Summary of Renal cortical necrosis
Transcript for Renal cortical necrosis
Content Reviewers:Rishi Desai, MD, MPH, Kyle Slinn, RN, BScN, MEd, Maria Fernanda Villareal, Vincent Waldman, PhD, Tanner Marshall, MS
Renal cortical necrosis
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.
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.