Renal cortical necrosis, defined as the ischemia of the renal cortex with sparing of the medulla, is a rare, but very dangerous and life-threatening complication of the acute renal injury. Anuria, hematuria and a profoundly poor overall general condition are important clinical features. The diagnosis, made through laboratory and imaging studies, must be made early on, in order to increase the chances of survival.
Renal cortical necrosis (RCN), responsible for approximately 2-7% of all acute kidney injuries (AKIs), can have a rapidly progressing clinical course that may result in death without early recognition . Diminished perfusion of the renal cortex in both kidneys (as the underlying diseases are primarily of systemic etiology), occurs as a result of vascular spasm, coagulation, or microvascular injury, which may be seen in a myriad of disorders: hemolytic-uremic syndrome (HUS), placental abruption, sepsis, hemorrhagic shock (during pregnancy as well), eclampsia, extensive burn injury or severe dehydration resulting in hypovolemia, pancreatitis, snake bites and malaria  . RCN may also be induced by several drugs, such as aminoglycosides, beta-lactam antibiotics, and non-steroidal anti-inflammatory drugs (NSAIDs), whereas post-nephrectomy of kidney donors may also result in RCN  . Because of the nature of the condition, RCN is predominantly encountered in early infancy (HUS, sepsis, dehydration) and in women of childbearing age, when puerperal sepsis and placental abruption are responsible for the majority of cases . Regardless of the underlying cause, an acute onset of absolute or relative anuria (defined as excretion of 0 or < 100 mL of urine per 24h, respectively) lasting for several days or even weeks is the typical clinical presentation . Abdominal pain and fever, which may be severe in sepsis, can also appear. In addition, hematuria, both gross and/or microscopic, gastrointestinal hemorrhage, pulmonary edema and profound uremia lead to shock and multiorgan failure in many patients, and a fatal outcome is often seen without immediate initiation of dialysis  . This condition usually results in acute kidney failure.
Rapid detection of kidney failure is detrimental in order to save the life of the patient, which is why a detailed patient history and a thorough physical examination that will assess vital signs, history of urinary output, and note accompanying symptoms, are essential steps. A detailed laboratory workup comprising serum electrolyte levels (sodium, potassium, chloride, calcium, bicarbonate), arterial blood gas analyses (ABGs), kidney function tests (blood urea nitrogen and creatinine), a complete blood count (CBC) and urinalysis must be performed immediately, whereas imaging studies of the kidneys, either through ultrasonography or computed tomography (CT) should be subsequently employed. In fact, contrast-enhanced CT is considered as a very effective non-invasive method for early detection of RCN because it may identify a hypoattenuated subcapsular rim of the renal cortex , while magnetic resonance imaging (MRI) and contrast-enhanced ultrasonography may be used as well   . Although recommended in only a subset of patients due to its potential risks, renal biopsy is the gold standard for the diagnosis of RCN , which is classified into two types based on histopathological findings: diffuse, characterized by widespread cortical destruction; and patchy, where 30-50% of the cortical tissue is affected by ischemic necrosis  .