Chapter 528 Cortical Necrosis
Renal cortical necrosis is a rare cause of acute renal failure occurring secondary to extensive ischemic damage of the renal cortex. It occurs most commonly in neonates and in adolescents of childbearing age.
In newborns, cortical necrosis is most commonly associated with hypoxic or ischemic insults caused by perinatal asphyxia, placental abruption, and twin-twin or fetal-maternal transfusion. Other causes include renal vascular thrombosis and severe congenital heart disease. After the neonatal period, cortical necrosis is most commonly seen in children with septic shock or severe hemolytic-uremic syndrome. In adolescents and women, cortical necrosis occurs in association with obstetric complications including septic abortion and intrauterine fetal demise.
Less-common causes of cortical necrosis include extensive burns, snakebite, infectious endocarditis, and medications (e.g., nonsteroidal anti-inflammatory agents).
Renal cortical necrosis is a rare disease entity accounting for only 2% of all cases of acute renal failure in developed countries. The incidence is higher in developing countries.
Grossly, areas of necrosis are limited to the cortex of the kidney. Histologic findings consist of acute ischemic infarction. Intravascular and intraglomerular thromboses are present. These changes are bilateral and may be patchy or involve the whole cortex.
Cortical necrosis develops as a result of acute severe decreased renal arterial blood flow secondary to vascular spasm from ischemia or hypoxia or from endothelial cell injury from toxins or HUS. This leads to glomerular and arteriolar microthrombi and consequent cortical necrosis.
Cortical necrosis manifests as acute renal failure in patients who have the previously mentioned predisposing causes. Urine output is diminished and gross and/or microscopic hematuria may be present. Hypertension is common, and thrombocytopenia may be present as a result of renal microvascular injury.
Laboratory results are consistent with acute renal failure: an elevated blood urea nitrogen (BUN) and creatinine, hyperkalemia, and metabolic acidosis. Anemia and thrombocytopenia are common. Urinalysis reveals hematuria and proteinuria.
Ultrasound examination with Doppler demonstrates decreased perfusion to both kidneys. A radionuclide renal scan shows decreased uptake with significantly delayed or absent function.
It is important to treat the underlying cause, where possible. Therapy involves medical management of acute renal failure as well as the initiation of dialysis, where necessary. Management is otherwise supportive and involves volume repletion, correction of asphyxia, and treatment of sepsis.
Untreated, renal cortical necrosis has a mortality rate >50%. Long-term recovery of renal function depends on the amount of surviving cortex. Children with partial recovery can require therapy for end-stage renal disease. All patients require continued follow-up for chronic kidney disease.
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