Renal cortical necrosis

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Renal cortical necrosis

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A 30-year-old woman, gravida 2 para 1, at 26 weeks gestation is brought to the emergency department for evaluation of abdominal pain and vaginal bleeding following a motor vehicle accident three hours ago. A stat transvaginal ultrasound reveals placental abruption. After adequate resuscitation, the patient is brought to the operating room for emergent c-section. Approximate blood loss is 2500 mL. Several hours following the surgery, she endorses sudden onset bilateral flank pain. Physical examination shows bilateral costovertebral angle tenderness. Urine output in the last 6 hours is measured at 30mL. Laboratory results are shown.

 
 Laboratory value  Result 
 Complete blood count 
 Hemoglobin  8.5 g/dL 
 Leukocytes  10,000 /mL 
 Platelets  330,000/mm3 
 Serum chemistry 
 Sodium  136 mEq/L 
 Potassium  5.8 mEq/L 
 Chloride  85 mEq/L 
 Bicarbonate  19 mEq/L 
 Creatinine  1.7 mg/dL 
 Blood urea nitrogen (BUN)  40 mg/dL 
 Urinalysis 
 Erythrocytes  30-32/hpf 
 Leukocyte esterase  Negative 
 Leukocytes  2/hpf 
 Protein  1.0 g/day 
 Urine osmolality  650 mOsm/kg 
 Dysmorphic red blood cells  Absent 
 Cast  Tubular cell casts 
   
A renal ultrasound demonstrates hypoechoic areas in the renal cortex. Which of the following pathologic processes is responsible for this patient’s clinical presentation?  

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Renal cortical necrosis, sometimes called diffuse cortical necrosis, can be explained by the name. Renal refers to the kidneys, cortical refers to the outer layer, and necrosis refers to tissue death, so renal cortical necrosis describes the outer layer of the kidney dying—usually because of ischemia or a lack of blood flow.

Normally, around 20% of the blood leaving the heart goes into the renal arteries and through cortical radial arteries to reach the renal cortex, which is where the glomeruli of the nephrons are located. And that’s a lot of blood, especially given that the kidneys are relatively smallish organs when you put them next to the brain and liver.

Literally millions of glomeruli in the kidneys work to filter that large volume of blood, and they do so at a rate called the glomerular filtration rate.

It’s also worth noticing that those cortical radial arteries are end arteries, meaning that they rarely anastomose with adjacent branches, and are, therefore, more susceptible to infarction—since a single blocked artery is all it takes to cause ischemia because the tissue cannot be saved by neighboring arteries.

Some causes of reduced blood flow or a complete blockage are thrombi, which are blood clots that fill the blood vessels, and vasospasm, which is the narrowing of the blood vessel.

Interestingly, renal cortical necrosis has been associated with pregnancy complications, like placental abruption—which is when the placental lining is separated from the uterus—as well as prolonged intrauterine fetal death—which is when the fetus dies and then remains dead inside the uterus—and infected abortion—which is when there's an infection of the remnants of the placenta or fetus.

All of these are obviously terrible complications, and they relate back to renal cortical necrosis because they can progress to septic shock or disseminated intravascular coagulation, both conditions that can lead to the widespread formation of blood clots.

So once there’s an obstruction to blood flow, tissue ischemia sets in, and it triggers inflammation in the renal cortex.

Resumen

Renal cortical necrosis is one of the causes of prerenal acute kidney injury, caused by a sudden drop in blood perfusion to the renal cortex resulting from acute tubular necrosis. Causes that can lead to this hypoperfusion of the renal cortex include spasms of the feeding arteries, microvascular injury, or disseminated intravascular coagulation.

Symptoms may include a sharp decrease in urine output, flank pain at the costovertebral angle, and hematuria. Diagnosis is usually made by imaging techniques such as computed tomography (CT) or magnetic resonance imaging (MRI). Treatment options are limited, and the main focus is usually on supportive care and management of underlying causes. Renal replacement therapy may be necessary in some cases.

Fuentes

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Cellular pathophysiology of ischemic acute kidney injury" Journal of Clinical Investigation (2011)
  6. "Acute kidney injury in late pregnancy in developing countries" Renal Failure (2010)
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