Factors affecting GFR | simple & easy
Factors affecting GFR | simple & easy

Factors affecting GFR | simple & easy

What is GFR?

The glomerular filtration rate (GFR) is the amount of filtration produced by both kidneys per unit time. An estimated GFR test (eGFR) shows the condition of the kidneys and how well they are working.

The normal range of GFR is 100-130 mL / min in men (125 on average) and 90-120mL / min in women. In children it is 110 mL / min.

When should GFR be tested?

GFR test should be done if the following symptoms appear.

  • More or less urination than usual
  • Itching
  • Fatigue or exhaustion
  • Swelling of hands, feet or feet
  • Muscle obstruction
  • Nausea and vomiting
  • Dislike of food
  • Diabetes
  • High blood pressure
  • Family history of kidney failure

Definition of GFR :

Adult human GFR is about 125mL / min or 180L / day. The GFR is determined by the following:

  • The sum of hydrostatic and colloid osmotic forces which gives net filtration pressure for or against GFR.
  • Glomerular Capillary Filtration Coefficient (Kf)
factors affecting gfr

The GFR can be expressed as:


Factors affecting GFR:

  • The GFR decreases as the hydrostatic pressure of the bowman’s capsule increases. That is, if PB increases, GFR will decrease.
  • Obstruction of the urethra by calcium or uric acid or stones in the urethra increases the pressure in the bowman’s capsule, resulting in a severe decrease in GFR.
  • Increased glomerular capillary colloid osmotic pressure decreases GFR. That is, if the amount of ug increases, the GFR decreases.
  • GFR increases when the rate of blood flow to the glomerulus increases and GFR decreases when the rate of blood flow to the glomerulus decreases.
  • As the arterial pressure increases, so does the glomerular hydrostatic pressure, which in turn increases the GFR.
  • GFR decreases as resistance of afferent arterioles increases.
  • Expansion of the afferent arterioles increases glomerular hydrostatic pressure which increases GFR.

Why it is important to control GFR :

Too much GFR increases the level of fluid flow through the tubule. As a result, the re-absorption of the required components cannot be done properly. That is, it reduces the reabsorption of filtration. If the peritubular capillaries cannot absorb properly, the amount of urine will increase and there will be frequent urination. In contrast, a decrease in GFR means a decrease in fluid flow to the tubule. Then the amount of reabsorption will increase so much that the peritubular capillaries will also absorb various wastes which are harmful to the body and should be expelled from the body. This will eventually increase the amount of nitrogen-containing waste products in the blood. Therefore both conditions of GFR are harmful for our body. Therefore, it is very important to control GFR.

GFR regulation:

GFR regulation
regulation of GFR

GFR regulation occurs in two ways – intrinsic (internal) and extrinsic (external). Intrinsic involves the process of autoregulation which occurs in two ways namely: myogenic and tubuloglomerular feedback mechanism. Extrinsic regulation occurs in four ways, among which hormonal control is widely discussed.

Autoregulation ( internal ):

The autoregulation mechanism occurs when the blood pressure range is between 75-160 mmHg. It may not work for extra blood pressure changes. The goal of autoregulation is to keep the amount of GFR and RBF constant when blood pressure changes to normal range (75-160mmHg). This means that in a normal kidney, only a few percent change in GFR occurs when arterial blood pressure is less than 75mmHg or more than 160mmHg. This means that if the blood pressure difference falls below 75mmHg and rises above 160mmHg, autoregulation will not work. Autoregulation prevents excessive changes in GFR with changes in blood pressure, so that the kidneys can continue to excrete wastes.

Note: Macula densa is a cluster of epithelial cells located at the beginning of a distal convoluted tubule. Macula densa cells detect the concentration of Na in the fluid in the tubule. NaCl is a substance that should be reabsorbed under normal conditions.

1. Tubuloglomerular feedback mechanism:

When blood pressure goes down:

As blood pressure decreases, blood flow to the renal tubules decreases, resulting in lower GFR. Due to which the reabsorption of the substance in the renal tubule is increased. This reduces the concentration of NaCl in macula densa cells. The macula densa then secretes the necessary material which subsequently maintains normal levels of GFR by causing expansion of the afferent arteriole and contraction of the efferent arteriole.

Net result: increase glomerular hydrostatic pressure and normalize GFR.

When blood pressure rises :

As blood pressure rises, blood flow to the renal tubules also increases, resulting in an increase in GFR. This reduces the level of reabsorption and increases the concentration of NaCl in the macula densa. The macula densa then regulates GFR by secreting the afferent arterioles and dilating the efferent arterioles by secreting the necessary material.

Net result: Reduces glomerular hydrostatic pressure and normalizes GFR.

2. Myogenic process:

The myogenic mechanism is the internal ability of blood vessels to constrict when blood pressure rises.

mechanism of myogenic regulation
mechanism of myogenic regulation

Increased blood pressure increases blood flow to the arteries. The pressure on the smooth muscles increases and these muscles have stretching sensors. These sensors can tell from the muscle stretching that the pressure has changed. This causes more Ca to enter the muscle which causes the blood vessels to constrict. This contraction prevents blood flow to the renal tubules and an excess of GFR.

When blood pressure decreases, the myogenic mechanism reduces vascular resistance and dilates the ducts.

Hormonal control of GFR ( external )

Juxtaglomerular apparatus secretes a hormone called renin which activates an inactive hormone called angiotensinogen from the liver which produces angiotensin I an active hormone. Angiotensin I is then converted to angiotensin II by the angiotensin converting enzyme (ACE). Angiotensin II causes contraction of the efferent and releases aldosterone from the adrenal cortex, which is used to retain salt and water.

hormonal control of GFR
hormonal control of GFR

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