Fig. 33.17 displays the net ultrafiltration pressure (PUF) at the afferent end of the glomerulus as 17 mm Hg, while at the efferent end it is 8 mm Hg (where PUF = PGC − PBS −πGC). Two important points to note about Starling forces and this pressure change are as follows: First, PGC decreases slightly along the length of the capillary due to flow resistance. Second, πGC increases as plasma is filtered and protein is retained within the glomerular capillary, leading to an increasing protein concentration along the capillary. The glomerular filtration rate (GFR) is determined by the sum of the Starling forces across the capillaries [(PGC − PBS) −σ(πGC −πBS)] multiplied by the ultrafiltration coefficient (Kf). This can be represented by Equation 33.10, where Kf is the product of the glomerular capillary's intrinsic permeability and the available surface area for filtration. The rate of glomerular filtration is significantly higher in glomerular capillaries compared to systemic capillaries due to Kf being approximately 100 times greater in glomerular capillaries. Additionally, PGC is approximately twice as high as the hydraulic pressure in systemic capillaries.

GFR can be altered by modifying Kf or any of the Starling forces. In normal individuals, changes in PGC mainly mediated by alterations in afferent or efferent arteriolar resistance regulate GFR. PGC is affected in three ways: 

1. Changes in afferent arteriolar resistance: Decreased resistance increases PGC and GFR, while increased resistance decreases PGC and GFR.
2. Changes in efferent arteriolar resistance: Decreased resistance reduces PGC and GFR, while increased resistance elevates PGC and GFR.
3. Changes in renal arteriolar pressure: An increase in blood pressure temporarily increases PGC (enhancing GFR), while a decrease in blood pressure temporarily decreases PGC (reducing GFR).

Blood flow through the kidneys serves several important functions: 

1. Modifying the rate of solute and water reabsorption by the proximal tubule.
2. Participating in concentration and dilution of urine.
3. Delivering O2, nutrients, and hormones to cells along the nephron and returning CO2, reabsorbed fluid, and solutes to the general circulation.

The equation representing blood flow through any organ is as follows:

A reduction in GFR in disease states is most often due to decreases in Kf caused by the loss of filtration surface area. Changes in PGC, πGC, and PBS also contribute to alterations in GFR in pathophysiological conditions.

1. Changes in Kf: Increased Kf enhances GFR, while decreased Kf reduces GFR. Some kidney diseases decrease Kf by reducing the number of filtering glomeruli (i.e., diminished surface area). Certain drugs and hormones that dilate glomerular arterioles also increase Kf. Conversely, drugs and hormones that constrict glomerular arterioles decrease Kf.

2. [Additional content from the excerpt not included in the paraphrasing request]
Fig. 33.17 , a net ultrafiltration pressure (PUF) of 17 mm Hg exists at the afferent end of the glomerulus, whereas at the efferent end it is 8 mm Hg (where PUF = PGC − PBS −πGC). Two additional points concerning Starling forces and this pressure change are important. First, PGC decreases slightly along the length of the capillary because of the resistance to flow along the length of the capillary. Second, πGC increases as plasma is filtered while protein is retained within the glomerular capillary, thereby progressively increasing the protein concentration along the length of the capillary. GFR is proportional to the sum of the Starling forces that exist across the capillaries [(PGC − PBS) −σ(πGC −πBS)] multiplied by the ultrafiltration coefficient (Kf). That is:
Equation 33.10
Kf is the product of the intrinsic permeability of the glomerular capillary and the glomerular surface area available for filtration. The rate of glomerular filtration is considerably greater in glomerular capillaries than in systemic capillaries, mainly because Kf is approximately 100 times greater in glomerular capillaries. Furthermore PGC is approximately twice as great as the hydraulic pressure in systemic capillaries.
GFR can be altered by changing Kf or by changing any of the Starling forces. In normal individuals, GFR is regulated by alterations in PGC that are mediated mainly by changes • Fig. 33.17 Idealized glomerular capillary and the Starling forces across it. The reflection coefficient (σ) for protein across the glomerular capillary is approximately 1. PBS, hydraulic pressure in Bowman’s space; PGC, hydraulic pressure in the glomerular capillary; PUF, net ultrafiltration pressure; πBS, oncotic pressure in Bowman’s space; πGC, oncotic pressure in the glomerular capillary. The negative signs for PBS and πGC indicate that these forces oppose formation of the glomerular filtrate.
in afferent or efferent arteriolar resistance. PGC is affected in three ways: 1.
Changes in afferent arteriolar resistance: A decrease in resistance increases PGC and GFR, whereas an increase in resistance decreases PGC and GFR.
2.
Changes in efferent arteriolar resistance: A decrease in resistance reduces PGC and GFR, whereas an increase in resistance elevates PGC and GFR.
3.
Changes in renal arteriolar pressure: An increase in blood pressure transiently increases PGC (which enhances GFR), whereas a decrease in blood pressure transiently decreases PGC (which reduces GFR).
Blood flow through the kidneys serves several important functions: 1.
2.
modifies the rate of solute and water reabsorption by the proximal tubule 3.
participates in concentration and dilution of urine 4.
delivers O2, nutrients, and hormones to cells along the nephron and returns CO2, reabsorbed fluid, and solutes to the general circulation 5.
Blood flow through any organ may be represented by the following equation:
A reduction in GFR in disease states is most often due to decreases in Kf because of the loss of filtration surface area. GFR also changes in pathophysiological conditions because of changes in PGC, πGC, and PBS.
1.
Changes in Kf: Increased Kf enhances GFR, whereas decreased Kf reduces GFR. Some kidney diseases reduce Kf by decreasing the number of filtering glomeruli (i.e., diminished surface area). Some drugs and hormones that dilate the glomerular arterioles also increase Kf. Similarly, drugs and hormones that constrict the glomerular arterioles also decrease Kf.
2.