Background
Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. The lesions are usually caused by significantly diminished renal arterial perfusion secondary to vascular spasm, microvascular injury, or intravascular coagulation. Renal cortical necrosis is usually extensive, although focal and localized forms occur. In most cases, the medulla, juxtamedullary cortex, and a thin rim of subcapsular cortex are spared. (See Etiology.)
Classification
Renal cortical necrosis is classified into 5 pathologic forms, depending on severity, as follows:
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Focal pathologic form - Kidneys show focally necrotic glomeruli without thrombosis and patchy necrosis of tubules
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Minor pathologic form - Larger foci of necrosis are evident with vascular and glomerular thrombi
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Patchy pathologic form - Patches of necrosis may occupy two thirds of the cortex
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Gross pathologic form - Almost the entire cortex is involved; thrombosis of the arteries is more widespread
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Confluent pathologic form - Kidneys show widespread glomerular and tubular necrosis with no arterial involvement
Complications
Acute renal failure is typical in patients with renal cortical necrosis, with associated complications (eg, hyperkalemia, fluid overload).
Chronic renal failure, occurring in 30-50% of patients, requires dialysis and transplantation. (See Treatment.)
Go to Acute Renal Failure and Acute Tubular Necrosis for complete information on these topics.
Etiology
Cases of renal cortical necrosis are usually bilateral. Although the pathogenesis of the disease remains unclear, the presumed initiating factor is intense vasospasm of the small vessels. If this vasospasm is brief and vascular flow is reestablished, acute tubular necrosis results. More prolonged vasospasm can cause necrosis and thrombosis of the distal arterioles and glomeruli, and renal cortical necrosis ensues.
In hemolytic-uremic syndrome (HUS) and septic abortion, an additional mechanism involves endotoxin-mediated endothelial damage that leads to vascular thrombosis.
Studies have shown that patients with HUS with thrombotic microangiopathy (TMA) involving arteries have a higher likelihood of progressing into acute cortical necrosis compared with patients with predominant glomerular TMA. [1]
Renal cortical necrosis in placental abruption may be due to a combination of a hypercoagulable state, endothelial injury, and intravascular thrombosis.
Neonatal risk factors
Neonatal conditions that may lead to renal cortical necrosis include the following:
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Congenital heart disease
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Fetal-maternal transfusion
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Dehydration
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Perinatal asphyxia
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Anemia
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Placental hemorrhage
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Severe hemolytic disease
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Sepsis
Childhood risk factors
Childhood conditions that may lead to renal cortical necrosis include the following:
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HUS
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Acute gastroenteritis with dehydration
Pregnancy-related risk factors
Pregnancy-related conditions (more than 50% of cases) [2, 3] that may lead to renal cortical necrosis include the following:
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Placental abruption
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Infected abortion
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Prolonged intrauterine fetal death
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Severe eclampsia
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Postpatrum hemorrhage [4]
Additional risk factors
Miscellaneous conditions that may lead to renal cortical necrosis include the following:
Epidemiology
Incidence in the United States
Renal cortical necrosis accounts for 2% of all cases of acute renal failure in adults and more than 20% of acute renal failure during the third trimester of pregnancy. Renal cortical necrosis was detected by postmortem examination in 5% of infants aged 3 months or younger at death.
International incidence
Renal cortical necrosis incidence is higher in developing countries, ranging from 6-7% of all cases of acute renal failure. The incidence of acute cortical necrosis has been decreasing in developing countries over the past years.
The incidence of renal cortical necrosis was reported to be 3.12% of all cases of acute renal failure based on a study from India. [12] Acute cortical necrosis due to obstetric causes was observed in 56.2% of patients, whereas nonobstetric causes accounted for acute renal failure in 43.8% of the patients.
Prakash et al recently reported that the incidence of renal cortical necrosis in obstetric acute kidney injury in developing countries is declining, likely a reflection of improving obstetric care. [13]
Race predilection
Renal cortical necrosis has no race predilection.
Sex predilection
In childhood, renal cortical necrosis equally affects both sexes. In adults, renal cortical necrosis occurs more frequently in women, because the most common cause is placental abruption (50% of all cases).
Age predilection
The first peak of renal cortical necrosis occurrence is in early infancy and is associated with severe perinatal events or conditions. Renal cortical necrosis in childhood is usually secondary to HUS or severe volume depletion. Occurrence also peaks in women of childbearing age because of obstetric causes. [14]
Prognosis
In untreated patients, the mortality rate from renal cortical necrosis exceeds 50%. Early initiation of dialysis significantly diminishes this rate.
The most important prognostic factors are the extent of necrosis, duration of oliguria, and severity of associated conditions.
Infant survival rates are low because of associated conditions.
Severe congenital heart disease is a major risk factor for death.
Of those patients who survive, most require dialysis for variable periods of time, depending on the extent of necrosis. Some patients have recovered renal function even after several months of oliguria.
Patient Education
For patient education information, see the Diabetes Center and the Kidneys and Urinary System Center, as well as Acute Kidney Failure and Blood in the Urine.
