Yenidoğanda Akut Böbrek Hasarı
Özet
Akut Böbrek Hasarı (ABH) yenidoğan popülasyonunda özellikle ileri prematüre bebeklerde mortalite ve morbiditeyi artıran önemli bir klinik tablodur. Böbrek fonksiyonlarında ani azalma, glomerüler filtrasyon hızında (GFH) düşüş ve azotlu atıkların birikimi ile karakterizedir. Modern neonatal yoğun bakım uygulamalarına rağmen insidansı %30’lara ulaşmaktadır. Böbrek gelişiminin gebeliğin 36. haftasına kadar sürmesi nedeniyle preterm doğumlarda mevcut olan fizyolojik immatürite böbrekleri hasara karşı savunmasız bırakmaktadır. Tanıda serum kreatinin düzeylerindeki değişimler ve idrar çıkışına dayanan Modifiye Neonatal Kidney Disease: Improving Global Outcomes (KDIGO) kriterleri kullanılmaktadır. Ancak yenidoğan döneminde serum kreatinin değerlerinin maternal geçişten etkilenmesi ve gestasyonel yaşa bağlı değişkenlik göstermesi dikkatli klinik değerlendirme gerektirir. Olguların büyük kısmını (%85) prerenal nedenler oluştururken sepsis, nefrotoksik ilaçlar ve asfiksiye bağlı intrinsik nedenler ile postrenal obstrüksiyon da etyolojide yer alır. Tedavi yaklaşımı altta yatan nedenin düzeltilmesi, sıvı-elektrolit dengesinin korunması ve nefrotoksik ajanlardan kaçınılmasına dayanır. Tedaviye dirençli hiperkalemi, ağır metabolik asidoz veya kontrolsüz sıvı yüklenmesinde renal replasman tedavileri uygulanabilir. Akut böbrek hasarı geçiren yenidoğanlar uzun dönemde kronik böbrek hastalığı açısından izlenmelidir.
Acute Kidney Injury (AKI) is an important clinical condition in the neonatal population, particularly in very preterm infants increasing both mortality and morbidity. It is characterized by a sudden decline in kidney function, a decrease in glomerular filtration rate (GFR) and the accumulation of nitrogenous waste products. Despite modern neonatal intensive care practices, its incidence can reach up to 30%. Since kidney development continues until 36 weeks of gestation physiological immaturity in preterm infants makes the kidneys highly vulnerable. Diagnosis relies on changes in serum creatinine and urine output according to the Modified Neonatal Kidney Disease: Improving Global Outcomes (KDIGO) criteria. However, neonatal serum creatinine is influenced by maternal transfer and varies with gestational age requiring careful clinical evaluation. The majority of cases (85%) are prerenal, but intrinsic causes such as sepsis, nephrotoxic drugs, and asphyxia, as well as postrenal obstruction, also contribute to the etiology. Management focuses on correcting the underlying cause, maintaining fluid–electrolyte balance and avoiding nephrotoxic agents. Renal replacement therapy may be required for treatment-resistant hyperkalemia, severe metabolic acidosis or uncontrolled fluid overload. Neonates who develop AKI should be monitored long-term for the risk of chronic kidney disease.
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