Biomedical subjects
Publications and source records attributed to Abdülgaffar Vural.
In renal transplant recipients, acute pyelonephritis may cause acute deterioration of renal function. We report a case with acute allograft failure due to acute pyelonephritis, which was confirmed by graft biopsy. After appropriate antimicrobial therapy, allograft function recovered.
BACKGROUND: Nephrotoxicity is one of the most frequent dose-limiting factors of high-dose chemotherapy to create tolerance of autologous peripheral blood stem-cell transplantation (PBSCT) for the treatment of malignant diseases. The relative importance of factors that may be responsible for the development of nephrotoxicity varied in different trials. METHODS: The factors affecting nephrotoxicity in the early period of high-dose ifosfamide, carboplatin and etoposide treatment (ICE) followed by autologous PBSCT was investigated in 47 patients. ICE was given as a conditioning regimen for 6 days. Nephrotoxicity was defined as an increase in the serum creatinine concentration of 0.5 mg/dl or more over individual baseline levels. RESULTS: Eleven patients developed nephrotoxicity (23.4%). There was no significant difference in baseline renal function between patients with nephrotoxicity and those without. No differences were found between the two groups in terms of average total doses of ICE, infections and antibiotic use. The age of patients was higher in those with nephrotoxicity (37+/-3.7 vs 26+/-1.7 years, P=0.019). The cumulative cisplatin dose administered prior to this regimen was higher in the group that developed nephrotoxicity (470 vs 227 mg/m(2), P=0.02). The overall mortality rate was 17%, but the transplant-related deaths were higher in the presence of nephrotoxicity (54.5 vs 5.5%, P=0.001). CONCLUSIONS: The cumulative dose of cisplatin is a strong risk factor for the development of nephrotoxicity in patients who receive high doses of ICE followed by PBSCT. Nephrotoxicity may occur with much lower doses than the currently recommended maximum doses.
A case of a renal transplant recipient with colchicine-induced myopathy is presented. He was on colchicine therapy for 10 months. He was hospitalized for investigation of fatigue, severe myalgia in the lower extremities and elevated serum aminotransferase levels. His viral markers and other factors that may cause myalgia and that may increase the serum aminotransferase levels were either normal or negative. Creatine phosphokinase (CK) levels were normal. Electrophysiological findings indicated myopathy and muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, the symptoms disappeared gradually and serum aminotransferase levels were normalized. We suggest that colchicine myopathy should be taken into account in patients who have been on colchicine therapy and had unexplained myalgia as well as elevated aminotransferase levels even with normal CK levels.