Abstract
Abstract
Preterm birth (In SVN, nephron mass is reduced because prematurity interrupts and an adverse intrauterine environment impairs nephron endowment. Maladaptive responses to low nephron mass include glomerular hyperfiltration, glomerular hypertension and glomerular sclerosis. In addition, complications of prematurity cause renal hypoperfusion and pharmacological treatment on the neonatal intensive care unit (NICU) can be nephrotoxic, both contributing to neonatal acute kidney injury (AKI). Neonatal AKI is common, has a high acute mortality and is a potentially modifiable second hit towards CKD.
Preventive strategies include optimizing maternal health to prevent SVN, improved detection and avoidance of neonatal AKI by reduction of nephrotoxicity and kidney hypoperfusion during NICU-treatment and systematic documentation of AKI at discharge. Physicians and families should be educated about the child’s lifelong CKD risk. Follow-up should be stratified by completed gestational weeks, birth weight, occurrence of AKI and comorbidities. Follow-up aims are early identification and treatment of CKD progression factors and complications.