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
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).
Causes of Renal Cortical Necrosis
Patient Group |
Causes |
|
Neonates |
Abruptio placentae (causes about 50% of cases) Dehydration Fetomaternal transfusion Perinatal asphyxia Renal vein thrombosis |
|
Children |
Dehydration |
|
Pregnant and postpartum women |
Pregnancy complications (cause > 50% of cases): Abruptio placentae, amniotic fluid embolism, intrauterine fetal death, placenta previa, preeclampsia, puerperal sepsis, uterine hemorrhage Sepsis (causes about 30%) |
|
Others |
Burns Drugs (eg, nonsteroidal anti-inflammatory drugs) Hyperacute renal allograft rejection Incompatible blood transfusion Nephrotoxic contrast agents Trauma |
Symptoms and Signs
Diagnosis
Diagnosis is suspected when typical symptoms occur in patients with a potential cause.
Imaging tests can sometimes confirm the diagnosis. CT angiography is usually preferred despite the risks of using an iodinated contrast agent. Because of the risk of nephrogenic systemic fibrosis, use of magnetic resonance angiography with gadolinium contrast is not recommended in these patients, who usually have severe renal dysfunction.
An alternative is isotopic renal scanning using diethylenetriamine penta-acetic acid. It shows enlarged, nonobstructed kidneys, with little or no renal blood flow. Renal biopsy is done only if the diagnosis is unclear and no contraindications exist. It provides definitive diagnosis and prognostic information.
Urinalysis, complete blood count (CBC), liver function tests, and serum electrolytes and renal function tests are done routinely. These tests often confirm renal dysfunction (eg, indicated by elevated creatinine and blood urea nitrogen and by hyperkalemia) and may suggest a cause. Severe electrolyte abnormalities may be present depending on the cause (eg, hyperkalemia, hyperphosphatemia, hypocalcemia). CBC often detects leukocytosis (even when sepsis is not the cause) and may detect anemia and thrombocytopenia if hemolysis, 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.
Prognosis
Treatment
Key Points
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Renal cortical necrosis is rare, typically occurring in neonates and in pregnant or postpartum women with sepsis or pregnancy complications.
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Suspect the diagnosis in patients at risk who develop typical symptoms (eg, gross hematuria, flank pain, decreased urine output, fever, hypertension).
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Confirm the diagnosis with renal vascular imaging, usually CT angiography.
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Treat the underlying disorder.
