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Acute tubular necrosis
Renal cortical necrosis
Renal papillary necrosis
IgA nephropathy (NORD)
Rapidly progressive glomerulonephritis
Focal segmental glomerulosclerosis (NORD)
Minimal change disease
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Chronic kidney disease
Renal tubular acidosis
Nephroblastoma (Wilms tumor)
Renal cell carcinoma
Renal artery stenosis
Acid-base disturbances: Pathology review
Congenital renal disorders: Pathology review
Electrolyte disturbances: Pathology review
Kidney stones: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Renal and urinary tract masses: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Renal cortical necrosis
0 / 3 complete
0 / 1 complete
|Complete blood count|
|Blood urea nitrogen (BUN)||40 mg/dL|
|Urine osmolality||650 mOsm/kg|
|Dysmorphic red blood cells||Absent|
|Cast||Tubular cell casts|
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.
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.
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