RESUMO
A 42-year-old female who was an asymptomatic carrier of hepatitis B virus (HBV) was diagnosed with antineutrophil cytoplasm antibody- (ANCA-) associated vasculitis and was induced to remission with 30 mg/day prednisolone nine years ago. Four years ago, she suffered recurrence of ANCA-associated vasculitis and with 30 mg/day prednisolone was induced to remission. This time, laboratory data showed 3-fold increase in myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) levels. Administration of 30 mg/day prednisolone was started. Three days later, she was admitted to our hospital suffering from fatigue. After admission, urinalysis showed glomerular hematuria. Despite administration of 30 mg/day prednisolone, MPO-ANCA titer had been of high level, ranging from 42 to 83 EU for 2.5 months. Furthermore, the adverse effects of steroid were seen. We decided the tapering of prednisolone (25 mg/day) and the start of mizoribine (4-carbamoyl-1-ß-D-ribofuranosyl imidazolium-5-olate) administration. After mizoribine treatment, MPO-ANCA titer was decreased without any mizoribine-related adverse effects. Six months later, MPO-ANCA titer was decreased to normal levels and she was induced to clinical remission without reactivation of HBV. We describe the effectiveness of mizoribine for the ANCA-associated vasculitis complicated with HBV-carrier.
RESUMO
Glomerular filtration rate(GFR) can be estimated from serum (s-) creatinine using the modification of diet in renal disease (MDRD). However, its calculation is sometimes cumbersome in clinical use. Cystatin C is less influenced by age, gender and muscle mass than serum creatinine, and it has been proposed as an alternative marker for estimating GFR (eGFR). The comparison of s-cystatin C with MDRD-eGFR from 245 Japanese outpatients with chronic kidney disease (CKD)resulted in the equation of eGFR = 82.8/s-cystatin C - 10.7 (r = 0.85, n = 245). Based on this equation, there were 22 patients above + SD, which was the high-group in which s-cystatin C levels were higher than the corresponding eGFR, and there were 21 patients below -SD, which was the low-group in which s-cystatin C levels were lower than the corresponding eGER. Between the two groups there was no significant difference in age, gender, weight, and body mass index. The high-group included 1 case of hyperthyroidism and 7 cases of steroid user. The low-group included 4 cases of hypothyroidism and 1 case of steroid user. In healthy individuals, MDRD-eGFR is unsuitable for estimating GFR. Thyroid dysfunction or glucocorticoid excess are known to influence s-cystatin C levels. An improved eGFR equation was provided from 144 cases excluding 88 with normal renal function (eGFR > 90 mL/min/1.73 m2), 5 with thyroid dysfunction and 8 steroid users. eGFR = 86.1/s-cystatin C - 13.6 (r = 0.94, n = 144). Each GFR estimation provided from males or from females yielded nearly the same results as this equation. The prediction of eGFR using s-cystatin C may be convenient and useful in clinical practice, and the comparison of s-cystatin C with creatinine-based eGFR may reveal some factors that affect s-cystatin C or s-creatinine levels independent of GFR.