Renal cortical necrosis is destruction of cortical tissue resulting from renal arteriolar injury and leading to acute kidney injury. This rare disorder typically occurs in neonates and in pregnant or postpartum women when sepsis or pregnancy complications occur. Symptoms and signs include gross hematuria, flank pain, decreased urine output, fever, and symptoms of uremia. Symptoms of the underlying disorder may predominate. Diagnosis is by ultrasonography, CT, or renal biopsy. Mortality rate at 1 year is 20%. Treatment is directed at the underlying disorder and at preserving renal function.
In renal cortical necrosis, which may be patchy or diffuse, bilateral renal arteriolar injury results in destruction of cortical tissues and acute kidney injury. Renal cortical tissues eventually calcify. The juxtamedullary cortex, medulla, and the area just under the capsule are spared.
Etiology of Renal Cortical Necrosis
Injury usually results from reduced renal artery perfusion secondary to vascular spasm, microvascular injury, or intravascular coagulation.
About 10% of cases occur in infants and children. Pregnancy complications increase risk of this disorder in neonates and in women, as does sepsis. Other causes (eg, disseminated intravascular coagulation [DIC]) are less common (see table Causes of Renal Cortical Necrosis).
Symptoms and Signs of Renal Cortical Necrosis
Gross hematuria, flank pain, and sometimes decreased urine output or abrupt anuria occur. Fever is common, and chronic kidney disease with hypertension develops. However, these symptoms are often overshadowed by symptoms of the underlying disorder.
Diagnosis of Renal Cortical Necrosis
Imaging study or renal biopsy
Diagnosis is suspected when typical symptoms occur in patients with a potential cause.
The diagnosis can usually be established by ultrasonography or CT. Renal biopsy is done only if the diagnosis is unclear and no contraindications exist. It provides definitive diagnosis and prognostic information.
hyperkalemia, hyperphosphatemia, hypocalcemia). CBC often detects leukocytosis (even when sepsis is not the cause) and may detect anemia and thrombocytopenia if hemolysis, disseminated intravascular coagulation (DIC), or sepsis is the cause. Transaminases may be increased in relative hypovolemic states (eg, septic shock, postpartum hemorrhage). If DIC is suspected, coagulation studies are done. They may detect low fibrinogen levels, increased fibrin-degradation products, and increasing prothrombin time (PT)/INR and partial thromboplastin time (PTT). Urinalysis typically detects proteinuria and hematuria.
Treatment of Renal Cortical Necrosis
Treatment of underlying cause
Preservation of renal function
Treatment is directed at the underlying disorder and at preserving renal function (eg, with early dialysis).
Prognosis for Renal Cortical Necrosis
Prognosis of renal cortical necrosis was poor in the past, with mortality > 50% in the first year. More recently, with aggressive supportive therapy, 1-year mortality can be about 20%, and up to 20% of survivors may recover some renal function.
Key Points
Renal cortical necrosis is rare, typically occurring in neonates and in pregnant or postpartum women with sepsis or pregnancy complications.
Suspect the diagnosis in patients at risk who develop typical symptoms (eg, gross hematuria, flank pain, decreased urine output, fever, hypertension).
Confirm the diagnosis with renal imaging or renal biopsy.
Treat the underlying disorder.
