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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 could be patchy or diffuse, bilateral renal arteriolar injury results in destruction of cortical tissues and acute renal failure. 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 2: Renovascular Disorders: Causes of Renal Cortical Necrosis ).
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Table 2
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Causes of Renal Cortical
Necrosis
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Patient Group
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Causes
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Neonates
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Abruptio placentae (causes about 50% of cases)
Congenital heart disease (severe)
Dehydration
Fetomaternal transfusion
Hemolytic anemia (severe)
Perinatal asphyxia
Renal vein thrombosis
Sepsis
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Children
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Dehydration
Hemolytic-uremic syndrome
Sepsis
Shock
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Pregnant and postpartum women
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Pregnancy complications (causes > 50% of cases): abruptio placentae, amniotic fluid embolism, intrauterine fetal death, placenta previa, preeclampsia, puerperal sepsis, uterine hemorrhage
Sepsis (causes about 30%)
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Others
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Burns
Disseminated intravascular coagulation
Drugs (eg, NSAIDs)
Hyperacute renal allograft rejection
Incompatible blood transfusion
Nephrotoxic contrast agents
Pancreatitis
Poisoning (eg, phosphorus, arsenic)
Sepsis
Snakebite
Trauma
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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.
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 pentaacetic 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 functions 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
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
Treatment is directed at the underlying disorder and at preserving renal function (eg, with early dialysis).
Last full review/revision April 2008 by Seyed-Ali Sadjadi, MD
Content last modified April 2008
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