Increased Risk for Cardiovascular Events in Patients with Diabetic Kidney Disease and Non-Alcoholic Fatty Liver Disease

Nephron ◽  
2018 ◽  
Vol 141 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Rajkumar Chinnadurai ◽  
Constantina Chrysochou ◽  
Philip A. Kalra
Author(s):  
Claudio Tana ◽  
Stefano Ballestri ◽  
Fabrizio Ricci ◽  
Angelo Di Vincenzo ◽  
Andrea Ticinesi ◽  
...  

New evidence suggests that non-alcoholic fatty liver disease (NAFLD) has a strong multifaceted relationship with diabetes and metabolic syndrome, and is associated with increased risk of cardiovascular events, regardless of traditional risk factors, such as hypertension, diabetes, dyslipidemia, and obesity. Given the pandemic-level rise of NAFLD—in parallel with the increasing prevalence of obesity and other components of the metabolic syndrome—and its association with poor cardiovascular outcomes, the question of how to manage NAFLD properly, in order to reduce the burden of associated incident cardiovascular events, is both timely and highly relevant. This review aims to summarize the current knowledge of the association between NAFLD and cardiovascular disease, and also to discuss possible clinical strategies for cardiovascular risk assessment, as well as the spectrum of available therapeutic strategies for the prevention and treatment of NAFLD and its downstream events.


2021 ◽  
Vol 12 ◽  
pp. 204062232110243
Author(s):  
Xiaoyan Cai ◽  
Lichang Sun ◽  
Xiong Liu ◽  
Hailan Zhu ◽  
Yang Zhang ◽  
...  

Background and Aims: Whether non-alcoholic fatty liver disease (NAFLD) is associated with an increased risk of incident chronic kidney disease (CKD) independent of established cardio-renal risk factors remains controversial. We aimed to provide a quantitative estimate of the association and strength between NAFLD and risk of CKD after adjustment for multiple cardio-renal risk factors. Methods: We searched electronic databases (PubMed, Embase, and Google Scholar) for studies published from database inception until 30 November 2020. Analysis included cohort studies that reported multivariable-adjusted risk ratios [including odds ratios, relative risks (RRs), or hazard ratios] and 95% confidence intervals (CIs) for CKD of NAFLD compared with individuals without NAFLD. Results: A total of 11 cohort studies were included comprising 1,198,242 participants (46.3% women) for analysis. The median follow-up duration was 3.7 years, with 31,922 cases of incident CKD. Compared with individuals without NAFLD, unadjusted models showed that NAFLD was associated with a higher risk of CKD (RR 1.54, 95% CI 1.38–1.71). After adjusting for multiple cardio-renal risk factors, the CKD risk was still significantly increased in patients with NAFLD (RR 1.39, 95% CI 1.27–1.52). Compared with individuals without NAFLD, the adjusted absolute risk increase in NAFLD for CKD was 5.1 (95% CI 3.5–6.8) per 1000 person-years. Conclusion: NAFLD is associated with an increased risk of incident CKD independent of established cardio-renal risk factors.


2020 ◽  
Vol 18 ◽  
Author(s):  
Zlatko Fras ◽  
Dimitri P. Mikhailidis

: IMPROVE-IT (IMProved Reduction of Outcomes: Vytorin Efficacy International Trial) was a randomized clini- cal trial (18,144 patients) that evaluated the efficacy of the combination of ezetimibe with simvastatin vs simvastatin mono- therapy in patients with acute coronary syndrome (ACS) and moderately increased low-density lipoprotein cholesterol (LDL-C) levels (of up to 2.6-3.2 mmol/L; 100-120 mg/dL). After 7 years of follow-up, combination therapy resulted in an additional LDL-C decrease [1.8 mmol/L, or 70 mg/dL, within the simvastatin (40 mg/day) monotherapy arm and 1.4 mmol/L, or 53 mg/dL for simvastatin (40 mg/day) + ezetimibe (10 mg/day)] and showed an incremental clinical benefit (composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary re- vascularization (≥30 days after randomization), or nonfatal stroke; hazard ratio (HR) of 0.936, and 95% CI 0.887-0.996, p=0.016). Therefore, for very high cardiovascular risk patients “even lower is even better” regarding LDL-C, independently of the LDL-C reducing strategy. These findings confirm ezetimibe as an option to treat very-high-risk patients who cannot achieve LDL-C targets with statin monotherapy. Additional analyses of the IMPROVE-IT (both prespecified and post-hoc) include specific very-high-risk subgroups of patients (those with previous acute events and/or coronary revascularization, older than 75 years, as well as patients with diabetes mellitus, chronic kidney disease or non-alcoholic fatty liver disease). The data from IMPROVE-IT also provide reassurance regarding longer-term safety and efficacy of the intensification of li- pid-lowering therapy in very-high-risk patients resulting in very low LDL-C levels. We comment on the results of several (sub) analyses of IMPROVE-IT.


2010 ◽  
Vol 69 (2) ◽  
pp. 211-220 ◽  
Author(s):  
J. Bernadette Moore

Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. As a disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. An estimated 20–35% of the general population has steatosis, 10% of whom will develop the more progressive non-alcoholic steatohepatitis associated with markedly increased risk of cardiovascular- and liver-related mortality. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The recognition that NAFLD is an independent risk factor for CVD is a major public health concern. There is a great need for a sensitive non-invasive test for the early detection and assessment of the stage of NAFLD that could also be used to monitor response to treatment. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression. Weight loss through diet and exercise is the primary recommendation in the clinical management of NAFLD. The application of systems biology to the identification of NAFLD biomarkers and factors involved in NAFLD progression is an area of promising research.


Gut ◽  
2021 ◽  
pp. gutjnl-2021-325724
Author(s):  
Tracey G Simon ◽  
Bjorn Roelstraete ◽  
Hannes Hagström ◽  
Johan Sundström ◽  
Jonas F Ludvigsson

ObjectiveSome data suggest a positive association between non-alcoholic fatty liver disease (NAFLD) and incident major adverse cardiovascular events (MACEs). However, data are lacking from large cohorts with liver histology, which remains the gold standard for staging NAFLD severity.DesignThis population-based cohort included all Swedish adults with histologically confirmed NAFLD and without cardiovascular disease (CVD) at baseline (1966–2016, n=10 422). NAFLD was defined from prospectively recorded histopathology and categorised as simple steatosis, non-fibrotic steatohepatitis, non-cirrhotic fibrosis and cirrhosis. Patients with NAFLD were matched to ≤5 population controls without NAFLD or CVD, by age, sex, calendar year and county (n=46 517). Using Cox proportional hazards modelling, we calculated multivariable adjusted HRs (aHRs) and 95% CIs for MACE outcomes (ie, ischaemic heart disease (IHD), stroke, congestive heart failure (CHF) or cardiovascular (CV) mortality).ResultsOver a median of 13.6 years, incident MACE was confirmed in 2850 patients with NAFLD and 10 648 controls. Patients with NAFLD had higher incidence of MACE than controls (24.3 vs 16.0/1000 person-years (PY); difference=8.3/1000 PY; aHR 1.63, 95% CI 1.56 to 1.70), including higher rates of IHD (difference=4.2/1000 PY; aHR 1.64, 95% CI 1.54 to 1.75), CHF (difference=3.3/1000 PY; aHR 1.75, 95% CI 1.63 to 1.87), stroke (difference=2.4/1000 PY; aHR 1.58, 95% CI 1.46 to 1.71) and CV mortality (difference=1.2/1000 PY; aHR 1.37, 95% CI 1.27 to 1.48). Rates of incident MACE increased progressively with worsening NAFLD severity (ptrend=0.02), with the highest incidence observed with cirrhosis (difference vs controls=27.2/1000 PY; aHR 2.15, 95% CI 1.77 to 2.61).ConclusionCompared with matched population controls, patients with biopsy-proven NAFLD had significantly higher incidence of MACE, including IHD, stroke, CHF and CV mortality. Excess risk was evident across all stages of NAFLD and increased with worsening disease severity.


2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii221-iii222
Author(s):  
Rajkumar Chinnadurai ◽  
Diana Vassallo ◽  
James Ritchie ◽  
Darren Green ◽  
Philip Kalra

2019 ◽  
Vol 16 (1) ◽  
pp. 39-45
Author(s):  
Cemal Kemaloglu ◽  
Melek Didem Kemaloglu

Objective: The aim of this study is to identify the relationship between carotid intima-media thickness (c-imt) and non-alcoholic fatty liver disease (NAFLD), and to determine whether NAFLD is an independent predictor for the progression of atherosclerosis.  Method: This is a prospective randomized controlled study. 103 NAFLD patients who have hepatosteatosis with grade II and above were enrolled in this study. Patients were divided into NAFLD with metabolic syndrome (MS) and NAFLD without MS groups and compared with 50 healthy people. Basal demographic characteristics and C-imt of all patients and control group were measured.  Results: C-imt and carotid cross sectional area rates in the NAFLD groups were significantly higher than those in the control group. The mean and max. c-imt levels were significantly higher in the NAFLD group with metabolic syndrome (p<0,001). Homeostatic Model of Assessment-Insulin Resistance (HOMA-IR) levels were increased in the group with metabolic syndrome than those in the group without metabolic syndrome, with statistical significance (p<0.001). There was no difference in c-imt levels between HOMA-IR positive and negative groups (p=0.254) in patients with NAFLD and without metabolic syndrome. There was only a mild positive corelation between c-imt levels and high sensitive C-Reactive protein (hs-CRP) levels in metabolic syndrome positive group (p=0.026 r=0.30).  Conclusion: NAFLD was a significant predictor to determine the increased risk of carotid atherosclerosis. 


Sign in / Sign up

Export Citation Format

Share Document