Acute Kidney Injury in Neonates
Our first aim is to describe how common a sudden decrease in renal function happens in infants in a neonatal intensive care unit. We also want to see how a sudden loss of renal function affects survival. Finally, we will explore non-invasive markers to identify a sudden decrease in renal function from urinary samples.
Advancements in the field of peri-natal medicine has improved the survival of critically ill neonates but yet many still do not survive, and many more are left with long-term damage to vital organ systems. Very little data is available on the impact that acute kidney injury (AKI) has on survival in term neonates, but adult and pediatric studies that show that even mild AKI independently impacts survival after correcting for severity of illness. The role that AKI impacts survival in neonates is likely to be greater than adults as this acute injury occurs in context of impaired and ongoing kidney development.
Our ability to improve outcomes in children and adults with AKI has been hampered by the inability to recognize AKI early in the disease process. Thus, the work on early non-invasive biomarkers of renal injury has brought great optimism to the field of AKI. Serum and urinary levels of neutrophil gelatinase-associated lipocalin (NGAL), urinary interleukin 18 (IL-18) others are markedly elevated several hours after AKI as opposed to serum creatinine which takes days to rise after the inciting event. Early non-invasive biomarkers of AKI have not been tested in neonates.
Inclusion criteria - Families of infants (birthweight >1500g) be asked to participate in the study.
Exclusion criteria - Infants with prenatal renal ultrasound diagnosis of severe hydronephrosis or other known renal abnormalities will be excluded
Time Perspective: Prospective
Acute Kidney Injury
University of Alabama at Birmingham
University of Alabama at Birmingham
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00572715
- ClinicalTrials.gov processed this data on April 01, 2015
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Medical and Biotech [MESH] Definitions
Abrupt reduction in kidney function defined as an absolute increase in serum CREATININE of more than or equal to 0.3. mg/dl, a percentage increase in serum creatinine of more than or equal to 50%, or a reduction in urine output. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal failure, either acute (KIDNEY FAILURE, ACUTE) or chronic (KIDNEY FAILURE, CHRONIC), requires HEMODIALYSIS.
A complication of kidney diseases characterized by cell death involving KIDNEY PAPILLA in the KIDNEY MEDULLA. Damages to this area may hinder the kidney to concentrate urine resulting in POLYURIA. Sloughed off necrotic tissue may block KIDNEY PELVIS or URETER. Necrosis of multiple renal papillae can lead to KIDNEY FAILURE.
A severe stage of acute renal insufficiency, characterized by the sudden decrease in GLOMERULAR FILTRATION RATE to less than 15 ml per min, sometime to less than 1 to 2 ml per min. It is usually associated with OLIGURIA; EDEMA; and increase in BLOOD UREA NITROGEN and serum CREATININE concentrations.