8th February 2024

Renal perfusion and glomerular filtration

Renal perfusion

Despite their size, the kidneys receive up to 25% of the resting cardiac output, equating to around 1200mls/minute.

The left and right renal arteries are branches of the abdominal aorta. They enter each kidney at the hilum before branching into segmental arteries and then into interlobar arteries that pass through the renal columns. Once they reach the base of the pyramids, they become known as arcuate arteries. These then divide into interlobular arteries, which pass through the renal lobules and supply each nephron with an afferent arteriole. 

From here, the blood supply enters a network of capillaries known as a glomerulus. Unlike other capillary bodies, the glomerulus is not followed by a venule but by a further arteriole known as the efferent arteriole. The efferent arteriole divides into a second capillary network known as the peritubular capillaries, which surround the proximal and distal tubules of the nephrons within the renal cortex. Tubules within medullary nephrons are supplied by long vasa recta capillaries, which also originate from the efferent arterioles.

The peritubular capillaries drain into the peritubular venules and the interlobular veins. Blood from the vasa recta drains directly into the interlobular veins. From here, blood enters the arcuate veins, followed by the interlobar veins, before exiting the kidney via the renal vein. 

Image Source: Pressbooks (2017). Urinary structures and function, Licensed under a creative commons licence. Available for free at: https://pressbooks.ccconline.org/bio106/chapter/urinary-structures-and-functions/  (Accessed: 9 January 2024).

Renal perfusion relies on total body volume, effective volume and cardiac output. Reducing any of these factors results in a reduced mean arterial pressure and, thus, reduced renal perfusion.

Glomerulus

Glomerular filtration is a passive process reliant on the hydrostatic pressure created by an ingoing wider afferent arteriole and an outgoing narrower efferent arteriole. The glomerular filtration rate is a measure of the kidney’s excretory function. Drugs such as NSAIDs and ACE inhibitors can reduce the GFR by reducing the hydrostatic pressure: 

• NSAIDS and tacrolimus cause constriction of the afferent arteriole, thus reducing the flow of blood into the glomerular bed.
• ACE inhibitors and ARBs cause dilation of the efferent arteriole, allowing blood to leave the glomerular bed more easily. 

Oncotic pressure counteracts the hydrostatic pressure. Other factors affecting the GFR include the permeability of the glomerulus. Factors that can reduce permeability include angiotensin II release (resulting in mesangial cell contraction) and inflammation of the glomerular basement membrane (GBM) thickening.

Serum creatinine is often a reliable measure for GFR as it is released from muscle cells at a constant rate and is freely filtered across the glomerular basement membrane with negligible further secretion or reabsorption as it passes through the nephron. When reviewing creatinine results, factors to consider are age and nutritional status – creatinine can be close to the normal range despite a drop in eGFR. Creatinine can also be unreliable in early renal disease.

Once the filtrate has passed through the glomerular basement membrane, it enters the renal tubule.

References

Kumar, P. and Clark, M., 2012. Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., & Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing. 

Tortora, G. J., & Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.