Renal cortical necrosis

Definitions & Key takeaways

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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Introduction0:00–0:27

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.

Physiology0:27–0:46

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.

Causes0:46–2:03

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.

Pathophysiology2:03–3:38

So once there’s an obstruction to blood flow, tissue ischemia sets in, and it triggers inflammation in the renal cortex.
That inflammation causes fluid to leak into the interstitium of the kidney—which is the space between the cells—and triggers vasoconstriction of the afferent arterioles which bring blood to the glomeruli of the nephrons.
That vasoconstriction reduces the glomerular filtration rate—which is the amount of blood that gets filtered over time. Also, some parts of the nephron that happen to be in the cortex, like the proximal tubule and the thick ascending loop of Henle, need more energy and therefore a bigger supply of blood, to carry out their job of reabsorption.
Since these cells are very energy demanding, having a reduced blood supply, means that they are the first to start dying and detaching when there’s renal ischemia.
The dead epithelial cells can clog up the lumen of the nephron, and cause an increase in the pressure within that nephron.
Since blood likes to move from a high pressure to low pressure space whenever possible, a higher pressure inside the nephron reduces glomerular filtration rate even more.
Up to this point, if the obstruction goes away and normal blood flow is recovered, the damage to the kidney cells is generally reversible, and this is also known as acute tubular necrosis.
If blood flow isn't recovered, though, and the ischemia persists, then the ischemic damage eventually leads to an irreversible necrotic injury to the renal cortex.
Broadly speaking, renal cortical necrosis is a type of prerenal acute kidney injury, which is a category that includes any cause of kidney injury that anatomically comes before the kidneys, like in this case a decreased blood flow in this case.

Symptoms3:38–4:11

The decrease in blood flow leads to one of the main symptoms which is a sharp decrease in urine output. Renal cortical necrosis makes the kidney swell up and stretches out the renal capsule, and that can cause flank pain at the costovertebral angle.
The diagnosis of renal cortical necrosis is often done by getting laboratory studies in the blood and urine. The blood typically has an excess of nitrogen waste products, like BUN and creatinine, as well as other serious electrolyte and metabolic imbalances, like hyperkalemia—increased potassium levels in blood—and metabolic acidosis.

Diagnosis4:11–5:12

The urine typically shows hematuria—blood in the urine, proteinuria—protein in the urine, and tubular cell casts which are dead tubule cells in the mold of the tubule.
Since there is no blood flow to the renal cortex, imaging studies—like a contrast-enhanced CT scan—usually shows a nonenhancing renal cortex.
Sometimes a very thin rim of contrast enhancement can happen, and this is known as the cortical rim sign. In a biopsy, the kidney cortex might show patchy necrosis and atrophy, whereas the renal medulla looks pretty normal.
Unfortunately, by the time renal cortical necrosis is treated, the damage is usually irreversible, so the main goal is to increase blood perfusion to the renal cortex.

Treatment5:12–5:28

Once kidney function is severely affected, hemodialysis may be needed. All right, as a quick recap, renal cortical necrosis is an irreversible type of prerenal acute kidney injury caused by a sudden drop in blood perfusion to the renal cortex, and it has been associated with pregnancy complications.

Review5:28–6:04

The reduced blood supply, due in part to the lack of anastomosis among radial end arteries, combined with the relatively high demand for blood in certain parts of the nephron like the proximal tubule and the thick ascending loop of Henle - causes ischemia to set in.
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