Search

rESultS: The mean age of 58 patients (30 women) in our study was 53.2±14.7 years and duration of PD was 41.3±8.3 months. Thirteen of the patients were not literate. 19 patients in the pre-dialysis period and 14 PD patients were using herbal products. Five of the patients who used HB in the pre-dialysis period continued using them after the initiation of PD. There was no relationship between the use of HPs and initiation of PD. Various herbs and plants were the most common products used and the most common supply source was sellers of herbs.

Aim: When kidney failure occurs the treatment choices for diabetes is narrowed. To evaluate the effect of vildagliptin, a DPP-4 inhibitor, in diabetic nephropathy patients we planned this study. Patients and methods: Twenty two patients (15 M, 7 F, mean age 59,3 + 7,4) admitted to our outpatient clinics within past two and half years with type 2 diabetes mellitus, more than 300 mg/g albuminuria, GFR less than 60 ml/min and started vildagliptin were evaluated retrospectively. Results: After 3 months of vildagliptin treatment HbA1c is tended to be reduced (basal 8,3±1,7; after 3 month: 7,7±1,6; p=0,08 ), eGFR (basal 45,7±19,8 ml/min; after 3 month:44,9±20,1 ml/min; p=0,57) and albuminuria (basal 1572,1 mg/G ± 1829,5; after 3 mo; 1590,1±1936,9; p=0,84) did not changed. Other parameters including

Background Amikacin has the largest spectrum among aminoglycosides, its nephrotoxic effect limits its utilization. Our purpose in this study is to review the protective effect of dexpanthenol against the nephrotoxic effect of amikacin, accompanied with histopathological and biochemical parameters. Methods 32 rats were randomly separated into four groups with eight in each (amikacin (1.2 mg/kg/day), amikacin (1.2 mg/kg/day) + dexpanthenol (500 mg/kg/day), dexpanthenol (500 mg/kg/day) and control). In order to assess the oxidative balance and renal damage between groups, biochemical parameters (total antioxidant capacity (TAS), total oxidant stress (TOS), catalase (CAT), paraoxonase (PON), arylesterase (ARES), urea, and creatinin) were studied from the blood samples. At the end of the 14th day, renal tissues were reviewed blindly by a pathologist. Results TOS and oxidative stress index (OSI) values were significantly lower in the group which was administered with dexpanthenol + amikacin compared to the group which only received amikacin (respectively, p = 0.001, p = 0.002). Antioxidant biochemical parameters (TAS, CAT, PON, and ARES) were significantly higher in the group which was administered with dexpanthenol + amikacin compared to the group administered only with amikacin (respectively, p = 0.007, p = 0.001, p = 0.003, p = 0.003). Urea and creatitin values were found to be significantly lower in the group which was administered with dexpanthenol + amikacin compared to the group administered only with amikacin (respectively, p = 0.002, p = 0.001). Histopathologic changes such as glomerular and tubular epithelium changes and interstitial edema were clearly observed in the group administered only with amikacin, such findings were insignificant in the group administered with dexpanthenol + amikacin. Conclusion It was revealed with biochemical and histopathologic data that nephrotoxic effects created by amikacin administration can be limited with dexpanthenol by using them together, and further advanced clinical studies are required.

Renal cholesterol crystal embolism (also called renal atheroembolism) is a cause of acute kidney injury with increasing frequency. It is usually seen in patients older than 60 years of age with diffuse atherosclerotic disease. Although it develops usually following vascular interventions; it may occur spontaneously. It presents with partial or total occlusion of small arteries due to distal embolization from cholesterol crystals from ruptured atherosclerotic plaques. It is in fact a part of systemic disease called cholesterol crystal embolization disease affecting kidneys, eyes, brain and gastrointestinal system. Livedo reticularis, especially purple discoloration of toes are clues for diagnosis. The pathognomonic finding of renal cholesterol crystal embolism is the cholesterol crystal clefts in renal biopsy specimen. Herein, we present a atypical case of acute kidney injury due to spontaneous cholesterol crystal embolization in a patient with functionally solitary kidney., Renal kolesterol kristal embolizimi (renal ateroembolizim) akut böbrek hasarının artan nedenlerinden biridir. Genellikle yaygın aterosklerozu olan 60 yaşının üzerindeki hastalarda görülmektedir. Vasküler girişimler sonrasında ortaya çıkabileceği gibi spontan olarak da meydana gelebilir. Rüptüre aterosklerotik plaklardan serbestleşen kolesterol kristallerinin distaldeki küçük arterleri total yada parsiyel olarak tıkaması sonucu ortaya çıkmaktadır. Aslında sistemik bir hastalık olan, böbrekler, gözler, beyin ve gastrointestinal sistemi tutabilen kolesterol kristal embolizimi hastalığının bir parçasıdır. Livedo retikülaris ve ayak parmaklarında mor renk değişiklikleri hastalığın ipuçları olabilir. Renal kolesterol kristal emboliziminin patognomonik bulgusu böbrek biyopsisinde kolesterol kleftlerinin gösterilmesidir. Bu yazıda fonksiyonel olarak tek böbrekli bir hastada spontan kolesterol kristal embolisine bağlı gelişen bir akut böbrek hasarı olgusu sunduk

Streptococcus salivarius is a Gram-positive bacteria that may cause infections like endocarditis and meningitis. However, it has not been reported as a causative agent of peritonitis in peritoneal dialysis patients. In this paper we present a rare case of peritonitis with Streptococcus salivarius admitted to our Clinic with abdominal pain, who had been on peritoneal dialysis treatment for 19 months. Streptococus salivarius was cultured from the effluent, sensitive to ampicillin and penicillin G. Patient was discharged completely cured. Peritonitis is the most important clinical issue that occurs in patients treated with peritoneal dialysis, and every effort should be invested to determine the causative agent while even rare bacteria as Streptococcus salivarius may be found.

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare cause of hemolytic anemia. The major outlines of clinical presentation comprises findings of hemolysis, venous thrombosis and findings of bone marrow failure. The presentation of the disease with acute kidney injury (AKI) is not frequent. Massive hemoglobinuria following a serious attack of hemolysis during the course of PNH may lead to AKI by way of causing acute tubular necrosis. Hemoglobin casts and accumulation of hemosiderin in the proximal tubule may be seen in renal biopsy. The treatment is not different from that of acute tubular necrosis. Herein, we present a case who was admitted to our clinic with AKI and diagnosed to have PNH during hospitalization. KEY wORdS: Paroxysmal nocturnal hemoglobinuria, Acute kidney injury, Hemolysis. doi: 10.5262/tndt.2013.1001.22 Yazisma Adresi: abdullah sumnu Haseki Egitim ve Arastirma Hastanesi, Nefroloji Klinigi, Istanbul, Turkiye Tel : 0 212 529 44 00 E-posta : drabdullahsumnu@yahoo.com Gelis Tarihi : 11.04.2012 Kabul Tarihi : 17.06.2012 Hastaligin ortaya cikisinda median yas 33’tur (5). Kliniginin ana hatlarini hemoliz bulgulari, venoz trombozlar ve kemik iligi yetersizlik bulgulari olusturmaktadir. Myelodisplastik sendrom veya akut losemiye ilerleyebilir (6). Hastaligin akut bobrek hasari (ABH) ile prezantasyonu sik degildir. PNH hastalarinda ortaya cikan ABH’nin patogenezi komplekstir ve bu hasar heme pigmenti iliskili ABH (pigment nefropatisi) basligi altinda incelenebilir. Literaturde PNH seyrinde hemodiyaliz gereksinimi olusturacak ABH vakalari bildirilmistir (7,8). Biz de ilk olarak ABH ile klinigimize basvuran ve yatisi sirasinda PNH tanisi koyulan bir olgu sunuyoruz. GIRIs Paroksismal nokturnal hemoglobinuri (PNH) nadir gorulen ve PIG-A (phosphatidylinositol glycan-complementation class A gene) genindeki somatik bir mutasyon sonucu ortaya cikan edinsel hematopoetik kok hucre hastaligina bagli bir hemolitik anemidir. PIG-A genindeki mutasyon, eritrosit hucre membranina cesitli proteinleri baglayan glikozil fosfatidil inozitolun capa seklindeki yapisini bozarak normal sartlarda hucre membraninda yerleserek komplemana bagli lizisi engelleyen CD55 ve CD59 gibi proteinlerin eksikligine yol acar. Sonuc olarak eritrositler kompleman sisteminin bir hedefi haline gelir ve intravaskuler bir hemoliz gerceklesir (1-4).