Mechanism and composition of the filtrate
The first stage of urine formation takes place in the renal corpuscle. Blood entering the glomerular capillaries undergoes ultrafiltration. Driven by high hydrostatic pressure, the liquid portion of the plasma is literally forced through the microscopic pores of the capillary wall into the cavity of Bowman's capsule. This is how primary urine is formed.
The filtration barrier functions as a strict physical filter: it reliably retains cellular blood elements and large proteins, keeping them circulating in the bloodstream. Meanwhile, water, electrolytes, amino acids, glucose molecules, as well as various vitamins and trace elements, freely penetrate the capsule cavity. Nitrogen metabolism products (urea, creatinine, uric acid), hormones (such as insulin), and pigments (urobilin, indican) are filtered along with them. In its chemical composition, the resulting filtrate is almost completely identical to blood plasma, with the exception of the absence of macromolecular compounds.
Effective filtration pressure (EFP)
The process of glomerular filtration is maintained by a delicate balance of Starling forces—the pressure difference on both sides of the barrier. The main hemodynamic indicator here is the effective filtration pressure (EFP). It represents the difference between the force that pushes fluid out of the blood vessels and the forces that tend to keep it inside.
Three key parameters are involved in the physiological calculation:
- Blood pressure (BP): this is the hydrostatic pressure of blood directly within the glomerular capillaries. It serves as the primary driving force for all filtration. Its normal value is 70 mm Hg.
- Oncotic pressure (OP): generated by plasma proteins (predominantly albumins) that have not passed through the filter, remained in the vessel, and attract water molecules to themselves, actively preventing its outflow. Its value is 30 mm Hg.
- Hydrostatic pressure of urine (UP): this is the resistance of the fluid located in the capsule cavity and renal tubules. It also impedes new filtration. It is 20 mm Hg.
The general formula for calculation is: $$EFP = BP - (OP + UP)$$
Substituting the normal values, we get: 70 - (30 + 20) = 20 mm Hg. It is this positive value that ensures the continuous and stable formation of primary urine.
Effect of arteriole tone on diuresis
The tone of the blood vessels supplying the renal corpuscle directly controls the volume of primary urine produced and overall diuresis.
- Constriction of the efferent arteriole: in this situation, blood outflow from the glomerular network is hindered. Blood accumulates in the capillaries, causing the hydrostatic pressure inside them to rise sharply. This naturally leads to an increase in EFP, an increase in filtration volume, and, as a direct consequence, an increase in diuresis.
- Spasm of the afferent arteriole: under this condition, the influx of fresh blood to the renal corpuscle drops. Hydrostatic pressure in the capillaries decreases, and the EFP plummets. As a result, the formation of primary urine is sharply reduced, and diuresis drops down to the development of oliguria (a pathologically small amount of urine) or anuria (complete cessation of urine formation).
Self-regulation of the process and markers
A healthy body strives to maintain the volume of primary urine at a strictly constant level, despite significant physiological fluctuations in systemic blood pressure over a wide range from 70 to 180 mm Hg.
This process is called self-regulation. It is carried out through a myogenic mechanism—the autonomous contraction or relaxation of precapillary sphincters without the participation of the nervous system and hormones. It is important to note that this mechanism is well expressed in cortical nephrons, but completely absent in juxtamedullary nephrons located at the border of the cortex and medulla.
Normally, plasma oncotic pressure is a strict constant. If the force balance is disrupted (for example, blood pressure rises uncontrollably or oncotic pressure drops critically), the hydrostatic pressure of the urine itself in the capsule increases compensatorily in response. This neutralizes shifts and keeps the glomerular filtration rate stable.
To accurately clinically assess the intensity of filtration, special marker substances are used: inulin and creatinine. Their feature is that they pass freely through the filtration barrier, but are completely reabsorbed in the renal tubules. Based on their concentration in the final urine, doctors objectively assess the quality of kidney function.
Briefly: answers to topical questions
What structural layers make up the filtration barrier of the renal corpuscle?
The filtration barrier of the renal corpuscle is described in sources as follows:
- Basement membrane — a specialized form of extracellular matrix; in renal glomeruli, it is located between two cell layers and acts as a highly selective filtration barrier.
- Podocytes — cells of the inner layer of the capsule; they contact the basement membrane via short processes called foot processes (pedicels).
- Between adjacent pedicels remain filtration slits, which communicate with the cavity of the renal corpuscle capsule and ensure the outflow of the filtrate.
- From the blood side, the liquid part of plasma passes through the capillary pores into the capsule.
What is the normal glomerular filtration rate (GFR) in milliliters per minute?
Normally, the glomerular filtration rate (GFR) is 115–125 ml/min.
Normal GFR values for a body weight of 70 kg and a body surface area of 1.73 m²:
- in men — 120–125 ml/min;
- in women — about 110 ml/min.
The GFR value is calculated in ml/min per 1.73 m² of body surface area.
Class and exam questions
What is effective filtration pressure?
This is the resultant force ensuring plasma filtration. It is calculated as the difference between the hydrostatic pressure of blood (pushing fluid out) and the sum of the plasma oncotic pressure and primary urine pressure (retaining fluid).
How does primary urine differ from blood plasma?
By chemical composition, primary urine is almost completely identical to plasma. The main difference is that blood cells and macromolecular compounds (proteins with a mass greater than 70 thousand units) are completely absent in it.
Why does spasm of the afferent arteriole lead to anuria?
During a spasm of the afferent arteriole, blood inflow to the glomerulus sharply decreases. Because of this, hydrostatic pressure in the capillaries drops so much that the effective filtration pressure decreases, stopping the urine formation process.
What else to study on this topic
- Structure of the filtration barrier of the renal corpuscle
- Differences between cortical and juxtamedullary nephrons
- Processes of tubular reabsorption of substances
- Clinical significance of creatinine clearance
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