September 06, 2017
2 min read

Chronic kidney disease risk increases with NAFLD severity

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The risk for chronic kidney disease increased as nonalcoholic fatty liver disease progressed in severity, according to a recently published study.

“Our findings suggest that NAFLD may play a pathophysiologic role in CKD development and may be useful to identify subjects with a higher risk of CKD development,” the researchers wrote. “NAFLD patients need to be carefully monitored for the development of CKD.”

The study comprised 41,430 adults from South Korea, 14,223 of whom had NAFLD. Researchers followed the participants for a median of 4.15 years, during which time 691 participants developed CKD. Baseline glomerular filtration rates were significantly lower in patients with NAFLD compared with those without NAFLD (89.7 vs. 91.4 mL/min/1.73 m2; P < .001).

After adjusting for age, sex and year of visit, the researchers observed that patients with NAFLD had a significantly higher risk for CKD (HR = 1.38; 95% CI, 1.19-1.6).

The association between NAFLD and CKD development remained significant after adjusting for history of smoking, alcohol use, BMI and baseline glomerular filtration rate (HR = 1.29; 95% CI, 1.1-1.52); systolic blood pressure, HbA1c, LDL cholesterol, use of antihypertensive medications, use of antidiabetic medications and use of lipid-lowering medications (HR = 1.22; 95% CI, 1.04-1.43); and time-varying development of diabetes and hypertension (HR = 1.21; 95% CI, 1.03-1.44).

Among patients with NAFLD, those with a NAFLD fibrosis score of –1.455 or higher had a significantly higher risk for CKD after each adjustment (final adjusted HR = 1.59; 95% CI, 1.31-1.93) compared with those with lower scores (HR = 1.1; 95% CI, 0.91-1.33).

Similarly, patients with NAFLD and aspartate aminotransferase to platelet ratio index (APRI) of 0.5 or higher (HR = 1.27; 95% CI, 0.9-1.83) and those with FIB-4 scores of 1.45 or higher (HR = 1.38; 95% CI, 1.11-1.7) had a higher risk for CKD compared with those with a lower APRI or FIB-4 scores, respectively.

“Although the exact pathophysiologic mechanisms linking NAFLD to CKD are not completely understood, several plausible mechanisms have been suggested,” the researchers concluded. “NAFLD may alter liver-kidney interactions, including altered rennin-angiotensin system activation, antioxidant defense, or lipogenesis, which may contribute to CKD. In addition, NAFLD may exacerbate systemic and hepatic insulin resistance, cause atherogenic dyslipidemia, and release a variety of pro-inflammatory, pro-coagulant, pro-oxidant, and pro-fibrogenic mediators that may result in the development and progression of CKD.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.