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Amaç: Pnömoni, KOAH, Bronşektazi, Hışıltı (Wheezing), Astım ve Bronşit tanıları ile göğüs hastalıkları servisine başvuruda bulunan hastaların balgam kültür sonuçlarında üreyen bakteri/bakterilerin antibiyotik direnç profillerinin belirlenmesidir. Materyal ve Metot: Ocak 2021- Şubat 2022 tarihleri arasında Göğüs Hastalıkları Servisinde yatarak tedavi gören Pnömoni, KOAH, Bronşektazi, Hışıltı (Wheezing), Astım ve Bronşit tanılı olgularda çalışılan balgam kültürleri, üreyen mikroorganizmalar ve antibiyotik dirençleri retrospektif olarak tarandı. 20-87 yaş arası; yaş ortalaması 36,2 olan, 295’i (%59) erkek, 205’i (%41) kadın olmak üzere toplam 500 hasta izlendi. Kültürde üremesi olmayan hastalar çalışmaya dahil edilmedi. Bulgular: 30 hastada Acinetobacter baumannii/haemolyticus, 16 hastada Enterobacter cloacae, 97 hastada Escherichia coli, 28 hastada Gram - Bacilli 12 hastada Haemophilus influenzae, 13 hastada Klebsiella oxytoca, 42 hastada Klebsiella pneumoniae, 13 hastada Klebsiella pneumoniae ssp ozaenae, 79 hastada Klebsiella pneumoniae ssp pneumoniae, 11 hastada Klebsiella species, 20 hastada Pseudomonas aeruginosa, 78 hastada Staphylococcus aureus ve 7 hastada Streptococcus pneumoniae) bakterisi üremiştir. Balgam kültürlerinde yoğun olarak üreyen bakterilerin antibiyotik dirençliliğine bakıldığımızda; Escherichia Coli, Amikasın (%16,4), Trimetoprim+ Sulfametaksazol (%8,24), Aztreonam (%9,27), Cefazolin (%6,18), Sefaperazon/Sulbaktam (%15,46), Ceftazidim (%20,61), Ampisilin+ Sulbaktam (%10,30), Cefotaxim (%13,40), Cefoxitim (%4,12), Piperasilin+ Tazobaktam (%14,43). Acinetobacter Baumanni, Amikasın (%13,33), Trimetoprim + Sulfametaksazol (%16,66), Aztreonam (%10,00), Cefazolin (%10,00), Sefaperazon/Sulbaktam (%3,33), Ceftazidim (%13,33), Ampisilin + Sulbaktam (%6,66), Cefotaxim (%10,00), Cefoxitim (%6,66), Piperasilin + Tazobaktam (%10,00). Pseudomonas Aeruginosa, Amikasın (%20,00), Trimetoprim + Sulfametaksazol (%15,00), Aztreonam (%10,00), Cefazolin (%10,00), Sefaperazon/Sulbaktam (%5,00), Ceftazidim (%5,00), Ampisilin + Sulbaktam (%15,00), Cefotaxim (%10,00), Cefoxitim (%5,00), Piperasilin + Tazobaktam (%5,00). Klebsiella Pneumonia Ssp, Amikasın (%8,86), Trimetoprim + Sulfametaksazol (%7,59), Aztreonam (%20,25), Cefazolin (%10,12), Sefaperazon/Sulbaktam (%5,06), Ceftazidim (%3,79), Ampisilin + Sulbaktam (%16,45), Cefotaxim (%11,39), Cefoxitim (%2,53), Piperasilin + Tazobaktam (%13,92). Sonuç: Pnömoni, KOAH, Bronşektazi, Wheezing, Astım ve Bronşit tanılı, mikroorganizma kökenli etkilenimi olan hastalarda izole edilen bakteriler ve bu bakterilere karşı duyarlılık-dirençlilik verilerine göre ampirik tedavi başlanması önemlidir.

WOS: 000443998400089 …

WOS: 000443998400058 …

Background Acute tubulointerstitial nephritis (TIN) is a significant cause of acute renal failure in paediatric and adult patients. There are no large paediatric series focusing on the aetiology, treatment and courses of acute TIN. Patients, design and setting We collected retrospective clinical data from paediatric patients with acute biopsy-proven TIN by means of an online survey. Members of four professional societies were invited to participate. Results Thirty-nine physicians from 18 countries responded. 171 patients with acute TIN were included (54%female, median age 12 years). The most frequent causes were tubulointerstitial nephritis and uveitis syndrome in 31% and drug-induced TIN in 30% (the majority of these caused by non-steroidal anti-inflammatory drugs). In 28% of patients, no initiating noxae were identified (idiopathic TIN). Median estimated glomerular filtration rate (eGFR) rose significantly from 31 at time of renal biopsy to 86mL/min/1.73m(2) 3-6 months later (p90mL/min/1.73m(2)), with only 3% having severe or end-stage impairment of renal function (

Background Alport syndrome (AS) is an inherited glomerular disease caused by mutations in COL4A3, COL4A4, or COL4A5. Associations between clinical manifestations and genotype are not yet well defined. Our study aimed to define clinical and genetic characteristics, establish genotype-phenotype correlations, and determine prognosis of AS in children. Methods A total of 87 children with AS from 10 pediatric nephrology centers, whom had genetic analyses performed at the Hacettepe University Nephrogenetics Laboratory between February 2017 and February 2019, were included. Data regarding demographics, family history, clinical and laboratory characteristics, histopathological and genetic test results, treatments, and yearly follow-up results were retrospectively analyzed. Results Of 87 patients, 16% presented with nephrotic syndrome. In patients with nephrotic syndrome, kidney biopsy findings showed focal segmental glomerulosclerosis (FSGS) in 79%, and COL4A3 mutations were the leading genetic abnormality (50%). Twenty-four percent of all patients progressed to chronic kidney disease (CKD). The rate of progression to CKD and the decline in the glomerular filtration rate of the patients with COL4A3 mutation were higher than other mutation groups (p < 0.001 and p = 0.04, respectively). In kidney survival analysis, nephrotic syndrome presentation, histopathology of FSGS, COL4A3 mutations, and autosomal recessive inheritance were found as independent risk factors for earlier progression to CKD. Cyclosporin A treatment did not improve kidney survival. Conclusions We emphasize that genetic testing is important for patients suspected as having AS. Furthermore, COL4A mutations should be considered in patients with FSGS and steroid-resistant nephrotic syndrome. This approach will shed light on the prognosis of patients and help with definitive diagnosis, preventing unnecessary and potentially harmful medications. C1 [Ozdemir, Gulsah; Gulhan, Bora; Duzova, Ali; Ozaltin, Fatih; Topaloglu, Rezan] Hacettepe Univ, Fac Med, Div Pediat Nephrol, TR-06230 Ankara, Turkey. [Atayar, Emine; Ozaltin, Fatih] Hacettepe Univ, Fac Med, Div Pediat Nephrol, Nephrogenet Lab, Ankara, Turkey. [Saygili, Seha] Istanbul Univ Cerrahpasa, Fac Med, Div Pediat Nephrol, Istanbul, Turkey. [Soylemezoglu, Oguz] Gazi Univ, Fac Med, Div Pediat Nephrol, Ankara, Turkey. [Ozcakar, Zeynep Birsin] Ankara Univ, Fac Med, Div Pediat Nephrol, Ankara, Turkey. [Eroglu, Fehime Kara] Dr Sami Ulus Matern & Childrens Hlth Hosp, Div Pediat Nephrol, Ankara, Turkey. [Candan, Cengiz] Istanbul Medeniyet Univ, Goztepe Training & Res Hosp, Div Pediat Nephrol, Istanbul, Turkey. [Demir, Belde Kasap] Tepecik Training & Res Hosp, Div Pediat Nephrol, Izmir, Turkey. [Soylu, Alper] Dokuz Eylul Univ, Fac Med, Div Pediat Nephrol, Izmir, Turkey. [Yuksel, Selcuk] Pamukkale Univ, Fac Med, Div Pediat Nephrol, Denizli, Turkey. [Alpay, Harika] Marmara Univ, Fac Med, Div Pediat Nephrol, Istanbul, Turkey. [Agbas, Ayse] Haseki Training & Res Hosp, Div Pediat Nephrol, Istanbul, Turkey. [Hayran, Mutlu] Hacettepe Univ, Fac Med, Dept Prevent Oncol, Ankara, Turkey.