Background Each year, millions face natural disasters, encountering mass fatalities and severe medical issues such as crush injuries and crush syndrome. Crush syndrome, marked by acute kidney injury (AKI) and hyperkalemia, correlates with mortality. This study focuses on presenting epidemiological data on kidney disease resulting from the February 6, 2023 earthquakes centered in Kahramanmaras. Methods This retrospective analysis included patients diagnosed with crush syndrome after the 2023 Kahramanmaras earthquakes, treated in regional hospitals or referred elsewhere in Turkey. Patient data were documented using the web-based system developed by the Turkish Nephrology Association Renal Disaster Working Group. Results Of the 1024 analyzed patients from 46 centers, 515 (50.3%) were women. The mean age was 41 ± 16 years, with a median duration of 12 h under rubble, and the median presentation time to the first health facility was 4 h after extrication from the rubble. Upon admission, 79.8% received intravenous fluid therapy, all potassium-free. Initial serum creatinine, K⁺, and creatinine kinase levels averaged 2.59 ± 2 mg/dl, 5.1 ± 1 mmol/L 38,305 ± 54,303 U/L, respectively. Intensive care unit (ICU) admissions were 53.6%, with mean hospital and ICU stays of 20 and 11 days, respectively. Compartment syndrome occurred in 40.8% of patients, with 75.8% undergoing fasciotomy. Acute kidney injury developed in 67.9% of patients, with 70.3% undergoing hemodialysis, totaling 3016 sessions on 488 patients. The overall in-hospital mortality rate was 9.8%. Conclusion Earthquakes have a significant impact on kidney health. Although our study indicates some progress compared to previous earthquake responses, there remains a crucial need for drills emphasizing post-earthquake initial response, fluid-electrolyte balance management, and emergency dialysis protocols. Graphical abstract

Intrapatient variability (IPV) in tacrolimus has been increasingly acknowledged as a risk factor for poor graft survival after kidney transplantation. Although past studies have mainly accounted for IPV in acute or chronic rejection states as due to underimmunosuppression, this is not yet clear. So far, tacrolimus IPV for BK virus-associated nephropathy (BKVN) and chronic calcineurin inhibitor toxicity (CNIT) has not been investigated. Here, we evaluated IPV in tacrolimus for BKVN and chronic CNIT, which are mainly considered as overimmunosuppression states. In this case–control study, kidney allograft biopsies conducted between 1998 and 2018 were included, with patients grouped by biopsy results as BKVN alone group, CNIT alone group, and normal graft function (control group). IPV was estimated as mean absolute deviation. Our study groups included 25 kidney transplant recipients with BKVN alone, 91 patients with CNIT alone, and 60 patients with normal 5-year graft survival (control group). In analyses of IPV in tacrolimus six months before graft biopsy, IPV was highest in the BKVN group (P = 0.001). The BKVN group also had the highest IPV in tacrolimus at 12 months after biopsy (P = 0.001), with all pairwise comparisons statistically different between groups. At 12 months after biopsy, five patients (20%) in the BKVN group and 10 patients (10.9%) in the CNIT group had graft loss. Among other risk factors, BKVN and chronic CNIT are consequences related to high IPV. Quantification of IVP for tacrolimus in clinical practice would help to optimize kidney transplant outcomes.

Background Growth differentiation factor (GDF)-15 is related to inflammation and mortality in many conditions. We aimed to determine if an elevated serum GDF-15 level is related to nutritional status of patients on hemodialysis (HD), and mortality. Materials and Methods Routine HD patients (n=158) were included in the study and followed for 18 months. Some malnutrition/inflammation scoring indexes (malnutrition/inflammation score (MIS), controlling nutritional status (CONUT) score, and prognostic nutritional index (PNI)), biochemical parameters, and GDF-15 were used to build Cox regression multivariate models to study the association with mortality. Results Among the patients, 90 (57 %) had a high MIS (?8) which associates with worse status. The serum GDF-15 level was higher in the same group (p = 0.003). The serum GDF-15 level differentiated malnutrition/inflammation according to the MIS (p = 0.031). Age, GDF15, and C-reactive protein (CRP) were significantly associated with higher all-cause mortality risk. Patients with both age and GDF-15 above the mean had a hazard ratio of 2.76 (p=0.006) when compared with those both < mean. Conclusion In HD patients the GDF-15 level is increased in worse nutritional status. Beyond the MIS, age, GDF-15 and CRP would be used together to estimate the worse clinical outcome in these patients.

Background/aim: Neutrophil gelatinase-associated lipocalin (NGAL) is used previously to estimate the etiology, severity, and clinical outcomes of acute kidney injury (AKI). However, the role of urinary NGAL (uNGAL) in the postrenal setting is not clear. In our study, we aimed to discover the cut-off value of uNGAL that can be used in the differential diagnosis of underlying AKI etiologies.Materials and methods: In this prospective cross-sectional study, we examined 82 subjects in four groups: patients that had (1) postrenal AKI; (2) AKI other than postrenal etiologies; (3) stable chronic kidney disease; and (4) healthy subjects. A renal function assessment was carried out by measuring serum creatinine (sCr) and uNGAL at the time of diagnosis [0th min (T0)]. We followed the study group for three months. Results: At the time of diagnosis, sCr (T0) was highest in the postrenal AKI and AKI groups in contrast to stable chronic kidney disease patients and healthy subjects (P < 0.001), as expected. T0 median uNGAL was highest in the postrenal group (P < 0.001). Area under curve (AUC) of uNGAL to estimate postrenal AKI presence was 0.957 (95% CI, 0.897–1.000; P < 0.001). The cut-off point of uNGAL was 42.625 ng/mL for this estimation. Conclusion: Patients with AKI must be classified according to the underlying etiologies as soon as possible. uNGAL may be useful to estimate the etiologies, and whether the problem is acute or chronic in the course. In postrenal kidney problems, to plan the urgency of the urologic procedures, it is crucial.

Renal Anatomi Orçun ALTUNÖREN Garip BEKFİLAVİOĞLU Renal Fizyoloji Ceren ÖNAL Bülent ALTUN Öykü ve Fizik İnceleme Tekin AKPOLAT Klirens Kavramı ve Glomerüler Filtrasyon Hızı Ölçüm Metotları Ebru SEVİNÇ OK İdrar Analizi ve Yorumlanması Çiğdem MENGÜŞ Ahmet Uğur YALÇIN Renal Görüntüleme Kenan TURGUTALP Caner ÖZER Renal Biyopsi ve Temel Patolojik İncelemeler Gökhan TEMİZ İlter BOZACI İdrar Miktarı Değişiklikleri (Poliüri, Oligüri, Anüri) Aydın ÜNAL İşeme Bozuklukları (Noktüri-Pollaküri-Dizüri-İdrar İnkontinansı) Murat Hayri SİPAHİOĞLU Sümeyra KOYUNCU Hematüriye Yaklaşım Cenk GÖKALP Soner DUMAN Proteinüriye Yaklaşım Serkan AKTÜRK Fatih DEDE Hücre Dışı Sıvı Volümü Düzenlenmesi ve Bozuklukları Seyhun KÜRŞAT Su ve Sodyum Metabolizması Bozuklukları Tevfik ECDER Potasyum Metabolizması ve Bozuklukları Bülent TOKGÖZ Cihan UYSAL Kalsiyum Metabolizması ve Bozuklukları Engin ONAN Özkan GÜNGÖR Fosfor Metabolizması ve Bozuklukları Aysel GÜRKAN TOÇOĞLU Savaş SİPAHİ Magnezyum Metabolizması ve Bozuklukları Eyüp KÜLAH Asit-Baz Dengesi Zeki AYDIN Metabolik Asidoz Özant HELVACI Galip GÜZ Metabolik Alkaloz Aykut SİFİL Solunumsal Asit-Baz Bozuklukları Halil AYDAR Garip ŞAHİN Karma Asit-Baz Bozuklukları Meltem SEZİŞ DEMİRCİ Gökhan ATAY Glomerüler Hastalıkların Patogenezi ve Sınıflaması Serhan TUĞLULAR Primer Glomerüler Hastalıkların Epidemiyolojisi Egemen CEBECİ Nefritik Sendrom İzzet Hakkı ARIKAN Nefrotik Sendrom Ferruh ARTUNÇ Minimal Değişim Hastalığı Meltem GÜRSU Membranöz Nefropati Savaş ÖZTÜRK İmmünglobülin A Nefropatisi Zerrin BİCİK BAHÇEBAŞI Fokal Segmental Glomerüloskleroz Abdülmecit YILDIZ Membranoproliferatif Glomerülonefrit ve C3 Glomerülopatisi Ahmet Burak DİRİM Yaşar ÇALIŞKAN Hızlı İlerleyen Glomerülonefritler Hayriye SAYARLIOĞLU Enfeksiyon İlişkili Glomerülonefritler Beyza ALGÜL DURAK Emre TUTAL İnce Bazal Membran Hastalığı Kamil DİLEK Diğer Glomerülonefritler Necmi EREN Serkan BAKIRDÖĞEN Lupus Nefriti Mustafa GÜLLÜLÜ Diğer Bağ Dokusu Hastalıkları ve Böbrek Didem TURGUT Diabetes Mellitus Epidemiyolojisi, Tanısı, Patogenezi, Kliniği ve Tedavisi Kültigin TÜRKMEN İsmail BALOĞLU Diyabetik Böbrek Hastalığı Neriman Sıla KOÇ Mustafa ARICI Gebelikte Böbrek Fizyolojisi Kübra KAYNAR Gebelikte Böbrek İlişkili Sorunlar Dilek TORUN Böbrek Hastalıklarında Gebelik Saime PAYDAŞ Üriner Sistem Enfeksiyonlarına Yaklaşım Faruk Hilmi TURGUT Kan Basıncı Kontrolü ve Hipertansiyon Fizyopatolojisi Ercan TÜRKMEN Nurol ARIK Primer Hipertansiyon ve Tedavisi Şükrü ULUSOY Gülsüm ÖZKAN Renovasküler Hipertansiyon Hadim AKOĞLU Endokrin Hipertansiyon Ayşa HACIOĞLU Züleyha KARACA Diğer Sekonder Hipertansiyon Nedenleri Ali Rıza UÇAR Halil YAZICI Hipertansif Aciller Kürşad ÖNEÇ Ülver BOZTEPE DERİCİ Ozmotik Diüretikler Özgür Akın OTO Tiazid ve Benzeri Diüretikler Ayça İNCİ Loop Diüretikleri Fatma AYERDEN EBİNÇ Diğer Diüretikler Yasemin COŞKUN YAVUZ Akuaretikler İrem PEMBEGÜL Kistik Böbrek Hastalıkları İsmail KOÇYİĞİT Eray EROĞLU Kalıtsal Tübüler Hastalıklar Ramazan ÇETİNKAYA Fabry Hastalığı Nurhan SEYAHİ Şeyda GÜL ÖZCAN Alport Hastalığı Ali Kemal KADİROĞLU Akut İnterstisyel Nefrit Ali GÜREL Ayhan DOĞUKAN Kronik İnterstisyel Nefrit Hakan AKDAM FMF ve Amiloidoz Harun AKAR Paraproteinemiler ve Miyelom Böbreği Vecihi BATUMAN Ürolojik Testler ve Değerlendirilmesi Aydın GÜÇLÜ Vezikoüreteral Reflü Funda SAĞLAM Böbrek Taş Hastalıkları Neslihan TEZCAN Rüya MUTLUAY Üriner Sistem Obstrüksiyonu Funda SARI Akut Böbrek Hasarının Tanımı ve Epidemiyolojisi Belda DURSUN Akut Böbrek Hasarında Klinik ve Komplikasyonlar Yelda GÜN Yavuz YENİÇERİOĞLU Akut Böbrek Hasarı Tedavisi Abdülmecit YILDIZ Alp İKİZLER Ezilme (Crush) Sendromu Mehmet Şükrü SEVER Trombotik Mikroanjiyopatiler Tuncay ŞAHUTOĞLU Ekrem KARA Yoğun Bakım Ünitesinde Akut Böbrek Hasarı ve Hemodinamik Destek Özlem USALAN Orhan ÖZDEMİR Yoğun Bakım Ünitesinde Renal Replasman Tedavileri Cuma Bülent GÜL Hepatitler ve Böbrek Alper AZAK Hepatorenal Sendrom Sinan KAZAN Sena ULU Kardiyorenal Sendrom: Patogenez ve Tanı Bülent HÜDDAM Kardiyorenal Sendrom: Tedavi İlter BOZACI Erhan TATAR Ürik Asitin Sistemik Hastalıklar ve Hipertansiyon Gelişimindeki Rolü Sidar ÇOPUR Mehmet KANBAY Gut ve Ürik Asit Nefropatisi Ender HÜR Aysun TORAMAN Kronik Böbrek Hastalığının Epidemiyolojisi ve Fizyopatolojisi...