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Higher Fibrotic Burden in HBV-Related Cirrhosis Related to Worse Kidney Outcomes – Renal and Urology News

Patients with hepatitis B virus (HBV)-related cirrhosis with a higher burden of fibrosis develop worse kidney outcomes, compared with patients with an absence of significant fibrosis, according to findings published in Journal of Infectious Diseases.

A growing body of research studies indicate that adverse kidney outcomes may be associated with fibrotic burden in patients with liver cirrhosis. Use of antiviral therapies in HBV-related cirrhosis are associated with liver fibrosis regression; however, 2 frequently prescribed antivirals — tenofovir dipivoxil fumarate (TDF) and adefovir — used to treat chronic hepatitis B infection, demonstrate increased nephrotoxicity. As such, risk stratification of patients with HBV-related cirrhosis to determine which individuals are likely to develop adverse kidney outcomes is critical prior to initiation of antiviral treatments.

To assess whether higher fibrotic burden was independently associated with adverse kidney outcomes in this patient population, researchers conducted a retrospective, longitudinal cohort study of 1691 patients (mean age, 53.4 years; men, 60.9%) with radiologically diagnosed HBV-related cirrhosis who did not demonstrate baseline chronic kidney disease (CKD).


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All patients underwent transient elastography (TE) to assess liver stiffness, reflective of fibrosis at 2 tertiary medical centers.

Liver cirrhosis was diagnosed via ultrasound or computed tomography scans in combination with laboratory studies, medical history, and clinical presentation. TE used mechanical and ultrasound waves to determine liver tissue elasticity reflective of liver fibrosis. Liver stiffness of 11.7 kilopascals (kPa) or greater indicated cirrhotic range of liver fibrosis, while liver stiffness between 7.9 and 11.7 kPa indicated significant to advanced liver fibrosis. Scores below 7.9 kPa suggested an absence of significant fibrosis.

At baseline and follow-up appointments, the researchers confirmed the presence of hypertension, diabetes, and acute kidney injury (AKI). AKI was defined as a change in serum creatinine of 0.3 mg/dL or greater within 48 hours or less or a 50% increase in serum creatinine from baseline.

Follow-ups took place every 3 to 6 months for a median 5.2 years to collect blood samples, perform a urinalysis, and assess kidney function. To assess kidney function, the researchers calculated estimated glomerular filtration rate (eGFR). Incident CKD was defined as eGFR of less than 60 mL/min/1.73 m2 or proteinuria on 2 or more consecutive outpatient follow-ups performed at least 3 months apart. Other adverse kidney outcomes that the researchers assessed included a decline in eGFR of 50% or more since baseline, onset of end-stage kidney disease (ESKD) requiring dialysis, or all-cause mortality.

Hypertension and diabetes increased as TE-confirmed fibrotic burden increased (P <.001). Approximately 60 (3.5%) of the 1691 patients experienced adverse kidney outcomes.

The researchers observed that the higher fibrotic burden — as evidenced by cirrhosis range liver stiffness (≥11.9 kPa) — was associated with a 2.77-fold increased risk for poorer kidney outcomes (95% CI, 1.16-6.63; P <.001), compared with patients with absence of significant liver fibrosis (<7.9 kPa). This relationship between liver stiffness and adverse kidney outcomes maintained significance even after adjusting for potential confounding factors.

“Higher fibrotic burden assessed using TE was independently associated with poorer kidney outcomes in patients with HBV-related cirrhosis but without baseline CKD,” study authors wrote. “The findings of this study provide rationale for detailed risk stratification of long-term kidney outcomes by assessing fibrotic burden in patients within the same disease category of HBV-related cirrhosis.”

Study limitations include the retrospective design, potential selection bias and confounding factors, lack of kidney biopsy to ascertain the mechanistic link between cirrhosis and adverse kidney outcomes, and lack of generalizability of findings outside of the South Korean population. Additionally, the researchers could not establish causality between liver fibrosis and kidney disease and did not examine the ability of antivirals to improve kidney outcomes with follow-up measurements of liver stiffness.

Disclosures: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of the author’s disclosures.

This article originally appeared on Gastroenterology Advisor