Acute Cortical Necrosis: Definition, Causes, and Management
Definition
Acute cortical necrosis (ACN) is a catastrophic renal condition characterized by patchy or diffuse ischemic destruction of all elements of the renal cortex resulting from severely diminished renal arterial perfusion due to vascular spasm, microvascular injury, and direct endothelial damage. 1, 2
- The pathophysiology involves both vascular spasm and direct endothelial injury, particularly in sepsis, eclampsia, hemolytic uremic syndrome (HUS), and snake envenomation, leading to endovascular thrombosis and subsequent renal ischemia. 2
- Progression to end-stage renal disease is the rule in diffuse cortical necrosis. 2
Causes
Obstetric Complications (Primary Cause in Developing Countries)
Obstetric complications account for 60-70% of ACN cases in developing countries, though this has declined from 20-30% to approximately 5% over the past two decades. 2, 3
Specific obstetric causes include:
The incidence of ACN in obstetrical acute kidney injury ranges from 1.44% to 42.8% depending on the region and time period studied. 2
Non-Obstetric Causes (30-40% of Cases)
Hemolytic uremic syndrome is the most common cause of ACN in the non-obstetrical group. 2
- Other non-obstetric causes include:
Epidemiology
- ACN accounts for only 1.9-2% of all acute kidney injury cases in developed countries, but 6-7% in developing countries. 2, 3
- Currently, ACN represents approximately 3% of all causes of acute kidney injury overall. 2
- Hospitalized patients with ACN have an approximate mortality rate of 37%. 1
Management
Immediate Supportive Care (First Priority)
Aggressive supportive care—including early dialysis initiation, hemodynamic stabilization, and treatment of the precipitating cause—is the cornerstone of ACN management. 1
Hemodynamic Stabilization
- After initial crystalloid resuscitation in volume-depleted patients, administer 20% albumin solution (approximately 1 g/kg, up to maximum dose) for two consecutive days. 1
- Daily urine output monitoring is essential; oliguria is associated with poorer prognosis. 1
Medication Management
- Stop all nephrotoxic medications immediately: NSAIDs, aminoglycosides, ACE inhibitors, ARBs, and iodinated contrast. 1
- Withdraw diuretics once ACN diagnosis is confirmed. 1
- Avoid additional nephrotoxic agents throughout the acute phase. 1
Infection Control
- Screen for and treat infections aggressively, as septicemia is a common precipitating factor, especially in obstetric-related ACN. 1
- Prophylactic antibiotics are not recommended due to unproven benefit. 1
- Avoid prophylactic bladder catheterization to reduce infection risk. 1
Renal Replacement Therapy
Hemodialysis should be initiated early based on clinical indications rather than waiting for specific biochemical thresholds. 1
Absolute Indications for Dialysis
- Severe or refractory hyperkalemia 1
- Metabolic acidosis unresponsive to medical management 1
- Volume overload unresponsive to diuretics 1
- Uremic manifestations (encephalopathy or pericarditis) 1
Modality Selection
- Continuous veno-venous hemofiltration (CVVH) is preferred for hemodynamically unstable patients, as it may improve renal blood flow when combined with inotropic support. 1
- Standard intermittent hemodialysis can be used in stable patients. 1
Diagnostic Confirmation
Magnetic resonance imaging (MRI) is the preferred non-invasive diagnostic tool for ACN. 1, 6
Characteristic MRI findings include:
Ultrasound contrast agents are not nephrotoxic and can be used to diagnose ACN in native kidneys. 1
Contrast-enhanced CT can also confirm ACN by showing contrasted medulla and thin subcapsular cortex without bilateral cortical enhancement. 4
Long-Term Management and Monitoring
The majority of patients progress to end-stage renal disease, making ongoing monitoring mandatory. 1, 2
Renal Function Monitoring
- Measure serum creatinine daily during the acute phase to stage acute kidney injury. 1
- Monitor ongoing renal function with serum creatinine and estimated glomerular filtration rate (eGFR). 1, 6
- Re-evaluate patients at three months after recovery for new or worsening chronic kidney disease, with follow-up extending from 12 to 74 months. 1
Chronic Kidney Disease Management
- Manage anemia and mineral-bone disorder according to established chronic kidney disease protocols. 1, 6
- Control blood pressure aggressively to limit further renal injury. 1, 6
- Monitor and correct electrolyte disturbances promptly, particularly hypocalcemia. 1
Nutritional Support
- Provide enteral nutrition (preferred over parenteral) at approximately 20-30 kcal/kg/day and 1.0-1.5 g protein/kg/day for patients on renal replacement therapy. 1
- Maintain careful fluid and electrolyte management with volume status monitoring. 6
Special Considerations
Anticoagulation in Thrombophilia
- In cases of ACN secondary to antiphospholipid syndrome or hyperhomocysteinemia, anticoagulation with low-molecular-weight heparin may be indicated. 5, 4
- For hyperhomocysteinemia, treat with folate supplementation and vitamin B12 injection. 5
Prognosis
- Most cases of ACN do not recover normal renal function despite intensive care. 7
- Rare cases of partial or complete renal recovery have been reported, even after years of dialysis dependence. 7, 5
- Prevention through better monitoring of pregnancies and early treatment of precipitating causes is critical to reducing the incidence of this catastrophic complication. 3