Hep C co-infection accelerates Kidney Disease

NKF 2009: Hepatitis C Virus Coinfection Accelerates Chronic Kidney Disease
by Bob Roehr
March 30, 2009 (Nashville, Tennessee)
— Add chronic kidney disease (CKD) to the list of diseases accelerated by hepatitis C virus (HCV) comorbidity, according to a study presented here at the National Kidney Foundation 2009 Spring Clinical Meetings. In a retrospective analysis (from 2001 through 2004), Lama Noureddine, MD, and colleagues from Indiana University, in Bloomington, identified 111 patients with biopsy-confirmed glomerulopathy who met the additional criteria of not being on dialysis at the time of biopsy, not having experienced acute renal or hepatic failure or a transplantation, and having at least 1 follow-up creatinine level available. "We were looking to see if patients with hepatitis C who had baseline CKD actually progressed to end-stage renal disease [ESRD]," Dr. Noureddine explained to Medscape Nephrology. "About 20% were hep C-positive [23], 60% were hep C-negative [68], and about 20% were not tested [20]" for antibodies to the virus. They evaluated 15 covariants that could possibly affect progression to ESRD or death. The hepatitis C patients were more likely to be African American, have diabetes, and have high liver-function scores due to that coinfection. "But otherwise, there were no significant differences in any of those 15 variables, aside from the AST and the ALT" at baseline, she said. "We found that if you were just hep C-positive (not necessarily with active or advanced disease), your odds ratio of [ESRD] or death was 4." That translated to an odds ratio of 2 for developing ESRD or death, compared with those who were negative for antibodies to HCV. "Our confidence interval did not pass 1, which is interesting for such a small number of patients," she said. In a multivariate analysis, only HCV-positive status and age predicted death or ESRD (P = .02). Looking at the change in creatinine over time, Dr. Noureddine found that those who were positive for HCV, "were at marginally statistically significant risk [P = .08] of having a worsening decline in creatinine. That is decent for the size of this cohort." She pointed to other studies suggesting that the deposition of circulating immune complexes stimulated by ongoing HCV replication might lead to accelerated kidney fibrosis. Dr. Noureddine acknowledged that a limitation of the study is that they did not have biopsy information for staging the patients' liver disease. Another issue is that industry-supported hepatitis C therapeutic trials generally exclude patients with CKD, so it is difficult to assess what, if any, effect treating 1 disease might have on progression of the other comorbidity.
In the United States, it is estimated that 1.3% to 1.9% of HCV patients aged 20 to 59 years have CKD. That rate increases to 4.3% in patients aged 40 to 49 years. Dr. Noureddine said an earlier study by her group suggests that HCV patients who do not have CKD at baseline are not likely to acquire the disease. In separate study presented at the meeting, Brian Mussio, MD, and colleagues reviewed all 76 kidney biopsies performed at the Cincinnati VA Medical Center, in Ohio, during a 12-year period ending in January 2008. They found that 18 patients (23.7%) were seropositive for HCV antibodies. Focal segmental glomerulosclerosis (FSGS) was the most commonly found pattern (5 of 18 patients) among those without diabetes. Patients with FSGS were younger (47.4 vs 53.7 years; P = .01), had lower serum creatinine levels at biopsy (2.0 vs 4.8 mg/dL; P = .01), and had a greater decline in glomerular filtration rate after biopsy (22.3 vs 2.2 mL/min/1.73m2; P = .02). Both analyses were conducted without industry support. The authors have disclosed no relevant financial relationships.
National Kidney Foundation (NKF) 2009 Spring Clinical Meetings: Abstracts 218 and 217. Presented March 27, 2009.
Chronic Kidney Disease Resource Center
Hepatitis C Resource Center