Renal Cortical Necrosis

Updated: Jul 03, 2018
Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD 



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.)


Renal cortical necrosis is classified into 5 pathologic forms, depending on severity, as follows:

  • Focal pathologic form - Kidneys show focally necrotic glomeruli without thrombosis and patchy necrosis of tubules

  • Minor pathologic form - Larger foci of necrosis are evident with vascular and glomerular thrombi

  • Patchy pathologic form - Patches of necrosis may occupy two thirds of the cortex

  • Gross pathologic form - Almost the entire cortex is involved; thrombosis of the arteries is more widespread

  • Confluent pathologic form - Kidneys show widespread glomerular and tubular necrosis with no arterial involvement


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.


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:

  • Congenital heart disease

  • Fetal-maternal transfusion

  • Dehydration

  • Perinatal asphyxia

  • Anemia

  • Placental hemorrhage

  • Severe hemolytic disease

  • Sepsis

Childhood risk factors

Childhood conditions that may lead to renal cortical necrosis include the following:

  • HUS

  • 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:

  • Placental abruption

  • Infected abortion

  • Prolonged intrauterine fetal death

  • Severe eclampsia

  • Postpatrum hemorrhage[4]

Additional risk factors

Miscellaneous conditions that may lead to renal cortical necrosis include the following:

  • Sepsis[5]

  • Shock

  • Trauma

  • Snakebite[6] ​[7]

  • Hyperacute kidney transplant rejection

  • Poisons

  • Drugs (eg, nonsteroidal anti-inflammatory drugs [NSAIDs])

  • Contrast media

  • Malaria[8]

  • Antiphospholipid syndrome[9] ​[10]

  • ​Smoking synthetic cannabinoids[11]


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]


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.




The following may be noted in the history of patients with renal cortical necrosis:

  • Renal failure (oliguria, hematuria, flank pain)

  • Neonatal conditions (perinatal asphyxia, bleeding, cyanotic heart disease)

  • Childhood conditions (diarrhea, vomiting, blood in stools, HUS)

  • Severe trauma

  • Snakebite (eg, sea snake, cobra, green pit viper, Russell viper)

  • Pregnancy (bleeding, abortion, symptoms of eclampsia)

Physical Examination

Kidney findings may include abdominal or bilateral costovertebral tenderness and/or palpable, tender kidneys.

Findings in patients with shock may include hypotension, tachycardia, and/or delayed capillary refill.

Findings in pregnancy may include lower abdominal tenderness, contracted uterus, and/or vaginal bleeding.



Diagnostic Considerations

Diagnostic considerations include the following:

  • Renal artery thromboembolism

  • Renal infarction

  • Renal vein thrombosis

Consider the diagnosis of renal cortical necrosis in a pregnant woman with sudden onset of abdominal pain, a tender uterus, and hematuria, especially during the third trimester.

Consider the diagnosis in a newborn or young child with dehydration, oliguria, and hematuria.

Differential Diagnoses



Approach Considerations

The diagnostic characteristics of renal cortical necrosis can be detected via the following[15] :

  • Serum electrolytes

  • Complete blood count (CBC)

  • Coagulation studies

  • Urinalysis

  • Radiography

  • Ultrasonography

  • Contrast-enhanced computed tomography (CT) scanning

  • Renal scanning

  • Kidney biopsy

Serum Electrolytes

Serum electrolyte measurements and renal function tests are used in patients with renal cortical necrosis (RCN) to check for hyperkalemia, hypocalcemia, metabolic acidosis, and elevated creatinine levels.


A CBC may reveal hemolytic anemia and thrombocytopenia.

Coagulation Studies

Coagulation studies detect low fibrinogen levels and increased fibrin-degradation products.


Urinalysis detects hematuria, proteinuria, red blood cell (RBC) casts, and granular casts.


Thin cortical shells or tram lines caused by calcification are a radiologic hallmark, but they develop only 4-5 weeks after the initial insult.


The ultrasonogram initially shows enlarged kidneys with reduced blood flow.[16] Cortical tissue becomes shrunken later in disease progression.

Contrast-Enhanced CT Scanning

Computed tomography (CT) scanning with contrast is the most sensitive imaging modality in renal cortical necrosis.

Diagnostic features of renal cortical necrosis include absent opacification of the renal cortex and enhancement of subcapsular and juxtamedullary areas and of the medulla without excretion of contrast medium.[17]

Initiating hemodialysis immediately after the procedure may be necessary to minimize contrast-mediated renal damage, although conclusive evidence for the efficacy of this practice is lacking.

Renal Scanning

Diethylenetriamine penta-acetic acid (DTPA) scanning reveals markedly diminished perfusion with delayed or no function.

Renal scan is the imaging technique of choice to diagnose renal cortical necrosis in transplant kidneys or if contrast-enhanced CT scanning is unavailable.

Kidney Biopsy

Kidney biopsy findings provide the definitive diagnosis and prognostic information; biopsy is indicated if the diagnosis is unclear and when no contraindications are present.



Approach Considerations

The cornerstones of renal cortical necrosis therapy are to restore hemodynamic stability, institute early dialytic therapy, and treat the underlying cause of the disease.

Most cases of renal cortical necrosis initially require intensive care.


Early institution of dialysis treatment for renal failure is crucial for patients who are oliguric.

Most patients require an access (eg, hemocatheter, peritoneal dialysis catheter) to institute dialysis.

Dietary Measures

Ensure adequate energy intake.

Patients with compromised kidney function require a low-potassium, low-phosphorus diet.

Activity Restriction

Activity should continue as tolerated.


Consult a nephrologist to manage acute renal failure and for ongoing chronic renal replacement therapy.

Consultation with other specialties may be needed, depending on the etiology of the renal cortical necrosis.



Medication Summary

The restoration of hemodynamic stability may require use of intravenous (IV) crystalloids, colloids, blood products, and/or pressors to maintain blood pressure and cardiac output.


Class Summary

These agents are used to maintain blood pressure and cardiac output.

Lactated Ringer with Normal Saline

Lactated Ringer is essentially isotonic and has restorative properties. It restores interstitial and intravascular volume.

Normal saline

Normal saline is used for restoration of interstitial and intravascular volume.


Class Summary

These agents are used for volume expansion to treat shock. They are preferred over crystalloids because the excessive administration of fluids can lead to extravasation caused by vascular leak, especially during the febrile and hypotensive stages.

Albumin (Albuminar, AlbuRx, Albutein, Flexbumin, Plasbumin)

Albumin is used for certain types of shock or impending shock. It is useful for plasma volume expansion and maintenance of cardiac output. Although theoretically attractive, the benefit of colloid resuscitation over isotonic crystalloids is not proven.


Class Summary

These agents maintain blood pressure and cardiac output in patients with renal cortical necrosis.


Dopamine stimulates both adrenergic and dopaminergic receptors. The hemodynamic effect depends on the dose. Low doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. High doses produce cardiac stimulation and renal vasodilation. After initiating therapy, increase the dose by 1-4 mcg/kg/min every 10-30 minutes until an optimal response is obtained. Maintenance dosing at less than 20 mcg/kg/min is satisfactory in greater than 50% of patients.

Norepinephrine (Levophed)

Norepinephrine is used in protracted hypotension after adequate fluid replacement. It stimulates beta1- and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility and the heart rate, as well as vasoconstriction. As a result, it increases systemic blood pressure and cardiac output. Adjust and maintain the infusion to stabilize blood pressure (eg, 80-100 mm Hg systolic) sufficiently to perfuse vital organs.

Vasopressin (Pitressin)

Vasopressin has vasopressor and antidiuretic hormone (ADH) activity. It increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.