Chronic kidney disease and the severity of non-alcoholic fatty liver disease: a systematic review

INTRODUCTION

Non-alcoholic fatty liver disease (NAFLD) has emerged as the leading cause of liver disease in developed countries, affecting more than one-third of the adult population¹. NAFLD encompasses a spectrum of diseases, ranging from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH), which can progress to liver cirrhosis and hepatocellular carcinoma².

NAFLD is now recognized as a multisystemic disease with extrahepatic involvement that affects the cardiovascular, endocrine, pulmonary, and renal systems. In the United States, NAFLD is expected to become the leading cause of liver transplantation in the next few years.

NAFLD is also associated with an increase in the incidence and prevalence of chronic kidney disease (CKD), which is defined as a glomerular filtration rate (GFR) <60 mL/min/1.73 m². These two diseases share several cardiometabolic risk factors, as well as profibrotic and proinflammatory molecular mechanisms³. Recent studies have reported CKD in 20–25% of individuals with NAFLD⁴ essential to establish primary prevention strategies for CKD and to implement appropriate interventions to manage this condition in patients with NAFLD.

This systematic review aims to contribute to the ongoing discussion of the relationship and impact of NAFLD severity on the development of CKD.

METHODS

This systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statements. The study protocol was registered on the PROSPERO platform under the number CRD42022307980 and followed a predefined protocol based on the systematic reviews guideline⁵.

To select articles, we conducted a literature search using the PUBMED, Web of Science, Scopus, Literatura Latino-americana e do Caribe em Ciências da Saúde (LILACS), and EMBASE databases. The search was conducted between May 2021 and September 2021.

The initial search was performed on PubMed to access the MEDLINE database, using the strategy defined below by the following descriptors (Non-alcoholic Fatty Liver Disease OR (non-alcoholic AND Fatty Liver AND disease) OR Nonalcoholic Steatohepatitis) AND “Renal Insufficiency, Chronic” OR “Chronic Renal Insufficiency.”

The entire process was conducted by two independent authors, who searched the databases, read the titles and abstracts of the articles, and applied the inclusion and exclusion criteria. Disagreements were resolved through consensus, and when necessary, a third reviewer was consulted.

Based on the articles found, we conducted the study according to the PECOS strategy (Participants, Exposure, Comparison, and Outcomes) and followed the inclusion criteria described below:

Inclusion criteria: prospective and retrospective cohort and cross-sectional studies assessing the association between NAFLD and CKD in patients aged 18 years, and the studies that evaluated renal dysfunction in adult patients with NAFLD fibrosis progression with the risk of CKD.

Exclusion criteria: review articles, clinical trials, case reports, editorials, and experimental studies; studies in specific populations such as diabetics and individuals with CKD from dialysis centers; and studies in patients with NAFLD diagnosis by non-invasive markers such as the fatty liver index (FLI)⁶ or by the parametric attenuation coefficient (PAC)⁷.

To assess the quality of the selected studies, we used the Newcastle-Ottawa Scale, which employs a scoring system from 0 to 9 in three domains: selection, comparability, and results. The higher score indicated better study quality, and a minimum score of 7 was established for the inclusion of the studies. The Rayyan Qari software was used to confirm the accuracy of the included articles.

CKD was diagnosed by estimating the GFR using the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) method.

We conducted a sensitivity analysis of the studies based on several factors, including the research site, length of stay in the study, methodology used in NAFLD follow-up, and NAFLD severity assessed by non-invasive methods, such as the FIB-4⁸-¹⁰ and NAFLD score¹¹,¹², liver elastography, or histological analysis.

RESULTS

A PRISMA flowchart (Figure 1) shows the studies evaluated in this review. Initially, 431 articles were identified during the literature search, of which 52 duplicated articles were excluded. Based on the title and abstract, 365 articles were reviewed, and 19 studies were selected for full text assessment.

Figure 1.
Preferred Reporting Items for Systematic Reviews and Meta-Analyses flowchart of the studies evaluated.

After excluding articles with an inadequate population (n=5), inadequate diagnostic method of steatosis (n=1), overlapping cohort (n=1), unreported outcome of interest (n=1), and inadequate study design (n=1), a total of 10 articles were included in the final analysis, and their quality was assessed.

Table 1 presents the main characteristics of the included studies. The presence of NAFLD was found to be associated with the presence of CKD in four studies¹³-¹⁶, and the development of NAFLD was found to increase the risk of CKD incidence in four additional studies¹⁷-²⁰. In these eight studies¹³-²⁰, the severity of liver disease was associated with a reduction in kidney function, regardless of known risk factors. Two studies did not find an association between NAFLD and CKD nor an increase in the incidence of CKD after adjusting for metabolic syndrome elements.

Table 1.
Overview of the included studies investigating the association between renal dysfunction in individuals with nonalcoholic fatty liver disease.

Author, year of publication	Country	Design of study	Number of subjects	Diagnosis of NAFLD	Setting	Definition of DRC	Statistical adjustment	NOS score
Targher, 201015	Japan	Cross-sectional Case-control	160	Liver biopsy	01 medical center	GFR <60 mL/min or albumin-to-creatinine ratio >3 mg/mmol	Age, gender, BMI, waist circumference, smoking, systolic BP, HOMA-IR score, and TG	08
Yasui, 201116	Japan	Cross-sectional Case-control	174	Liver biopsy	02 medical center	GFR <60 mL/min (Japanese Society of Nephrology)	BMI, SAH, age, sex, the presence of T2DM or dyslipidemia, levels of AST, ALT, or γ-GTP	08
Sinn, 201718	South Korea	Cohort	41430	Ultrasonography	Samsung Medical Center	CKD-EPI <60 mL/min	Smoking, alcohol consumption, BMI, and estimated GFR at baseline, systolic blood pressure, HbA1c, LDL-C, use of diabetes, lipid lowering, and antihypertensive medications
Sirota, 201224	USA	Cross-sectional Case-control	11469	Ultrasonography	NHANES program	GFR <60 mL/min or GFR >60 mL/min with albuminuria	Model adjusted for age, sex and race (Model 1); and a model adjusted for history of hypertension, history of diabetes, systolic BP, waist circumference, TG, HDL-C, and HOMA-IR score	08
Wilechansky, 201925	USA	Cohort	987	Tomography	Framingham Heart Study	CKD-EPI GFR <60 mL/min/1.73 m² and/or microalbuminuria (sex-specific urinary albumin-creatinine ratio)	Age, sex, smoking status, drinks per week, systolic blood pressure, diastolic blood pressure, use of antihypertensive medications, HDL-C, total cholesterol, regular aspirin use, and T2DM	08
Zhang, 202020	USA and China	Cross-sectional	65087	Ultrasonography	NHANES and dataset chinese	CKD-EPI GFR <60 mL/min/1.73 m² and/or abnormal albuminuria and/or overt proteinuria	Age, sex, BMI, history of T2DM, and history of SAH	08
Liu, 202014	Taiwan	Cross-sectional Case-control	37825	Ultrasonography	Taipei Tzu Chi Hospital	Proteinuria or GFR ≤60 mL/min/1.73 m²	Sex, age, current smoking, T2DM, SAH, low HDL-C, high TG, ALT, and systolic BP	07
Kaps, 202017	Germany	Cohort	48057		Disease Analyzer Database		Diabetes, obesity, SAH, and ischaemic heart diseases	08
Zuo, 202119	China	Cohort	4402	Ultrasonography	Medical center	Albumin-to-creatinine ratio >3 mg/mmol or GFR <60 mL/min/1.73 m²	Age, sex, smoking status, drinks, physical activity BMI, SBP, HbA1c, white blood cell count, UACR, eGFR, use of antidiabetic medications, antihypertensive, and use of lipid lowering medications	08
Cao, 202113	China	Cross-sectional Case-control	3872	Ultrasonography	Medical center	Albumin-to-creatinine ratio >3 mg/mmol or GFR <60 mL/min/1.73 m²	Age, sex, and T2DM	07

• CKD was defined as a urinary albumin-to-creatinine ratio (UACR) ≥30 mg/g, an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m² or both. BMI: body mass index; HOMA-IR: homeostatic model of insulin resistance; HDL-C: high-density lipoprotein cholesterol; TG: triglycerides; LDL-C: low-density lipoprotein cholesterol; NOS: Newcastle Ottawa Scale; SAH: systemic arterial hypertension; T2DM: Type 2 diabetes mellitus; SBP: systemic blood pressure; HbA1c: hemoglobin A1C.

Table 2 presents the studies that were excluded after evaluation. Three studies were excluded because they focused on a cohort of individuals with pre-existing CKD. Two studies focused solely on the molecular mechanisms involved in the condition being studied. Seven studies evaluated only specific populations of individuals. One study had a small sample size. One study examined only the effect of fibrosis. In one study, the outcome was not of interest to the researchers. Finally, one study used a non-imaging or biopsy-based diagnosis of steatosis, which may not be sufficiently reliable for this investigation.

Table 2.
Studies that were evaluated in full text and were excluded.

No.	First author	Year	Title	Reason for exclusion
1	Chinnadurai	2019	Non-alcoholic fatty liver disease and clinical outcomes in chronic kidney disease	Cohort of individuals who already had CKD
2	Mikolasevic	2013	Chronic kidney disease and nonalcoholic fatty liver disease proven by transient elastography	Cohort of individuals with CKD
3	Musso	2015	Emerging liver-kidney interactions in nonalcoholic fatty liver disease	Molecular study
4	Kasim	2019	Correlation between non-alcoholic fatty liver and chronic kidney disease	Small number of subjects in the study
5	Li	2014	Association between non-alcoholic fatty liver disease and chronic kidney disease in population with prediabetes or diabetes	Specific population with diabetes
6	Paik	2019	Chronic kidney disease is independently associated with increased mortality in patients with nonalcoholic fatty liver disease	Outcome was not of interest
7	Targher	2014	Nonalcoholic fatty liver disease is independently associated with an increased incidence of chronic kidney disease in patients with type 1 diabetes	Specific population with diabetes
8	Xu	2016	High FIB-4 index as an independent risk factor of prevalent chronic kidney disease in patients with nonalcoholic fatty liver disease	Associates only the effect of fibrosis
9	Targher	2008	Increased risk of CKD among type 2 diabetics with nonalcoholic fatty liver disease	Specific population
10	Aubert	2021	Role of non-alcoholic fatty liver disease in the evolution of renal function in patients with diabetes mellitus	Specific population
11	Targher	2012	Increased prevalence of chronic kidney disease in patients with Type 1 diabetes and non-alcoholic fatty liver	Specific population
12	Lu	2020	Non-alcoholic fatty liver disease increases the prevalence of maintenance haemodialysis in patients with chronic kidney disease	Specific population with chronic kidney disease
13	Machado	2012	Impaired renal function in morbid obese patients with nonalcoholic fatty liver disease	Specific population with obesity
14	Zeng	2017	Association between non-invasively diagnosed hepatic steatosis and chronic kidney disease in Chinese adults on their health check-up	Non-imaging or biopsy diagnosis of steatosis
15	Musso	2016	Fatty liver and chronic kidney disease: novel mechanistic insights and therapeutic opportunities	Molecular study
16	Chon	2020	Decrease in waist-to-hip ratio reduced the development of chronic kidney disease in non-obese non-alcoholic fatty liver disease	Specific population without obesity

DISCUSSION

In this systematic review of 10 observational longitudinal studies, comprising a total of 165,246 participants from different countries, we found a positive association between the presence of NAFLD and CKD stage ≥3, defined as the occurrence of eGFR <60 mL/min/1.73 m², with or without accompanying overt proteinuria. Moreover, the prevalence of CKD increased with the severity of NAFLD.

This systematic review is relevant because less is still known about the relationship between the evolution of NAFLD and the incidence of CKD. In recent years, this association has aroused increasing scientific interest, mainly due to the knowledge that NAFLD, in its broad spectrum, is associated with the development and progression of cardiovascular diseases.

There is now increasing evidence that the severity of NAFLD predicts the development and progression of CKD, suggesting that NAFLD-associated CKD might involve some unique mechanisms. Indeed, the hepatic and systemic vaso-regulatory changes seen in NAFLD may evoke the hepatorenal reflex and impair renal function²¹.

According to the literature, the study developed by Targher et al.¹⁵ demonstrated for the first time that individuals with NASH confirmed by liver biopsy had a moderate decrease in GFR and more frequent albuminuria than controls without NASH. This study was carried out with 80 non-obese patients, and adjustments were made for the main confounding factors such as age, gender, waist circumference, Homeostases Model Assessment-Insulin Resistance (HOMA-IR) score, systolic blood pressure, and triglycerides. Thus, it is possible to speculate that NASH is not associated with CKD because of shared cardiovascular risk factors, but NASH itself may contribute to the development of CKD.

Yasui et al.¹⁶ studied 92 individuals with NASH and found a high prevalence of CKD (21%) in those with NASH when compared to control without NASH. The study also identified obesity and NASH as risk factors for CKD in NASH.

In addition, a cohort study by Sinn et al.¹⁸ assessed the longitudinal association between NAFLD and the incidence of CKD over a 10-year period. The study concluded that CKD developed more frequently in participants with NAFLD compared to those without NAFLD. This association was not explained by the emergence of systemic arterial hypertension (SAH) and type 2 diabetes mellitus (T2DM) and persisted after adjustments for risk factors and potential metabolic mediators.

These findings further support the association between NAFLD and CKD and highlight the need for early detection and management of NAFLD to prevent the development and progression of CKD.

This cohort also observed the strong association between NAFLD and CKD in individuals with more advanced fibrosis, indicated by the high NAFLD fibrosis score (NFS) score⁹, and that fibrosis markers bring additional risk stratification, being used to identify the patients with NAFLD at increased risk of renal complications.

The European Association for the Study of the Liver recommends the evaluation of serum markers of fibrosis in hepatic steatosis²². The NFS can identify patients at low risk of advanced fibrosis and has been externally validated in ethnically diverse populations with NAFLD²³.

Despite the literature being likely to understand that NAFLD would act directly in the pathogenesis of CKD, other divergent studies in the literature have emerged. Sirota et al.²⁴ developed a large cross-sectional study with 11,469 adults who participated in the National Health and Nutrition Examination Survey, 1988–1994 (NHANES III). The hypothesis was that NAFLD was associated with CKD and that the severity of NAFLD would bring a greater chance of CKD. They concluded that there is a positive association between the presence and severity of NAFLD and CKD, but this association was attenuated after adjusting for confounding factors.

There are multiple possibilities for such discordant results found in studies examining the association between NAFLD and CKD. Some studies did not adjust for important confounding factors, such as antihypertensive drug use and smoking. Additionally, studies conducted in hospitals may have selected individuals with more advanced liver disease, including NASH and fibrosis²⁵. It is possible that only those with more advanced NAFLD, particularly with NASH or liver fibrosis, may be at increased risk for CKD.

More recently, cross-sectional studies with a large number of individuals²⁰,¹⁴ and long-term cohorts¹⁷ have confirmed that NAFLD is an independent risk factor for CKD. Zuo et al.¹⁹ confirmed this hypothesis but suggested that the progression of liver fibrosis in individuals with NAFLD is a more significant predictor for the development of CKD than baseline levels of metabolic diseases.

The biological mechanisms underlying this association are still not well understood. Possible factors include the activation of the renin-angiotensin system, hepatic insulin resistance, atherogenic dyslipidemia, proinflammatory, procoagulants, and pro-oxidants mediators, as well as alterations in the intestinal microbiota¹³.

This review has certain limitations inherent to the design of the studies included. First, the observational design of the eligible studies prevents us from establishing causality. Second, although most of the eligible studies adjusted the results for age, sex, obesity, hypertension, and diabetes, residual confounding due to some unmeasured factors cannot be excluded. Additionally, none of the eligible studies provide a histological characterization of NAFLD-associated kidney disease.

CONCLUSIONS

This systematic review suggests a positive association between the presence and severity of NAFLD and CKD. However, further follow-up studies are needed to confirm these findings.

ETHICAL STATEMENT

The authors declare that all experiments were conducted in accordance with the Declaration of Helsinki.

REFERENCES

• ^1.
  Targher G, Byrne CD. Non-alcoholic fatty liver disease: an emerging driving force in chronic kidney disease. Nat Rev Nephrol. 2017;13(5):297-310. https://doi.org/10.1038/nrneph.2017.16
  » https://doi.org/10.1038/nrneph.2017.16
• ^2.
  Haskins IN, Chang J, Nor Hanipah Z, Singh T, Mehta N, McCullough AJ, et al. Patients with clinically metabolically healthy obesity are not necessarily healthy subclinically: further support for bariatric surgery in patients without metabolic disease? Surg Obes Relat Dis. 2018;14(3):342-6. https://doi.org/10.1016/j.soard.2017.11.032
  » https://doi.org/10.1016/j.soard.2017.11.032
• ^3.
  Mantovani A, Petracca G, Beatrice G, Csermely A, Lonardo A, Schattenberg JM, et al. Non-alcoholic fatty liver disease and risk of incident chronic kidney disease: an updated meta-analysis. Gut. 2022;71(1):156-62. https://doi.org/10.1136/gutjnl-2020-323082
  » https://doi.org/10.1136/gutjnl-2020-323082
• ^4.
  Zou ZY, Fan JG. Incidence of chronic kidney disease in patients with non-alcoholic fatty liver disease. J Hepatol. 2020;73(1):214-6. https://doi.org/10.1016/j.jhep.2020.03.003
  » https://doi.org/10.1016/j.jhep.2020.03.003
• ^5.
  Page MJ, Moher D, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. PRISMA 2020 explanation and elaboration: updated guidance and exemplars for reporting systematic reviews. BMJ. 2021;372:n160. https://doi.org/10.1136/bmj.n160
  » https://doi.org/10.1136/bmj.n160
• ^6.
  Bedogni G, Bellentani S, Miglioli L, Masutti F, Passalacqua M, Castiglione A, et al. The Fatty Liver Index: a simple and accurate predictor of hepatic steatosis in the general population. BMC Gastroenterol. 2006;6:33. https://doi.org/10.1186/1471-230X-6-33
  » https://doi.org/10.1186/1471-230X-6-33
• ^7.
  Lédinghen V, Vergniol J, Foucher J, Merrouche W, Bail B. Non-invasive diagnosis of liver steatosis using controlled attenuation parameter (CAP) and transient elastography. Liver Int. 2012;32(6):911-8. https://doi.org/10.1111/j.1478-3231.2012.02820.x
  » https://doi.org/10.1111/j.1478-3231.2012.02820.x
• ^8.
  McPherson S, Hardy T, Dufour JF, Petta S, Romero-Gomez M, Allison M, et al. Age as a confounding factor for the accurate non-invasive diagnosis of advanced NAFLD fibrosis. Am J Gastroenterol. 2017;112(5):740-51. https://doi.org/10.1038/ajg.2016.453
  » https://doi.org/10.1038/ajg.2016.453
• ^9.
  Shah AG, Lydecker A, Murray K, Tetri BN, Contos MJ, Sanyal AJ, et al. Comparison of noninvasive markers of fibrosis in patients with nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol. 2009;7(10):1104-12. https://doi.org/10.1016/j.cgh.2009.05.033
  » https://doi.org/10.1016/j.cgh.2009.05.033
• ^10.
  Sterling RK, Lissen E, Clumeck N, Sola R, Correa MC, Montaner J, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection. Hepatology. 2006;43(6):1317-25. https://doi.org/10.1002/hep.21178
  » https://doi.org/10.1002/hep.21178
• ^11.
  Angulo P, Hui JM, Marchesini G, Bugianesi E, George J, Farrell GC, et al. The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD. Hepatology. 2007;45(4):846-54. https://doi.org/10.1002/hep.21496
  » https://doi.org/10.1002/hep.21496
• ^12.
  Treeprasertsuk S, Björnsson E, Enders F, Suwanwalaikorn S, Lindor KD. NAFLD fibrosis score: a prognostic predictor for mortality and liver complications among NAFLD patients. World J Gastroenterol. 2013;19(8):1219-29. https://doi.org/10.3748/wjg.v19.i8.1219
  » https://doi.org/10.3748/wjg.v19.i8.1219
• ^13.
  Cao Y, Deng Y, Wang J, Zhao H, Zhang J, Xie W. The association between NAFLD and risk of chronic kidney disease: a cross-sectional study. Ther Adv Chronic Dis. 2021;12:20406223211048649. https://doi.org/10.1177/20406223211048649
  » https://doi.org/10.1177/20406223211048649
• ^14.
  Liu HW, Liu JS, Kuo KL. Association of nonalcoholic fatty liver and chronic kidney disease: an analysis of 37,825 cases from health checkup center in Taiwan. Ci Ji Yi Xue Za Zhi. 2019;32(1):65-9. https://doi.org/10.4103/tcmj.tcmj_233_18
  » https://doi.org/10.4103/tcmj.tcmj_233_18
• ^15.
  Targher G, Bertolini L, Rodella S, Lippi G, Zoppini G, Chonchol M. Relationship between kidney function and liver histology in subjects with nonalcoholic steatohepatitis. Clin J Am Soc Nephrol. 2010;5(12):2166-71. https://doi.org/10.2215/CJN.05050610
  » https://doi.org/10.2215/CJN.05050610
• ^16.
  Yasui K, Sumida Y, Mori Y, Mitsuyoshi H, Minami M, Itoh Y, et al. Nonalcoholic steatohepatitis and increased risk of chronic kidney disease. Metabolism. 2011;60(5):735-9. https://doi.org/10.1016/j.metabol.2010.07.022
  » https://doi.org/10.1016/j.metabol.2010.07.022
• ^17.
  Kaps L, Labenz C, Galle PR, Weinmann-Menke J, Kostev K, Schattenberg JM. Non-alcoholic fatty liver disease increases the risk of incident chronic kidney disease. United Euro Gastroenterol J. 2020;8(8):942-8. https://doi.org/10.1177/2050640620944098
  » https://doi.org/10.1177/2050640620944098
• ^18.
  Sinn DH, Kang D, Jang HR, Gu S, Cho SJ, Paik SW, et al. Development of chronic kidney disease in patients with non-alcoholic fatty liver disease: a cohort study. J Hepatol. 2017;67(6):1274-80. https://doi.org/10.1016/j.jhep.2017.08.024
  » https://doi.org/10.1016/j.jhep.2017.08.024
• ^19.
  Zuo G, Xuan L, Xin Z, Xu Y, Lu J, Chen Y, et al. New nonalcoholic fatty liver disease and fibrosis progression associate with the risk of incident chronic kidney disease. J Clin Endocrinol Metab. 106(10):e3957-68. https://doi.org/10.1210/clinem/dgab425
  » https://doi.org/10.1210/clinem/dgab425
• ^20.
  Zhang M, Lin S, Wang MF, Huang JF, Liu SY, Wu SM, et al. Association between NAFLD and risk of prevalent chronic kidney disease: why there is a difference between east and west?. BMC Gastroenterol. 2020;20(1):139. https://doi.org/10.1186/s12876-020-01278-z
  » https://doi.org/10.1186/s12876-020-01278-z
• ^21.
  Lonardo A, Mantovani A, Targher G, Baffy G. Nonalcoholic fatty liver disease and chronic kidney disease: epidemiology, pathogenesis, and clinical and research implications. Int J Mol Sci. 2022;23(21):13320. https://doi.org/10.3390/ijms232113320
  » https://doi.org/10.3390/ijms232113320
• ^22.
  Marchesini G, Day CP, Dufour JF, Canbay A, Nobili V, Ratziu V, et al. EASL-EASD-EASO clinical practice guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-402. http://doi.org/10.1016/j.jhep.2015.11.004
  » https://doi.org/10.1016/j.jhep.2015.11.004
• ^23.
  Musso G, Gambino R, Cassader M, Pagano G. Meta-analysis: natural history of non-alcoholic fatty liver disease (NAFLD) and diagnostic accuracy of non-invasive tests for liver disease severity. Ann Med. 2011;43(8):617-49. https://doi.org/10.3109/07853890.2010.518623
  » https://doi.org/10.3109/07853890.2010.518623
• ^24.
  Sirota JC, McFann K, Targher G, Chonchol M, Jalal DI. Association between nonalcoholic liver disease and chronic kidney disease: an ultrasound analysis from NHANES 1988-1994. Am J Nephrol. 2012;36(5):466-71. https://doi.org/10.1159/000343885
  » https://doi.org/10.1159/000343885
• ^25.
  Wilechansky RM, Pedley A, Massaro JM, Hoffmann U, Benjamin EJ, Long MT. Relations of liver fat with prevalent and incident chronic kidney disease in the Framingham Heart Study: a secondary analysis. Liver Int. 2019;39(8):1535-44. https://doi.org/10.1111/liv.14125
  » https://doi.org/10.1111/liv.14125

• Funding: none.

Publication Dates

• Publication in this collection
  17 July 2023
• Date of issue
  2023

History

• Received
  16 Apr 2023
• Accepted
  25 Apr 2023