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Glomerular filtration rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time. [4] Central to the physiologic maintenance of GFR is the differential basal tone of the afferent (input) and efferent (output) arterioles (see diagram).
The Glomerular filtration rate (GFR) is regarded as the best overall measure of the kidney's ability to carry out these numerous functions. An estimate of the GFR is used clinically to determine the degree of kidney impairment and to track the progression of the disease. The GFR, however, does not reveal the source of the kidney disease.
GFR on its own is the most common and important measure of renal function. However, in conditions such as renal artery stenosis, blood flow to the kidneys is reduced. Filtration fraction must therefore be increased in order to perform the normal functions of the kidney. Loop diuretics and thiazide diuretics decrease filtration fraction.
Renin release activates RAAS leading to many outcomes including an increased GFR. The critical target of the trans-JGA signaling cascade is the glomerular afferent arteriole; its response consists of an increase in net vasoconstrictor tone resulting in reductions of glomerular capillary pressure (PGC) and glomerular plasma flow.
Patients had been diagnosed with aHUS for a median of 10 months before the start of the study, and 71% had severe renal impairment, with an estimated glomerular filtration rate (eGFR) <30 mL/min/1 ...
The glomerular filtration rate (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow. Because the filtration fraction, which is the ratio of the glomerular filtration rate (GFR) to the renal plasma flow (RPF), has increased, there is less plasma fluid in the downstream peritubular capillaries.
Pressure in glomerular capillaries is therefore maintained and glomerular filtration rate remains adequate. However, in a state of very high angiotensin II for a prolonged period of time, the colloid oncotic pressure of the capillaries will increase, counteracting the increased hydrostatic pressure from the efferent constriction.
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