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HCV Drives Down Kidney Function
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MedPage Today
October 29, 2009
"Progression to chronic kidney disease and end-stage renal disease is more rapid in patients with HCV infection," he added. "Progression to chronic kidney disease is independent of diabetes."...."We conclude that hepatitis C is associated with the development of chronic kidney disease and poorer renal survival.".......HCV has been reported to cause glomerular disease, increase the risk of albuminuria, and accelerate progression of diabetic nephropathy. Additionally, HCV particles or antigens have been identified in glomeruli and tubules, said Satapathy.......To test the hypothesis they performed a retrospective analysis of medical records on HCV-positive patients seen between January 2003 and October 2006 in a gastroenterology clinic"
from Jules: these data provide information to support considering earlier therapy for HCV rather than delaying therapy.
SAN DIEGO -- Hepatitis C infection almost doubles the risk of chronic kidney disease and significantly increases progression to end-stage renal disease, according to data reported here.
Action Points
* Explain to patients that two different studies showed an association between hepatitis C infection and chronic kidney disease.
* Both studies were retrospective evaluations of medical records and therefore do not prove that HCV infection causes chronic kidney disease.
* Note that these studies were published as abstracts and presented at a conference. These data and conclusions should be considered preliminary until published in a peer-reviewed journal.
The association remained significant regardless of whether chronic kidney disease was defined in terms of creatinine clearance, proteinuria, glomerular filtration rate (GFR), or a combination of the parameters, according to Sanjaya Satapathy, MD, of the Mayo Clinic in Rochester, Minn., and colleagues.
The disparity between patients who have HCV infection and those who don't increased with age, reaching a five-fold difference in the prevalence of chronic kidney disease in patients older than 70, Satapathy said in a presentation at the American College of Gastroenterology meeting.
"There is a higher prevalence of chronic kidney disease and proteinuria in patients with hepatitis C infection," he said. "Baseline viral load is higher in patients with chronic kidney disease and is an independent positive predictor for chronic kidney disease."
"Progression to chronic kidney disease and end-stage renal disease is more rapid in patients with HCV infection," he added. "Progression to chronic kidney disease is independent of diabetes."
"We conclude that hepatitis C is associated with the development of chronic kidney disease and poorer renal survival."
Several lines of evidence have linked HCV infection and kidney disease. HCV has been reported to cause glomerular disease, increase the risk of albuminuria, and accelerate progression of diabetic nephropathy. Additionally, HCV particles or antigens have been identified in glomeruli and tubules, said Satapathy. However, data on the association have been inconsistent.
Satapathy and his colleagues hypothesized that HCV increases the risk of chronic kidney disease and accelerates its progression.
To test the hypothesis they performed a retrospective analysis of medical records on HCV-positive patients seen between January 2003 and October 2006 in a gastroenterology clinic. Patient data were traced back to June 1, 1999 or the date of first visit.
The chart review yielded 552 patients who tested positive for anti-HCV antibodies. They were matched with a 313-patient, non-HCV, control group.
Satapathy and colleagues used two sets of criteria to define chronic kidney disease.
One definition stipulated persistence of proteinuria and/or serum creatinine >1.5 mg/dL in men or >1.3 mg/dL in women for more than three months.
The second definition conformed to the National Kidney Foundation (NKF) guidelines that include structural or functional evidence of kidney damage for three months or GFR <60mL/min/1.73 m2 for three months with or without evidence of kidney damage.
Proteinuria was defined as ≥30 mg/dL by dipstick measurement, and investigators used three months as the cutoff between intermittent and persistent proteinuria.
The HCV and control groups did not differ with respect to baseline characteristics, with the exception of a higher prevalence of HIV infection (7.6% versus 1.3%, P<0.0005) and positive history of injection drug use (23.2% versus 1.9%, P<0.0005) in the HCV group.
At baseline, 3.3% of the HCV group and 3.2% of the control group had chronic kidney disease, as defined by NKF criteria.
At follow-up, the prevalence had increased to 8.3% in the HCV-positive group compared with 4.5% of the control group (P=0.032).
Combining proteinuria with GFR resulted in a prevalence of 9.6% in the HCV group and 5.1% in the control group (P=0.019).
When chronic kidney disease was defined by serum creatinine level, 6.7% of the HCV group and 3.5% of the control group had chronic kidney disease (P=0.049).
Adding proteinuria to serum creatinine resulted in rates of 7.8% and 4.2% in the HCV and control groups, respectively (P=0.037).
Analysis of the data by age groups, showed that 1% to 2% of patients younger than 40 had chronic kidney disease in both the control and HCV groups.
With increasing age, more patients in the HCV group had chronic kidney disease compared with the control group, although none of the differences was statistically significant:
* 40 to 49, 4.6% versus 3%
* 50 to 59, 9.8% versus 5.2%
* 60 to 69, 22.7% versus 10.9% (P=0.083)
* >70, 40% versus 8.3% (P=0.054)
Rates of intermittent proteinuria were similar between the groups, but HCV patients had a significantly greater rate of persistent proteinuria (6.8% versus 2.9%, P=0.024).
HCV had a significant adverse effect on kidney survival compared with the control group, whether defined by onset of chronic kidney disease (P<0.0005) or time to end-stage renal disease (P=0.005). HCV infection had a similar adverse effect on renal survival in patients with and without diabetes.
Satapathy reported that HCV patients who developed CKD had significantly higher baseline viral loads (P=0.006).
A similar relationship was observed in a second, smaller study reported at the meeting. That study involved 19 HCV-positive patients who had a persistently elevated viral load (>1 million copies/mL) during follow-up for more than 1.5 years and 17 HCV patients who had a persistently low viral load (<10,000 copies/mL) during follow-up.
At the beginning of follow-up, patients in the two groups had similar kidney function (GFR 110 mL/min/1.73 m2 in patients with a high viral load and 96 mL/min/1.73 m2 in the patients with a low viral load), said Fadi Rzouq, MD, of the University of Washington in Seattle.
During 2.6 years of follow-up during which time none of the patients received treatment for HCV, mean GFR decreased by 27.6 mL/min/1.73 m2 in patients with a persistently elevated viral load, whereas GFR declined by <0.2 mL/min/1.73 m2 during 1.9 years of follow-up in the patients who had a persistently low viral load (P=0.003).
The results "point toward the possibility of a direct renal toxicity induced by HCV, although this conclusion needs to be confirmed by more studies," said Rzouq.
Satapathy and co-investigators reported no disclosures.
Rzouq reported no disclosures.
Primary source: American College of Gastroenterology
Source reference:
Satapathy S, et al "Higher prevalence of chronic kidney disease and poor renal survival in patients with chronic HCV infection" ACG 2009; Abstract 57.
Additional source: American College of Gastroenterology
Source reference:
Hatoum HH, Rzouq F "The direct impact of hepatitis C viral load on kidney function" ACG 2009; Abstract P192.
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