18 research outputs found

    Exenatide-Induced Acute Renal Failure: A Case Report

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    Exenatide is a glucagon-like peptide-1 receptor agonist that is commonly used in the treatment of type II diabetes mellitus for its effects on the incretin system. The use of exenatide is also related to weight loss and it has reportedly been known to induce acute renal failure (ARF) according to clinical reports. We observed ARF and severe weight loss two months after beginning the treatment with exenatide in a 59-year-old female patient with type II diabetes mellitus. We present this case in which ARF was considered to be a rare adverse effect of exenatide use. In conclusion, renal functions should be closely monitored, especially in patients prescribed nephrotoxic agents and for those with a high risk of nephropathy and dehydration due to their treatment with exenatide. The usage of this drug should also be carefully planned in these patients. Turk Jem 2013; 17: 68-7

    Arterial Stiffness in Breast Cancer Patients Treated with Anthracycline and Trastuzumab-Based Regimens

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    Aims. Cardiovascular diseases are the primary cause of premature morbidity and mortality in early breast cancer patients after treatment with cardiotoxic chemotherapeutic agents. Arterial stiffness is an independent risk factor for future cardiovascular diseases and can be used as a predictive marker of subclinical cardiac damage. The aim of this study is to analyze the arterial stiffness in breast cancer patients who are in the follow-up period after receiving anthracycline-based chemotherapy regimens with trastuzumab. Methods and Material. We enrolled 45 HER2-positive breast cancer patients who are on follow-up at least for six months after completion of adjuvant chemotherapy with trastuzumab, and cardiovascular risk matched 30 control volunteers. The measurements were done with pulse wave analyzing machine. Results. Mean pulse wave velocity was higher in breast cancer patients compared to controls. The pulse wave velocity was significantly higher in patients receiving aromatase inhibitors compared to patients under tamoxifen. It was also significantly higher in postmenopausal breast cancer patients than postmenopausal controls. Conclusions. Arterial stiffness measurements may predict the breast cancer survivors with higher risk for cardiovascular events earlier in the follow-up period, and necessary preventive approaches and/or treatments can be applied

    A Retrospective, Single-Center Study Analyzing Kidney Functions in Sarcoidosis

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    Objective: Sarcoidosis is a complex chronic disease of unknown etiology that is characterized by non-caseating granulomas. Lung and lymph node involvement is most common; however, various kidney function disorders may occur in these patients. This study aimed to investigate kidney and rarely assessed features in patients with sarcoidosis. Methods: This study evaluated pulmonary sarcoidosis patients aged 18 years and over, who presented to the nephrology outpatient clinic of SBU Tepecik Training and Research Hospital. In addition to the general sarcoidosis parameters, serum 25(OH)D level, tubular functions, and aortic arch calcification were also investigated. Results: Our study included 105 patients, of whom 74 (70.5%) were females and 31 (29.5%) were males. The mean age was 46.78 ± 12.54 years. The history of nephrolithiasis was present in 21 (20%) and aortic calcification was determined in 18 (17.1%) patients. The 25(OH)D level was below 20 ng/mL in 75 (71.4%) patients, and 21 (20%) patients were hypercalcemic. Smoking history was determined in 24 (22.9%) patients, and 25(OH)D levels (cut-off 20 ng/mL) were higher in smokers than non-smokers. Additionally, a rare finding of asymptomatic renal tubular acidosis was detected in 4 (3.8%) patients. The 24-hour urine calcium excretion was >250 mg/day in 27 (25.7%) patients, and 40 (38.1%) patients were hypercalcemic and/or hypercalciuric. Conclusion: Our study revealed a low 25(OH)D level. The incidence of aortic arch calcification as a possible marker of atherosclerosis was also higher than expected and the frequency was higher in patients with higher 25(OH)D levels. As a rarely examined entity in patients with sarcoidosis, renal tubular acidosis type I was detected in 4 patients. Beyond classical kidney findings other features should be analyzed in sarcoidosis

    Effect of thrombocytapheresis on blood rheology in healthy donors: Role of nitric oxide

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    Platelet transfusions are increasingly being used to treat thrombocytopenic conditions. Because of anticoagulation, changes in blood composition and extracorporeal circulation, donor apheresis may cause alterations in hemorheology. This study aimed at investigating the effects of thrombocytapheresis on donor blood rheology. The effect of nitric oxide (NO) on donor red blood cell (RBC) deformability after thrombocytapheresis was also studied. Platelets were collected by a Haemonetics MCS 3p cell seperator. Blood samples were obtained before and 15 min after thrombocytapheresis. RBC deformability and aggregation were measured using an ektacytometer, whole blood viscosity (WBV) was determined with a cone-plate rotational viscometer. Donor RBCs were shown to be less deformable at all stress levels except 0.30 Pa after thrombocytapheresis and NO donor sodium nitroprusside (SNP, 10-6 M) reversed the reduced deformability caused by thrombocytapheresis. It was observed that donor apheresis induces a decrement in RBC aggregation and WBV measured at standard hematocrit (Hct). No significant alterations were observed in WBV values determined at native Hct values. Thrombocytapheresis also resulted in a decrement in fibrinogen, total protein, cholesterol and albumin levels whereas Hct was found to be increased and serum glucose, triglyceride, hemoglobin levels unaltered after apheresis. These results suggest that, thrombocytapheresis causes alterations in hemorheological parameters and hence in the perfusion of the microvasculature of the donors and NO appears to have a protective effect on the impairment observed in RBC deformability. Crown Copyright © 2008
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