Femoral artery: An alternative cannulation localization in the angiographic treatment of dysfunctional arteriovenous fistulas. Single center experience

Bu çalışma, 26-28 Şubat 2021 tarihlerinde Sapanca-İstanbul düzenlenen 13. Çapa Nefroloji Günleri Kongresi‘nde bildiri olarak sunulmuştur.Endovasküler girişimler, disfonksiyonel arteriovenöz fistüllerin (AVF) tedavisinde en sık kullanılan tedavi modaliteleri olsa da optimal ponksiyon yeri konusunda bir fikir birliği yoktur. Bu retrospektif, tek merkezli çalışmada, femoral arter yoluyla disfonksiyonel AVF'lere yönelik endovasküler girişimlerin kısa vadeli klinik başarı oranlarını ve komplikasyonlarını sunuyoruz. Ocak 2016 ile Aralık 2019 arasında AVF disfonksiyonu tanısı alan ve bu nedenle perkütan transluminal anjiyoplasti (PTA) uygulanan toplam 29 hemodiyaliz hastası bu çalışmaya dahil edildi. Tüm PTA'lar aynı deneyimli girişimsel kardiyolog tarafından yapıldı. Hastaların demografik, klinik verileri, birincil açıklık ve işlem komplikasyonlarına ilişkin veriler hastane veri tabanından ve/veya hastanın kendi hemodiyaliz merkezinin elektronik kayıtlarından elde edildi. İşlem sonrası “thrill”in saptanması, başarılı kanülasyon ve tedaviden hemen sonra yeterli hemodiyaliz yapılabilmesi klinik başarı olarak kabul edildi. Toplam 29 hemodiyaliz hastasına AVF disfonksiyonu nedeniyle PTA uygulandı. Hastaların ortanca yaşı 61 (IQR 55.0-68.0) olup, %72.4'ü erkekti. Hastaların %41'i diyabetikti. Ortanca AVF yaşı 44.0 (24.0-92.0) aydı. Jukstaanastomotik (%48.3) ve efferent ven darlığı (%37.9) AVF işlev bozukluğunun ana nedenleriydi. 27 hastaya paklitaksel salınımlı balon anjiyoplasti uygulandı. Girişimlerin klinik başarı oranı %93.1 idi. İki hastada femoral arter ponksiyon yerinde lokal hematom gelişmesi dışında diğer hastalarda başka bir majör veya minör komplikasyon gözlenmedi. Femoral arter yoluyla yapılan PTA girişimleri AVF disfonksiyonlarında etkili ve güvenli bir tedavi yöntemidir.Although endovascular interventions are the most commonly used treatment modalities in the treatment of dysfunctional AVFs, there is no consensus on the optimal puncture site. In this retrospective single-center study, we present the short-term clinical success rates and complications of our interventions for dysfunctional AVFs via the femoral artery. 29 hemodialysis patients who were diagnosed with AVF dysfunction between January 2016 and December 2019 and therefore underwent percutaneous transluminal angioplasty (PTA) were included in this study. All PTAs were performed by the same experienced interventional cardiologist. Demographic, clinical data of the patients, and data on primary patency and procedural complications used were obtained from the hospital database and electronic records of the patient's own hemodialysis center. Detection of "thrill" after the procedure, successful cannulation, and adequate hemodialysis immediately after the treatment was considered a clinical success. A total of 29 hemodialysis patients underwent PTA due to AVF dysfunction. The median age of the patients was 61 (IQR 55.0-68.0) and 72.4% were male. 41% of patients were diabetic. The Median AVF age was 44.0 (24.0-92.0) months. Juxtaanastomotic (48.3%) and efferent venous stenosis (37.9%) were the main causes of AVF dysfunction. Paclitaxel-released balloon angioplasty was performed on 27 patients. The clinical success rate of the procedure was 93.1%. Two patients developed a local hematoma at the femoral artery puncture site; no other major or minor complications were detected. PTA via the femoral artery is an effective and safe treatment modality for AVF dysfunctions

Akut ve kronik lösemilerde survivin ve EPR-1 (Effektör Hücre Proteaz -1) ekspresyonunun prognostik önemi

TEZ5375Tez (Uzmanlık) -- Çukurova Üniversitesi, Adana, 2005.x, 72 s. : res. ; 29 cm.The inhibition of apoptosis is responsible not only for leukemia etiopathogenesis, but also for chemotherapy resistance which is a serious problem and affects survival negative. The expression of Survivin, an antiapoptotic protein, and EPR-1, as it is known to be Survivin's antisense, in acute and chronic leukemia's were assessed by RT-PCR assey in our research. The number of the patients included in the study was 110; 40 (37%) were with AML, 33 (30%) were with ALL, 24 (22%) were with CML and 13 (11%) were with CLL. Survivin expression were positive in 39 patients with AML (95.1%), 27 patients with ALL (%81.8) 12 patients with CML (52.2%) and 6 patients with CLL (46.2%). These ratios for EPR-1 were 7 (17.1%), 8 (24.2%), 1 (4.3%), 2 (15.4%) for AML, ALL, CML and CLL, respectively There was a statistically significant positive correlation between Survivin and LDH (p=0.005). Similarly, a statistically significant positive correlation between EPR-1 and Survivin was also found (p<0.001) And there were negative correlations between Survivin and white blood cells (p<0.05), Hb (p<0.001), EPR-1 and age were negatively correlated (p<0.0001), while it was positively correlated with CD33 (p=0.003) Hct (p<0.0001) and platelets (p<0.0005). Mean survival was shorter with positive Survivin; 24 months against 12 months in acute leukemias (p=0.1) and 54 months against 71 months in chronic leukemias (p=0.1) In subgroup analyses, there was a statistically significant survival in Survivin positive patients with AML (p=0.05). Mean survival of patients with acute leukemia with positive EPR-1 was longer (27 months) than those with negative expression (10 months), and this was statistically significant (p=0.001). Patients with AML who were EPR-1 positive had statistically significant longer survival (mean survival was 36 months against 6 months) (p=0.0006) When all the patient groups were evaluated, mortality ratios and Survivin expressions were correlated. Mortality ratios of those with positive Survivin were higher (84.5% against 61.5%) (p=0.01) EPR-1 negative. patients also had higher mortality ratios (61.1% against 82.6%) (p=0.04). The shortest survival was seen in Survivin(+)/EPR-1(-) group while the longest one was in Survivin(-)/EPR-1(-) group Survivin expression affects survival negatively in both acute and chronic leukemias, and EPR-1 affects survival positively by acting as Survivin's natural antisense.Apoptozis inhibisyonu yalnız lösemi etyopatogenezinde değil, aynı zamanda tedavi sırasında ciddi problem oluşturan ve sağkalımı olumsuz yönde etkileyen kemoterapi direncinden de sorumludur. Çalışmamızda bir antiapoptotik protein olan Survivin ve onun antisensi olduğu kabul edilen EPR-1'in akut ve kronik lösemilerdeki ekspresyonu RT-PCR yöntemi ile araştırıldı. Toplam hasta sayısı 110 olup bunların 40'i (%37)AML, 33'ü (%30) ALL, 24'ü (%22) KML ve 13'ü (%11) KLL idi. 39 AML'li (%95.1), 27 ALL'li , 12 KML'li (%52.2), 6 KLL'li (%46.2) hastada Survivin ekspresyonu saptandı. EPR-1 için bu oranlar AML, ALL, KML, KLL'de sırasıyla 7 (%17.1), 8 (%24.2), 1 (%4.3), 2 (%15.4) idi. Survivin ile LDH arasında istatistiksel olarak anlamlı pozitif korelasyon vardı (p=0.005). EPR-1 ile Survivin arasında istatistiksel olarak anlamlı pozitif korelasyon saptandı(p<0,001). Survivin ile beyaz küre (p<0.05), Hb (p<0.001), Hct (p<0.001) ve trombosit düzeyleri (p<0.005) ile negatif korelasyon saptandı. EPR-1 ekspresyonu ile yaş arasında negatif (p=0.045), CD33 arasında pozitif korelasyon saptandı (p= 0.003). Survivin pozitif akut lösemili hastalarda ortalama sağkalım daha kısa bulundu. (ortalama 12 aya karşın 24 ay) (p=0.1) Survivin pozitif kronik lösemili hastalarda ortalama sağkalım daha kısa idi (54 aya karşın 71 ay) (p=0.1). Alt grup analizlerinde Survivin ekspresyonu olan AML'li hastalarda istatistiksel olarak anlamlı bir şekilde daha uzun sağkalım süresi saptandı (p=0.05). EPR-1 pozitif akut lösemili hastalarda ortalama sağkalım negatif hastalara göre istatistiksel olarak anlamlı bir şekilde uzun bulundu (ortalama sağkalım 27 aya karşın 10 ay) (p=0.001). EPR-1 ekspresyonu olan AML'li hastalar istatistiksel olarak anlamlı bir şekilde daha uzun sağkalıma sahiplerdi (ortalama sağkalım 34 aya karşın 6 ay) (p=0.0006). Tüm hasta grupları değerlendirildiğinde Survivin pozitif olanlarda mortalite oranları daha yüksekti (%84.5 karşın %61.5) (p=0.01). EPR-1 negatif olanlarda hastalarda ise mortalite oranları daha yüksekti (%61.1'e karşın %82.6) (p=0.04). En kısa sağkalım, Survivin (+)/EPR-1 (-) grupta gözlenirken en uzun sağkalım Survivin (-)/EPR-1 (-)grupta gözlendi. Survivin ekspresyonu hem akut hem kronik lösemilerde sağkalımı olumsuz yönde etkilemektedir. EPR-1 ise Survivin'in doğal antisensi gibi davranarak sağkalımı olumlu yönde etkilemektedir

The Pathophysiology of Left Ventricular Hypertrophy, beyond Hypertension, in Autosomal Dominant Polycystic Kidney Disease

Heart disease is one of the leading causes of death in autosomal dominant polycystic kidney disease (ADPKD) patients. Left ventricular hypertrophy (LVH) is an early and severe complication in ADPKD patients. Two decades ago, the prevalence of LVH on echocardiography in hypertensive ADPKD patients was shown to be as high as 46%. Recent studies using cardiac magnetic resonance imaging have shown that the prevalence of LVH in ADPKD patients may be lower. The true prevalence of LVH in ADPKD patients is controversial. There is evidence that factors other than hypertension contribute to LVH in ADPKD patients. Studies have shown that young normotensive ADPKD adults and children have a higher left ventricular mass index compared to controls and that the prevalence of LVH is high in patients with ADPKD whose blood pressure is well controlled. Polycystin-1 (PC-1) and polycystin-2 (PC-2) control intracellular signaling pathways that can influence cardiac function. Perturbations of PC-1 or PC-2 in the heart can lead to profound changes in cardiac structure and function independently of kidney function or blood pressure. PC-1 can influence mammalian target of rapamycin and mitophagy and PC-2 can influence autophagy, processes that play a role in LVH. Polymorphisms in the angiotensin-converting enzyme gene may play a role in LVH in ADPKD. This review will detail the pathophysiology of LVH, beyond hypertension, in ADPKD

THE KIDNEY AT RISK: UNDERSTANDING CRUSH SYNDROME-RELATED ACUTE KIDNEY INJURY RİSK ALTINDAKİ BÖBREK: EZİLME SENDROMUNA BAĞLI AKUT BÖBREK HASARI

Crush syndrome (systemic manifestations of traumatic rhabdomyolysis) is the second leading cause of death after earthquakes or other destructive disasters. Crush-related acute kidney injury (AKI) is the most important Component of crush syndrome, and medical professionals living in disaster-prone regions should know about its pathophysiology, clinical and laboratory features, complications, and treatment. Pathogenesis of AKI on the basis of crush injuries is multifaceted. The most important mechanism is compartment syndrome-related hypovolemia, and consequent renal hypoperfusion, which may result in ischemic acute tubular necrosis. Also, rhabdomyolysis-related myoglobinuria may result in the formation of kidney-damaging myoglobin casts and direct tubular toxicity. Formation of uric acid plugs, oxidant injury, increased serum levels of cytokines, and still many other factors may take a role in the pathogenesis as well. Crush syndrome can cause serious electrolyte imbalances, sepsis, and bleeding, which can further exacerbate AKI. Early recognition and appropriate management, which includes aggressive hydration and management of electrolyte imbalances can help to prevent or minimize kidney damage. This review provides an overview of the pathophysiology, complications, and treatment of AKI in the context of Crush syndrome