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Non-alcoholic fatty liver and chronic kidney disease: Retrospect, introspect, and prospect.

ABSTRACT: With the growing prevalence of obesity and diabetes in the United States and across the world, a rise in the overall incidence and prevalence of non-alcoholic fatty liver disease (NAFLD) is expected. The risk factors for NAFLD are also associated with the development of chronic kidney disease (CKD). We review the epidemiology, risk factors, genetics, implications of gut dysbiosis, and specific pathogenic mechanisms linking NAFLD to CKD. Mechanisms such as ectopic lipid accumulation, cellular signaling abnormalities, and the interplay between fructose consumption and uric acid accumulation have led to the emergence of potential therapeutic implications for this patient population. Transplant evaluation in the setting of both NAFLD and CKD is also reviewed. Potential strategies for surveillance and management include the monitoring of comorbidities, the use of non-invasive fibrosis scoring systems, and the measurement of laboratory markers. Lastly, we discuss the management of patients with NAFLD and CKD, from preventative measures to experimental interventions.

SUBMITTER: Heda R

PROVIDER: S-EPMC8108029 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature

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Non-alcoholic fatty liver and chronic kidney disease: Retrospect, introspect, and prospect.

Heda Rajiv R Yazawa Masahiko M Shi Michelle M Bhaskaran Madhu M Aloor Fuad Zain FZ Thuluvath Paul J PJ Satapathy Sanjaya K SK

World journal of gastroenterology 20210501 17

With the growing prevalence of obesity and diabetes in the United States and across the world, a rise in the overall incidence and prevalence of non-alcoholic fatty liver disease (NAFLD) is expected. The risk factors for NAFLD are also associated with the development of chronic kidney disease (CKD). We review the epidemiology, risk factors, genetics, implications of gut dysbiosis, and specific pathogenic mechanisms linking NAFLD to CKD. Mechanisms such as ectopic lipid accumulation, cellular sig ...[more]

PMID: 34007127

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Project description:BackgroundChronic kidney disease (CKD) is a frequent, under-recognized condition and a risk factor for renal failure and cardiovascular disease. Increasing evidence connects non-alcoholic fatty liver disease (NAFLD) to CKD. We conducted a meta-analysis to determine whether the presence and severity of NAFLD are associated with the presence and severity of CKD.Methods and findingsEnglish and non-English articles from international online databases from 1980 through January 31, 2014 were searched. Observational studies assessing NAFLD by histology, imaging, or biochemistry and defining CKD as either estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 or proteinuria were included. Two reviewers extracted studies independently and in duplicate. Individual participant data (IPD) were solicited from all selected studies. Studies providing IPD were combined with studies providing only aggregate data with the two-stage method. Main outcomes were pooled using random-effects models. Sensitivity and subgroup analyses were used to explore sources of heterogeneity and the effect of potential confounders. The influences of age, whole-body/abdominal obesity, homeostasis model of insulin resistance (HOMA-IR), and duration of follow-up on effect estimates were assessed by meta-regression. Thirty-three studies (63,902 participants, 16 population-based and 17 hospital-based, 20 cross-sectional, and 13 longitudinal) were included. For 20 studies (61% of included studies, 11 cross-sectional and nine longitudinal, 29,282 participants), we obtained IPD. NAFLD was associated with an increased risk of prevalent (odds ratio [OR] 2.12, 95% CI 1.69-2.66) and incident (hazard ratio [HR] 1.79, 95% CI 1.65-1.95) CKD. Non-alcoholic steatohepatitis (NASH) was associated with a higher prevalence (OR 2.53, 95% CI 1.58-4.05) and incidence (HR 2.12, 95% CI 1.42-3.17) of CKD than simple steatosis. Advanced fibrosis was associated with a higher prevalence (OR 5.20, 95% CI 3.14-8.61) and incidence (HR 3.29, 95% CI 2.30-4.71) of CKD than non-advanced fibrosis. In all analyses, the magnitude and direction of effects remained unaffected by diabetes status, after adjustment for other risk factors, and in other subgroup and meta-regression analyses. In cross-sectional and longitudinal studies, the severity of NAFLD was positively associated with CKD stages. Limitations of analysis are the relatively small size of studies utilizing liver histology and the suboptimal sensitivity of ultrasound and biochemistry for NAFLD detection in population-based studies.ConclusionThe presence and severity of NAFLD are associated with an increased risk and severity of CKD. Please see later in the article for the Editors' Summary.

Project description:ObjectiveEctopic lipid accumulation in the liver and kidneys is a hallmark of metabolic diseases leading to non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). Moreover, recent data have highlighted a strong correlation between NAFLD and CKD incidences. In this study, we use two mouse models of hepatic steatosis or CKD, each initiated independently of the other upon the suppression of glucose production specifically in the liver or kidneys, to elucidate the mechanisms underlying the development of CKD in the context of NAFLD-like pathology.MethodsMice with a deletion of G6pc, encoding glucose-6 phosphatase catalytic subunit, specifically in the liver (L.G6pc-/- mice) or the kidneys (K.G6pc-/- mice), were fed with either a standard diet or a high fat/high sucrose (HF/HS) diet during 9 months. These mice represent two original models of a rare metabolic disease named Glycogen Storage Disease Type Ia (GSDIa) that is characterized by both NAFLD-like pathology and CKD. Two other groups of L.G6pc-/- and K.G6pc-/- mice were fed a standard diet for 6 months and then treated with fenofibrate for 3 months. Lipid and glucose metabolisms were characterized, and NAFLD-like and CKD damages were evaluated.ResultsLipid depot exacerbation upon high-calorie diet strongly accelerated hepatic and renal pathologies induced by the G6pc-deficiency. In L.G6pc-/- mice, HF/HS diet increased liver injuries, characterized by higher levels of plasmatic transaminases and increased hepatic tumor incidence. In K.G6pc-/- mice, HF/HS diet increased urinary albumin and lipocalin 2 excretion and aggravated renal fibrosis. In both cases, the worsening of NAFLD-like injuries and CKD was independent of glycogen content. Furthermore, fenofibrate, via the activation of lipid oxidation significantly decreased the hepatic or renal lipid accumulations and prevented liver or kidney damages in L.G6pc-/- and K.G6pc-/- mice, respectively. Finally, we show that L.G6pc-/- mice and K.G6pc-/- mice developed NAFLD-like pathology and CKD independently.ConclusionsThis study highlights the crucial role that lipids play in the independent development of both NAFLD and CKD and demonstrates the importance of lipid-lowering treatments in various metabolic diseases featured by lipid load, from the "rare" GSDIa to the "epidemic" morbid obesity or type 2 diabetes.

Project description:Background/Aims:The number of patients with nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) is on the rise. Epidemiological studies have shown the role of hyperuricemia in the development of NAFLD and CKD through oxidative stress and inflammatory mediators. Therefore, this study was conducted to investigate the prevalence and risk factors of hyperuricemia in patients with CKD and NAFLD in Iran. Patients and Methods:This study was conducted in 450 CKD patients. NAFLD was diagnosed by ultrasonography. According to the serum uric acid level, all CKD+ NAFLD+ patients were divided into non-hyperuricemia and hyperuricemia groups. The patients' demographic and clinical data such as age, sex, abdominal obesity, metabolic syndrome, diabetes, hypertension, CRP, hepatic steatosis, blood pressure, serum uric acid (UA), lipid and creatinine were collected for analysis. Results:A total of 279 cases (62%) were diagnosed with NAFLD. The prevalence rate of NFALD in CKD patients was significantly lower in normal UA level than hyperuricemia (42.7% vs 57.3%) (P=0.039). The prevalence of hyperuricemia was about 57.3% in patients with CKD and NAFLD. Accordingly, 279 CKD patients with NAFLD were enrolled and divided into hyperuricemia (n =160) and non-hyperuricemia groups (n =119). Patients with hyperuricemia showed higher creatinine and lipid levels, and a lower GFR compared to patients with normal uric acid levels (P< 0.05). However, no significant difference was observed in age, sex, abdominal obesity, metabolic syndrome, hypertension, type 2 diabetes, CRP, and steatosis between hyperuricemia and non-hyperuricemia groups (P>0.05). Three factors, including type 2 diabetes, hyperlipidemia, and a low GFR, serve as independent risk factors for hyperuricemia (P<0.05). Conclusion:The results showed a high prevalence of hyperuricemia in patients with CKD and NAFLD. A more comprehensive strategic management is necessary to address the potential harmful effects of hyperuricemia on the health of CKD+ NAFLD+ cases.

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Non-alcoholic fatty liver and chronic kidney disease: Retrospect, introspect, and prospect.

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Non-alcoholic fatty liver and chronic kidney disease: Retrospect, introspect, and prospect.

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