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Renal Cortical Necrosis

By Zhiwei Zhang, MD, Associate Professor of Medicine;Attending Nephrologist, Loma Linda University;VA Loma Linda Healthcare System

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Renal cortical necrosis is destruction of cortical tissue resulting from renal arteriolar injury and leading to chronic kidney disease. 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 MRI, CT, isotopic renal scanning, or renal biopsy. Mortality rate at 1 yr 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.


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



Abruptio placentae (causes about 50% of cases)

Congenital heart disease (severe)


Fetomaternal transfusion

Hemolytic anemia (severe)

Perinatal asphyxia

Renal vein thrombosis




Hemolytic-uremic syndrome



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%)



Disseminated intravascular coagulation

Drugs (eg, NSAIDs)

Hyperacute renal allograft rejection

Incompatible blood transfusion

Nephrotoxic contrast agents


Poisoning (eg, phosphorus, arsenic)




Symptoms and Signs

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.


  • Imaging, usually with CT angiography

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, 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 BUN 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 PT/INR and PTT. Urinalysis typically detects proteinuria and hematuria.


Prognosis of renal cortical necrosis was poor in the past, with mortality > 50% in the first year. More recently, with aggressive supportive therapy, 1-yr mortality can be about 20%, and up to 20% of survivors may recover some renal function.


Treatment is directed at the underlying disorder and at preserving renal function (eg, with early dialysis).

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 vascular imaging, usually CT angiography.

  • Treat the underlying disorder.

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