Mehmet Soydan

Acute Renal Failure under Dasatinib Therapy

Dasatinib is a second-generation tyrosine kinase inhibitor that is approved for the treatment of imatinib-resistant or imatinib-intolerant chronic myeloid leukemia. It has a 325 times stronger in vitro activity against to native BCR-ABL when comparing with imatinib. Little is known about the effects of dasatinib on renal function. A literature review revealed only one case with imatinib-resistant chronic myeloid leukemia that developed renal failure after being placed on dasatinib therapy. Here we report a patient with imatinib-resistant chronic myeloid leukemia who developed gastroenteritis and acute renal failure after a short time from the initiation of dasatinib therapy. After dasatinib interruption, these side effects resolved completely in days. In summary, dasatinib is a potent drug in the treatment of chronic myeloid leukemia, but close clinical monitoring and the timely interruption of the therapy in patients who developed acute renal failure are warranted.

Renal hemosiderosis and rapidly progressive glomerulonephritis associated with primary hemochromatosis

Abstract Hereditary hemochromatosis leads to the accumulation of iron in many organs including the liver, spleen and heart and results in injury and dysfunction of these organs. On the other hand, iron accumulation and functional impairment in kidney is extremely rare. We report a 61-year-old male patient with hereditary hemochromatosis, in whom the renal function was deteriorated rapidly. Renal biopsy revealed crescentic glomeruli and hemosiderin accumulation in tubular epithelial cells.

Cerebral Sinovenous Thrombosis Associated with Factor V Leiden and Methylenetetrahydrofolate Reductase A1298C Mutation in Adult Membranous Glomerulonephritis

Abstract Thromboembolic diseases are accepted as the most important complications in adult nephrotic syndrome, particularly membranous nephropathy. As renal vein thrombosis is usually seen in patients with membranous nephropathy, cerebral venous thrombosis is a very rare condition, which has not been reported previously in adult patients with membranous nephropathy. Although acquired dysfunctions of coagulation and fibrinolytic systems are responsible for hypercoagulopathy in patients with nephrotic syndrome, the two most common causes of hereditary venous thrombosis [the mutations of factor V Leiden and methylenetetrahydrofolate reductase (MTHFR)] facilitate thrombosis in arterial and venous system in these patients. We report a 56-year-old man with sinovenous thrombosis, diagnosed as membranous nephropathy and detected to have mutations in factor V Leiden and MTHFR A1298C. Our patient is important because he had genetic risk of thrombotic conditions and was the first adult patient with membranous nephropathy.

Colonization of peritoneal catheter with a thermophilic fungus, Thermoascus crustaceus: a case report

Thermoascus crustaceus is a thermophilic fungus and the teleomorph form of Paecilomyces crustaceus. Thermoascus spp. have been rarely isolated from human mycoses as etiological fungal agents. We believe that our patient is the first case of catheter colonization with Thermoascus crustaceus. In a 50-year-old male patient undergoing chronic peritoneal dialysis, the mold was isolated from three separate, consecutive dialysate fluid specimens and peritoneal catheter tip. The patient had slight clinical findings and he was treated by early catheter removal without antifungal treatment. Therefore this case was considered as the colonization of the peritoneal catheter rather than peritonitis. Consequently, we think that the human pathogen fungal spectrum will continue to enlarge.

Tuberculous peritonitis in a case receiving continuous ambulatory peritoneal dialysis(CAPD) treatment

BackgroundTuberculosis continues to be an important health problem in the world. Besides pulmonary involvement extrapulmonary involvement becomes an affair in developing countries, even in developed countries.Case presentationA thirty-six year old male patient was admitted with abdominal pain, diarrhea, nausea, vomiting and fever which had started one week before. The patient had been followed up with predialisis Chronic Renal Failure(CRF) diagnosis for 4 years and receiving continuous ambulatory peritoneal dialysis (CAPD) treatment for 4 months. In peritoneal fluid, 1600/mm3 cells were detected and 70% of them were polymorphonuclear leukocytosis. The patient begun nonspesific antibiotherapy but no benefit was obtained after 12 days and peritoneal fluid bacterial cultures remained negative. Peritoneal smear was positive for Asid-fast basilli (AFB), and antituberculosis therapy was started with isoniazid, rifampicine, ethambutol and pyrazinamide. After 15 days his peritoneal fluid cell count was decreased and his symptoms were relieved. Peritoneal fluid tuberculosis culture was found positive.ConclusionConsidering this case, we think that in patients with CAPD catheter and peritonitis; when peritoneal fluid leukocytes are high and PMNL are dominant, AFB and tuberculosis culture must be investigated besides bacterial culture routinely.

Prostaglandin-lndependent Decrease of Sheep Ureter Contractility Induced by Bradykinin

The mechanisms that mediate the actions of bradykinin on ureteral motility are poorly defined and mediation via prostaglandins has not been examined. Therefore, the effects of bradykinin on contractility and the possible mediator role of prostaglandins have been investigated in sheep ureter. At the concentrations of 10(-8), 10(-7) and 10(-6) M, bradykinin elicited marked reductions in contractile force. When ureteral strips were treated separately with 10(-6) M indomethacin, 2 x 10(-6) M sodium salicylate and 10(-5) M aspirin, each drug produced a significant decrease in contractile force. In strips in which prostaglandin synthesis was inhibited by the above concentrations of indomethacin, sodium salicylate and aspirin, 10(-7) M bradykinin significantly decreased the contractility. From these data, we concluded that in ureter bradykinin decreases contractility via a mechanism not involving prostaglandin generation.

Assessment of genetic risk factors for thromboembolic complications in adults with idiopathic nephrotic syndrome.

AIMS Nephrotic syndrome (NS) may occur with acquired hypercoagulability, however, the fact that it is accompanied by an underlying hereditary thrombophilia, especially combined hereditary thrombophilia would lead to thrombotic events. In this study, we aimed to evaluate the contribution of genetic thrombophilia to development of thrombotic events in adult patients with NS. MATERIAL AND METHODS Factor V Leiden (FVL), prothrombin, and methylenetetrahydrofolate reductase (MTHFR) gene mutation were studied in 51 newly diagnosed idiopathic NS patients and age- and gender-matched 20 healthy control subjects included in the study. Renal vein Doppler ultrasound was conducted in order to investigate the prevalence of subclinical renal vein thrombosis. RESULTS Of 51 patients, 6 (11.8%) were established to have thromboembolic (TE) complications at the time of diagnosis (4 symptomatic, 2 subclinical), and no recurring thrombotic episode was observed. Genetic mutation was established in all patients that were found to have TE complications. Acquired hypercoagulability factors were similar in patients without and with TE complication. CONCLUSIONS The coexistence of inherited thrombophilia in NS may facilitate thromboembolic complications. If the cause of thrombosis cannot be explained by the usual factors attributed to the occurrence of thrombosis in NS, screening for the other factors, such as FVL, MTHFR, and prothrombin gene mutation, may be beneficial.

Haemostatic Changes in Patients with Diabetic Nephropathy due to Proteinuria

OBJeCTIVe: It is known that diabetes may cause to hypercoagulability. The pathogenetic mechanism of coagulation activation is not completely clear and the origin is multifactorial. While chronic hyperglycemia is considered to be the main underlying pathology, there are various comments on the association between glycemic control and haemostatic disorders. In this study, we have aimed to compare patients with diabetic nephropathy and patients with idiopathic nephrotic syndrome with respect to haemostatic differences. mATeRIAL and meThODS: We compared 10 newly diagnosed idiopathic nephrotic syndrome patients with 10 normoalbuminuric, 10 microalbuminuric and 10 macroalbuminuric Type II diabetic patients in terms of haemostatic disorders. We included 12 healthy controls in the study. In all groups, protein C activity, free protein S, Antithrombin III, Factor VII, VIII, IX, XI, plasminogen, fibrinogen and platelet count were evaluated. ReSuLTS: Antithrombin III levels of patients with nephrotic syndrome were significantly lower than the control group and macroalbuminuric diabetics but fibrinogen levels were significantly higher than controls. Fibrinogen levels of microlalbuminuric diabetics were significantly higher than controls. Other haemostatic parameters were all in normal range in all patient groups. COnCLuSIOnS: These findings suggest that the mechanism of hypercoagulation works in a different pathway than the hypercoagulation in nephrotic patients.