8th February 2024

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.