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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of recent standardized definitions of acute kidney injury (AKI) has allowed us to begin understanding pediatric AKI epidemiology and risk factors and to stratify outcome by AKI severity. AKI incidence will vary with illness severity of the population studied and definition type, ranging from less than 1% when need for dialysis is used to 82% when less conservative definitions (such as > or =1.5 times baseline serum creatinine) are used to define AKI. The most common AKI causes are secondary, such as sepsis, nephrotoxic medication, and ischemia, each leading to acute tubular necrosis (ATN). Children undergoing cardiopulmonary bypass surgery, stem cell transplantation, or with multiple organ dysfunction syndrome are at high risk for these events. A key feature in diagnosis and management includes identifying the presence of ATN versus a reversible hypovolemic state because patients with ATN may quickly develop fluid overload with overaggressive fluid therapy, requiring dialytic removal. Despite advances in acute pediatric dialysis therapy and in overall care of critically ill children, severe AKI still is associated with a high mortality rate, necessitating more research in early AKI identification and therapeutic trials.
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PMID:Epidemiology and diagnosis of acute kidney injury. 1879 Mar 63

Acute kidney injury (AKI) is a clinical condition considered to be the consequence of a sudden decrease (> 25%) or discontinuation of renal function. The term AKI is used instead of the previous term acute renal failure, because it has been demonstrated that even minor renal lesions may cause far-reaching consequences on human health. Contemporary classifications of AKI (RIFLE and AKIN) are based on the change of serum creatinine and urinary output. In the developed countries, AKI is most often caused by renal ischemia, nephrotoxins and sepsis, rather than a (primary) diffuse renal disease, such as glomerulonephritis, interstitial nephritis, renovascular disorder and thrombotic microangiopathy. The main risk factors for hospital AKI are mechanical ventilation, use of vasoactive drugs, stem cell transplantation and diuretic-resistant hypervolemia. Prerenal and parenchymal AKI (previously known as acute tubular necrosis) jointly account for 2/3 of all AKI causes. Diuresis and serum creatinine concentration are not early diagnostic markers of AKI. Potential early biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), interleukins 6, 8 and 18, and liver-type fatty acid-binding protein (L-FABP). Early detection of kidney impairment, before the increase of serum creatinine, is important for timely initiated therapy and recovery. The goal of AKI treatment is to normalize the fluid and electrolyte status, as well as the correction of acidosis and blood pressure. Since a severe fluid overload resistant to diuretics and inotropic agents is associated with a poor outcome, the initiation of dialysis should not be delayed. The mortality rate of AKI is highest in critically ill children with multiple organ failure and hemodynamically unstable patients.
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PMID:[Acute kidney injury in children]. 2503 98


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