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. 2022 Jul 14;12(7):1142.
doi: 10.3390/jpm12071142.

Increased Risk of NAFLD in Adults with Glomerular Hyperfiltration: An 8-Year Cohort Study Based on 147,162 Koreans

Dae-Jeong Koo  1 , Mi Yeon Lee  2 , Inha Jung  3 , Sun Joon Moon  4 , Hyemi Kwon  4 , Eun-Jung Rhee  4 , Cheol-Young Park  4 , Won-Young Lee  4 , Ki Won Oh  4 , Se Eun Park  4
Affiliations

Increased Risk of NAFLD in Adults with Glomerular Hyperfiltration: An 8-Year Cohort Study Based on 147,162 Koreans

Dae-Jeong Koo et al. J Pers Med. .

Abstract

This study evaluated whether glomerular hyperfiltration (GHF) could predict nonalcoholic fatty liver disease (NAFLD) and fibrosis. A longitudinal cohort study including 147,479 participants aged 20-65 years without NAFLD and kidney disease at baseline was performed. GHF cutoff values were defined as age- and sex-specific estimated glomerular filtration rate (eGFRs) above the 95th percentile, and eGFR values between the 50th and 65th percentiles were used as reference groups. NAFLD was diagnosed via abdominal ultrasonography, and the fibrosis status was evaluated using the NAFLD fibrosis score and Fibrosis-4. During 598,745 person years of follow-up (median, 4.6 years), subjects with GHF at baseline had the highest hazard ratio (HR) for the development of NAFLD (HR 1.21; 95% CI 1.14-1.29) and fibrosis progression (HR 1.42; 95% CI 1.11-1.82) after adjusting for confounding factors. A higher baseline eGFR percentile maintained a higher risk of NAFLD and fibrosis probability. The persistent GHF group during follow-up had the highest HR for NAFLD compared to the persistent non-GHF group (HR 1.31; 95% CI 1.14-1.51). These results were consistent in all subgroups and statistically more prominent in participants without diabetes. GHF was positively associated with increased risk of NAFLD and probability of liver fibrosis in healthy adults.

Keywords: cohort study; glomerular filtration rate; insulin resistance; liver fibrosis; nonalcoholic fatty liver disease; obesity.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Diagram of study enrollment. eGFR: estimated glomerular filtration rate, HBs Ag: hepatitis B virus surface antigen, HCV Ab: hepatitis C virus antibody, USG: ultrasonography.
Figure 2
Figure 2
HR for the development of NAFLD (A) and advanced liver fibrosis of NAFLD based on NFS (B) according to baseline eGFR percentile. Adjusted for age, sex, muscle mass, BMI, smoking status, regular exercise, history of diabetes, dyslipidemia, hypertension, hs-CRP, and HOMA-IR. BMI: body mass index, eGFR: estimated glomerular filtration rate, GHF: glomerular hyperfiltration, HOMA-IR: homeostasis model assessment of insulin resistance, HR: hazard ratio, hs-CRP: high-sensitivity C-reactive protein, NAFLD: nonalcoholic fatty liver disease, NFS: NAFLD fibrosis score, Non-GHF: non-glomerular hyperfiltration.
Figure 3
Figure 3
Cumulative incidence of NAFLD by glomerular hyperfiltration status at baseline (A) and cumulative incidence of NAFLD by glomerular hyperfiltration status at baseline and at the end of the follow-up (B). GHF: glomerular hyperfiltration, NAFLD: nonalcoholic fatty liver disease, Non-GHF: non-glomerular hyperfiltration.
Figure 4
Figure 4
Subgroup analysis for comparing participants with GHF to those without GHF at baseline. 1 Adjusted for age, sex, muscle mass, BMI, smoking status, regular exercise, diabetes, dyslipidemia, hypertension, hs-CRP, and HOMA-IR. 2 Low HOMA-IR was defined as the value of <50 percentile of study participants. 3 High HOMA-IR was defined as the value of ≥50 percentile of study participants. GHF was defined as an eGFR value of ≥95th percentile of study participants in each stratified group. BMI: body mass index, eGFR: estimated glomerular filtration rate, GHF: glomerular hyperfiltration, HOMA-IR: homeostasis model assessment of insulin resistance, hs-CRP: high-sensitivity C-reactive protein, NAFLD: nonalcoholic fatty liver disease.
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