The Treatment of Post Transplant Tuberculosis: Rifampin Sparing Regimen / 대한이식학회지

BACKGROUND: Rifampin reduces the blood levels of cyclosporin (CsA) and steroids by increasing the activity of hepatic cytochrome P450 system and the inclusion of rifampin in the anti-tuberculosis treatment protocol increases the risk of acute allograft rejection and mortality due to its interaction with cyclosporine. We report the successful treatment outcome of post-renal transplant tuberculosis patients who were treated with quinolone substituted for rifampin in anti-tuberculosis regimen. METHODS: This was a retrospective study of 14 patients with tuberculosis diagnosed among 218 transplant recipients from Feb. 1988 through Dec. 2003 at Daejeon St. Mary's hospital of catholic university of Korea and 6 patients with tuberculosis who underwent transplantation in other hospital and followed up in our hospital. RESULTS: The incidence of post-renal transplant tuberculosis was 6.4%. The mean time to diagnosis of tuberculosis after transplantation was 58.6 months (3.3~180.7). 9 were pulmonary and 11 were extrapulmonary tuberculosis. The graft failure was not occurred in quinolone group (0/15) and 2 of 3 in rifampin group. The serum creatinine levels before tuberculosis were not different to that of post-treatment in quinolone group. (P=0.58) The CsA levels before tuberculosis were not also different to that of posttreatment in quinolone group (P=0.68). CONCLUSIONS: The treatment of post-renal transplant tuberculosis with rifampin sparing anti-tuberculosis regimen was successful. Rifampin, although a mainstay drug in the treatment of tuberculosis, can be avoided in patients receiving cyclosporine, thus avoiding the risk of precipitating allograft rejection.

The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury / 대한신장학회지

PURPOSE:Preconditioning due to activation of AMPK might reduce ischemia-reperfusion (I/R) injury in the kidney, based on the key role of AMPK in preserving ATP. To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, before sustained ischemia was investigated. METHODS:Adult male Sprague-Dawley rats weighing approximately 220-250 g were used. To induce renal ischemia, a laparotomy was performed under ketamine and xylazine hydrochloride, and the blood supply to both kidneys was interrupted by placement of vessel clamps at the level of the renal pedicles. Reflow was initiated by removing the clamps. The following experimental groups were defined 1. Acute renal ischemia 0 sec, 10 min, 15 min, 2. AICAR treatment, 3. Sham group (S), 4. Ischemia/ Reperfusion group (I/R), 5. AICAR+I/R group (A+I/R), 6. AraA (Adenine-9-b-D-arabinofuranoside, an AMPK) inhibitor+AICAR+I/R group (AraA+A+I/R) RESULTS:There was only faint AMPK phosphorylation in the sham group. After 10 minutes of ischemia, or AICAR preconditioning however, Thr172 phosphorylation of AMPK was increased (p<0.05). The serum levels of BUN and creatinine were significantly decreased in AICAR preconditioning group (A+I/R). (128.0+/-7.33 mg/dL, 4.18+/-0.27 mg/dL vs. 90.2+/-11.13 mg/dL, 2.58+/-0.7 mg/dL, p<0.05), but these effects were attenuated by AMPK inhibitor, AraA (AraA+A+I/R group). In quantitative analysis of tubular injury, tubular injury score in AICAR preconditioning group significantly decreased (p<0.05). CONCLUSION:The AMPK activator AICAR has a protective effect against renal I/R injury.

The Clinical Differentiations between Diabetic Nephropathy and Non-diabetic Renal Disease in Type 2 Diabetic Patients / 대한신장학회지

PURPOSE: It is important to differentiate non-diabetic renal diseases (NDRD) from diabetic nephropathy (DN) in type 2 diabetes. Our study was reviewing the clinical data and treatment strategies from diabetic patients performed renal biopsy to determine the clinical indicators suggestive of NDRD METHODS: We reviewed the medical records of type 2 patients who underwent renal biopsy from Jan. 1995 to Dec. 2007. RESULTS: Seventy four patients were included. Mean age was 52.0+/-12.5 years and 41 (55%) patients were male suddenly developed. Nephrotic syndrome [34 cases (46%)] was the leading reason for renal biopsy. There were 37 cases (50%) with a pathologic diagnosis of DN, 31 (42%) with NDRD, and 6 (8%) with concurrent DN and NDRD. IgA nephropathy (35%) was the most common lesion found in patients with NDRD. Thirty one patients (84%) with DN and 26 (84%) with NDRD had follow-up periods of more than 6 months. Of 26 patients with NDRD, 12 were treated with immune suppressants and 6 achieved complete remission. Thirteen patients with DN and one with NDRD developed end-stage renal disease. Patients with NDRD tended to show shorter duration of diabetes, lower systolic blood pressure (SBP) and lower serum triglyceride, and had significantly lower incidence of diabetic retinopathy (DR). In the univariate regression analysis, diabetes duration, SBP, triglyceride and DR showed statistically significance. And SBP and DR were identified as independent correlating factors by multivariate regression analysis. CONCLUSION: In this study, the absence of retinopathy could predict the presence NDRD among NIDDM patients presenting with renal disease. And additional disease-specific therapies may be helpful for the patients with NDRD.