Page created on December 16, 2018. Last updated on January 2, 2019 at 16:03
The kidneys receive a lot of blood: 20 – 25% of resting CO.
The oxygen extraction is very low, because the abundant circulation isn’t meant to serve oxygen but to be filtered. The tubules are what need the most oxygen in the kidneys.
In normal cases does the cortex receive much more blood than the medulla. However, when the RBF is decreased will the ratio be reduced – the cortex will still receive most blood of the two, but the difference won’t be as large.
The kidneys are built to tolerate hypoperfusion, so that blood can be redistributed from them to other organs when necessary. Of course, a significant hypoperfusion will damage them. Tubular hypoxia occurs first, manifesting as acute tubular nephropathy.
The RBF is autoregulated between a MAP of 60 – 160 mmHg. Because it is mostly constant does the kidney rely more on the composition of blood (hypoxaemia and anaemia) than the perfusion as triggers for erythropoietin production.
Kidneys adapt well to arterial stenosis by activating RAAS. They don’t adapt as well to congestion however, as in venous congestion, and stagnation hypoxia may occur.
The definition of cardiorenal syndrome isn’t entirely clear, as scientists haven’t agreed on what it actually includes. Most recently it has been defined as multiple clinical conditions where heart and kidney dysfunction overlap. It describes a condition where failure of one of these organs impairs the function of the other.
In heart failure is RAAS permanently activated as a compensatory mechanism. Angiotensin II vasoconstricts the renal artery, causing a lasting decrease in the renal circulation. This may lead to the production of reactive oxygen species, which damage the renal parenchyme.
Angiotensin II also activates NF-κB, inducing inflammatory processes in the kidney. Chemokines are produces that attract leukocytes that produce TNF-α, IL-1 and IL-6. This causes a chronic inflammation of the kidney.
The sympathetic tone is also increased in heart failure. This increases renin secretion which, together with ROS, leads to thickening of the walls of intrarenal vessels.
Angiotensin II promotes myocardial hypertrophy. This is especially important in primary kidney disease with activated RAAS and explains how kidney disease can worsen heart failure.