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Assistant Professor Division of Nephrology Department of Internal Medicine Medical Faculty Yüzüncü Yil University 65200 Van, Turkey fax 90 432 2155051 hayriyesayarlioglu{at}yahoo.com
Associate Professor Division of Nephrology Department of Internal Medicine Medical Faculty Yüzüncü Yil University
Fellow Division of Nephrology Department of Internal Medicine Medical Faculty Yüzüncü Yil University
Assistant Professor Division of Rheumatology Department of Internal Medicine Medical Faculty Yüzüncü Yil University
Assistant Professor Division of Nephrology Department of Internal Medicine Medical Faculty Yüzüncü Yil University
Published Online, January 25, 2005. www.theannals.com, DOI 10.1345/aph.1E419
Case Reports. Case 1. A 41-year-old male HBV carrier with nephrotic syndrome was admitted to the hospital. Laboratory findings were as follows: urinary protein excretion 10 g/day, serum creatinine (SCr) 0.8 mg/dL, cholesterol 386 mg/dL, triglycerides 372 mg/dL, and albumin 2.3 g/dL. Other biochemical parameters, such as glucose, C3, C4, immunoglobulins, thyroid-stimulating hormone, and electrolytes, were within normal ranges. Serologies for hepatitis A virus (HAV), hepatitis C virus (HCV), and HIV were negative. The HBV markers were positive for HBsAg and anti-HBe antibodies and negative for HBV DNA. A renal biopsy revealed membranous glomerulonephritis. Although the patient was an HBV carrier and had symptomatic nephrotic syndrome, no evidence of liver disease was obvious. MMF was started at 500 mg twice daily. At this time, the patient was taking statins and angiotensin-converting enzyme (ACE) inhibitor treatment, which were not withdrawn during treatment. After the sixth month of treatment, proteinuria decreased to 1.3 g/day, with serum albumin 3.2 g/dL, SCr 0.8 mg/dL, and cholesterol 230 mg/dL. Although alanine aminotransferase and aspartate aminotransferase levels were normal, control evaluation of HBV DNA was positive (9549 copies/mL). MMF treatment was stopped.
Case 2. A 29-year-old man with nephrotic syndrome was admitted to the hospital. The laboratory test results were as follows: SCr 1.1 mg/dL, cholesterol 230 mg/dL, triglycerides 215 mg/dL, and albumin 2.4 g/dL; urinary protein excretion was 7 g/day. Other biochemical parameters, such as glucose, C3, C4, immunoglobulins, thyroid-stimulating hormone, and electrolytes, were in the normal range. Serologies for HAV, HCV, and HIV were negative. Hepatitis markers were HBsAg positive, antiHBeAb positive, and HBV DNA negative. The biopsy revealed membranoproliferative glomerulonephritis type l. MMF 500 mg twice daily was started; statins and ACE inhibitor treatments were also given. Six months later, daily proteinuria was 2 g, SCr 1.4 mg/dL, albumin 2.8 g/dL, and cholesterol 104 mg/dL. HBV DNA was 1 000 000 copies/mL. MMF treatment was stopped.
Discussion. MMF treatment has been shown to reduce proteinuria and stabilize SCr in various glomerulonephropathies.1,2 Mycophenolic acid (MPA), the active compound of MMF, has been shown to inhibit the replication of a number of viruses, including Epstein-Barr virus.3 Gong et al.4 reported that MPA has an inhibitory effect on HBV replication in vitro. However, Ben-Ari et al.5 observed that, in 3 of 4 HBV-positive patients with liver transplants, viral replication increased after MMF treatment. We observed that MMF treatment alone stimulated the viral replication in patients with glomerulonephritis who were HBV carriers. We did not give antiviral agents initially because viral replication was not present (as indicated by negative HBV DNA, normal liver function tests, and positive anti-HBe.)
In patients with glomerulonephritis and HBsAg positivity without apparent liver disease and viral replication, MMF may reduce proteinuria, but this treatment carries the risk of viral induction. Further study is needed to determine whether prophylactic antiviral therapy may be needed.
References
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