DEVELOPMENT DEGREE AND THE ROLE OF ENDOTHELIAL DYSFUNCTION IN THE DEVELOPMENT AND PROGRESSION OF NON-ALCOHOL FATTY LIVER DISEASE AND CHRONIC KIDNEY DISEASE IN PATIENTS WITH OBESITY

ObjectivesTo investigate if non-alcoholic fatty liver disease (NAFLD) impacts mortality and adverse outcomes for individuals with chronic kidney disease (CKD).DesignSystematic review.Data sourcesPubMed, EMBASE and Web of Science were searched up to 1 February 2020 with no restriction on the earliest date.Eligibility criteria for selecting studiesObservational cohort studies that reported either the risk of all-cause mortality, incidence of non-fatal cardiovascular events (CVE) or progression of kidney disease among adults with established CKD who have NAFLD compared with those without.Data extraction and synthesisTwo reviewers extracted data and assessed bias independently.ResultsOf 2604 records identified, 3 studies were included (UK (n=852), South Korea (n=1525) and USA (n=1413)). All were judged to have a low or moderate risk of bias. Data were insufficient for meta-analysis. Two studies examined the influence of NAFLD on all-cause mortality. One reported a significant positive association for NAFLD with all-cause mortality for individuals with CKD (p<0.05) (cardiovascular-related mortality p=ns), which was lost following adjustment for metabolic risk factors; the second reported no effect in adjusted and unadjusted models. The latter was the only study to report outcomes for non-fatal CVEs and observed NAFLD to be an independent risk factor for this (propensity-matched HR=2.00, p=0.02). Two studies examined CKD progression; in one adjusted rate of percentage decline in estimated glomerular filtration rate per year was found to be increased in those with NAFLD (p=0.002), whereas the other found no significant difference.ConclusionsFew studies have examined the influence of NAFLD on prognosis and major adverse clinical outcomes within the CKD population. The studies identified were diverse in design and results were conflicting. This should be a focus for future research as both conditions continue to rise in prevalence and have end-stage events associated with significant health and economic costs.PROSPERO registration numberCRD42020166508.

Download Full-text

Non-alcoholic fatty liver disease and risk of developing chronic kidney disease: a new piece of a recent puzzle from a large Asian study

AME Medical Journal ◽

10.21037/amj.2018.02.08 ◽

2018 ◽

Vol 3 ◽

pp. 37-37

Author(s):

Alessandro Mantovani

Keyword(s):

Chronic Kidney Disease ◽

Liver Disease ◽

Kidney Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Alcoholic Fatty Liver ◽

Asian Study ◽

Alcoholic Fatty Liver Disease

Download Full-text

Complement C3 and Nonalcoholic Fatty Liver Disease in Chronic Kidney Disease Patients: A Pilot Study

Kidney & Blood Pressure Research ◽

10.1159/000504172 ◽

2020 ◽

Vol 45 (1) ◽

pp. 61-69

Author(s):

Binbin Pan ◽

Xin Wan ◽

Mengqing Ma ◽

Changchun Cao

Keyword(s):

Chronic Kidney Disease ◽

Glomerular Filtration Rate ◽

Liver Disease ◽

Kidney Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Filtration Rate ◽

Glycated Hemoglobin ◽

Complement C3 ◽

Nonalcoholic Fatty Liver

Context: Evidences have suggested complement C3 is a biomarker for nonalcoholic fatty liver disease (NAFLD) in the general population. Objective: The present study was conducted to explore the predictive function of C3 for NAFLD in chronic kidney disease (CKD) patients. Design, Setting, and Participants: CKD patients were recruited for evaluation of their liver function, kidney function, serum lipids, glycated hemoglobin, blood, and immune function. The glomerular filtration rate was calculated using the CKD-EPI equation. NAFLD was diagnosed according to predefined ultrasonographic criteria. Results: A total of 648 consecutive CKD patients were included, with 216 (33.3%) patients diagnosed with NAFLD. The NAFLD group had significant higher levels of serum protein, serum albumin, triglycerides, glycated hemoglobin, complement C3, hemoglobin (p = 0.001), alanine aminotransferase (p = 0.002), estimated glomerular filtration rate (p = 0.007), and C4 (p = 0.043) and lower levels of cystatin C, β2-microglobulin, proteinuria (p = 0.001), and high-density lipoprotein cholesterol (p = 0.008). In a logistic regression model, only complement C3 (OR = 1.003; 95% CI 1.002–1.004, p = 0.001) was associated with a higher likelihood of being diagnosed with NAFLD. Finally, we constructed ROC curves for complement C3 for prediction of having NAFLD. The best cut-off for complement C3 was 993.5 mg/L and it yielded a sensitivity of 63.9% and a specificity of 70.1%. Conclusion: Our study revealed that complement C3 can be used as a surrogate biomarker of NAFLD in CKD patients.

Download Full-text