.94 per 100 patient-years) and CV mortality (aHR 1.42 [0.56–3.59]; event rates 0.52 vs. 0.41 per 100 patient-years) were not significantly different in both SBP goal arms. Conclusion: The combination of statin therapy and intensive SBP management leads to improved survival in hypertensive patients with CKD.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
A M Okba ◽  
H S Abdelawi ◽  
R Y Shaheen ◽  
M N Amin ◽  
M M Amin ◽  
...  

Abstract Objectives Chronic kidney disease and atherosclerosis are considered to be inflammatory process in which T cells and cytokines participate. This study determines the effect of statin therapy as an anti-inflammatory agent on the level of CD4+CD28null T lymphocyte population, and subsequently on atherosclerosis in patients with chronic renal disease. Methods We recruited 90 chronic kidney disease patients. The patients were divided into three groups according to carotid intimal medial thickness (CIMT) as an indicator of atherosclerosis. Two groups (group A in whom CIMT above 0.95 mm and B in whom CIMT below 0.95 mm) were given statin (atorvastatin 20mg) while the third group (group C in whom CIMT below 0.95 mm) continue only on the conservative treatment for CKD patients. CD4+CD28null T cells was measured in the three groups at the beginning of the study and after 6 months of statin therapy. Results CD4+CD28null T cells was decreased in statin groups (group A and B) when compared to no-statin group (group C) at the end of the study. Multivariable regression analysis for the effect of statin therapy showed that statin can independently increase the percentage of decrease both CD4+CD28null cells at the end of our study (p-value &lt;0.0001). Conclusion Our study demonstrates that statins reduce CD4+CD28null T cells in CKD patients especially with atherosclerosis suggesting that statins may help in altering the inflammatory process that lead to atherosclerosis.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jingyi Xu ◽  
Zuowei Pei ◽  
Meng Yu ◽  
Xiang Li ◽  
Lu Wang ◽  
...  

A number of metabolic disorders, including hyperlipidemia, potentially cause chronic kidney disease (CKD), one of their major chronic complications and comorbidities. Rosuvastatin is one of the widely used antiatherogenic drugs among hyperlipidemic patients. Meanwhile, sarpogrelate is not only a 5-hydroxytryptamine receptor antagonist but also an antiplatelet agent, inhibiting platelet-stimulated blood coagulation and improving peripheral circulation. In this study, a combination of sarpogrelate and/or rosuvastatin was used on CKD mice induced by a high-fat diet for 8 weeks. The mice were tested for pathological changes using histological evaluation. Tremendous alterations were found, including a remarked increase in total cholesterol and low-density lipoprotein cholesterol levels, glomerular endothelial proliferation, and mesangial expansion. Also, tubular damage and extracellular matrix accumulation occurred, namely, a marked increase in the macula densa, scattered and apoptotic loss of the apical brush border with vacuolated basophilic cytoplasm and heavily stained nuclei, and expanded Bowman’s space, which were at least partially ameliorated by sarpogrelate and/or rosuvastatin treatment. The analysis of expression profiles at both the RNA and protein levels, using real-time quantitative polymerase chain reaction and Western blot analysis, indicated that LDL-R/CD68/LOX-1-positive monocyte/macrophage-mediated enhanced proinflammatory activation, including the significant upregulation of tumor necrosis factor-α and interleukin-6, was actually attenuated by sarpogrelate and/or rosuvastatin treatment. The findings indicated that sarpogrelate and/or rosuvastatin treatment potentially ameliorates CKD progression in patients with the aforementioned comorbid metabolic disorders.


2013 ◽  
Vol 34 (24) ◽  
pp. 1807-1817 ◽  
Author(s):  
Wanyin Hou ◽  
Jicheng Lv ◽  
Vlado Perkovic ◽  
Lihong Yang ◽  
Na Zhao ◽  
...  

2006 ◽  
Vol 36 (8) ◽  
pp. 519-527 ◽  
Author(s):  
O. M. Steinmetz ◽  
U. Panzer ◽  
R. A. K. Stahl ◽  
U. O. Wenzel

2021 ◽  
Vol 12 ◽  
Author(s):  
Collins N. Khwatenge ◽  
Marquette Pate ◽  
Laura C. Miller ◽  
Yongming Sang

Obesity prevails worldwide to an increasing effect. For example, up to 42% of American adults are considered obese. Obese individuals are prone to a variety of complications of metabolic disorders including diabetes mellitus, hypertension, cardiovascular disease, and chronic kidney disease. Recent meta-analyses of clinical studies in patient cohorts in the ongoing coronavirus-disease 2019 (COVID-19) pandemic indicate that the presence of obesity and relevant disorders is linked to a more severe prognosis of COVID-19. Given the significance of obesity in COVID-19 progression, we provide a review of host metabolic and immune responses in the immunometabolic dysregulation exaggerated by obesity and the viral infection that develops into a severe course of COVID-19. Moreover, sequela studies of individuals 6 months after having COVID-19 show a higher risk of metabolic comorbidities including obesity, diabetes, and kidney disease. These collectively implicate an inter-systemic dimension to understanding the association between obesity and COVID-19 and suggest an interdisciplinary intervention for relief of obesity-COVID-19 complications beyond the phase of acute infection.


2019 ◽  
Vol 23 (6) ◽  
pp. 83-91 ◽  
Author(s):  
E. O. Bogdanova ◽  
O. N. Beresneva ◽  
I. M. Zubina ◽  
G. T. Ivanova ◽  
M. M. Parastaeva ◽  
...  

BACKGROUND. The molecular mechanisms of the initial stages of inorganic phosphate (Pi) metabolic disorders in chronic kidney disease (CKD) remain poorly understood.THE AIM. To test the hypothesis about changes in canonical Wnt signaling pathway inhibitors biosynthesis and a concomitant decrease in bone turnover as one of early mechanisms of Pi imbalance in CKD.MATERIAL AND METHODS. Creatinine (Cr), inorganic phosphate (Pi), serum parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), osteoprotegerin (OPG), sclerostin (SOST) and Dickkopf-1 (DKK), renal SOST and DKK mRNA expression, albuminuria (Alb), proteinuria (uTP) levels, fractional (FEPi) and daily (uPi24) Pi excretion were analyzed in SHR rats (N = 52) with 3/4 nephrectomy (NE) or sham operation (SO) and observation periods of 2, 4, and 6 months.RESULTS. Experimental model was comparable with 1-2 stages of CKD. In groups NE4 and NE6, the concentration of sPi and renal Pi excretion (FEPi and uPi24) were significantly higher vs corresponding controls SO4 (p = 0.006, p <0.010) and SO6 (p = 0.002, p = 0.028). Serum concentrations of FGF23 and PTH in NE and SO animals did not change significantly. In NE4 and NE6 groups, serum SOST and DKK concentrations were significantly higher vs controls (p <0.049, p <0.043), while the kidney expression SOST and DKK mRNA in NE rats did not change significantly or decreased (p = 0.002, p <0.011). The serum concentration of OPG was higher in the NE6 vs SO6 control (p = 0.028).CONCLUSION. The initial stages of experimental CKD are characterized by an increase in serum concentrations of Dikkopf-1, sclerostin and osteoprotegerin. The obtained data suggest the possible role of canonical Wnt signaling inhibition and reduction of bone turnover in the pathogenesis of Pi metabolic disorders in early stages of CKD.


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