Renal blood flow

Renal blood flow
MeSHD012079
Parameter Value
renal blood flow RBF = 1000 mL/min
hematocrit HCT = 40%
glomerular filtration rate GFR = 120 mL/min
renal plasma flow RPF = 600 mL/min
filtration fraction FF = 20%
urine flow rate V = 1 mL/min
Sodium Inulin Creatinine PAH
SNa = 150 mEq/L SIn = 1 mg/mL SCr = 0.01 mg/mL SPAH =
UNa = 710 mEq/L UIn = 150 mg/mL UCr = 1.25 mg/mL UPAH =
CNa = 5 mL/min CIn = 150 mL/min CCr = 125 mL/min CPAH = 420 mL/min
ER = 90%
ERPF = 540 mL/min

In the physiology of the kidney, renal blood flow (RBF) is the volume of blood delivered to the kidneys per unit time. In humans, the kidneys together receive roughly 25% of cardiac output, amounting to 1.2 - 1.3 L/min in a 70-kg adult male. It passes about 94% to the cortex. RBF is closely related to renal plasma flow (RPF), which is the volume of blood plasma delivered to the kidneys per unit time.

While the terms generally apply to arterial blood delivered to the kidneys, both RBF and RPF can be used to quantify the volume of venous blood exiting the kidneys per unit time. In this context, the terms are commonly given subscripts to refer to arterial or venous blood or plasma flow, as in RBFa, RBFv, RPFa, and RPFv. Physiologically, however, the differences in these values are negligible so that arterial flow and venous flow are often assumed equal.

Renal plasma flow

Renal plasma flow
MeSHD017595

Renal plasma flow is the volume of plasma that reaches the kidneys per unit time. Renal plasma flow is given by the Fick principle:

This is essentially a conservation of mass equation which balances the renal inputs (the renal artery) and the renal outputs (the renal vein and ureter). Put simply, a non-metabolizable solute entering the kidney via the renal artery has two points of exit, the renal vein and the ureter. The mass entering through the artery per unit time must equal the mass exiting through the vein and ureter per unit time:

where Pa is the arterial plasma concentration of the substance, Pv is its venous plasma concentration, Ux is its urine concentration, and V is the urine flow rate. The product of flow and concentration gives mass per unit time.

As mentioned previously, the difference between arterial and venous blood flow is negligible, so RPFa is assumed to be equal to RPFv, thus

Rearranging yields the previous equation for RPF:

Measuring

Values of Pv are difficult to obtain in patients. In practice, PAH clearance is used instead to calculate the effective renal plasma flow (eRPF). PAH (para-aminohippurate) is freely filtered, is not reabsorbed, and is secreted within the nephron. In other words, not all PAH crosses into the primary filtrate in Bowman's capsule and the remaining PAH in the vasa recta or peritubular capillaries is taken up and secreted by epithelial cells of the proximal convoluted tubule into the tubule lumen. In this way PAH, at low doses, is almost completely cleared from the blood during a single pass through the kidney. (Accordingly, the plasma concentration of PAH in renal venous blood is approximately zero.) Setting Pv to zero in the equation for RPF yields

which is the equation for renal clearance. For PAH, this is commonly represented as

Since the venous plasma concentration of PAH is not exactly zero (in fact, it is usually 10% of the PAH arterial plasma concentration), eRPF usually underestimates RPF by approximately 10%. This margin of error is generally acceptable considering the ease with which PAH infusion allows eRPF to be measured.

Finally, renal blood flow (RBF) can be calculated from a patient's renal plasma flow (RPF) and hematocrit (Hct) using the following equation:

.[1]

Autoregulation and kidney failure

If the kidney is methodologically perfused at moderate pressures (90–220 mm Hg performed on an experimental animal; in this case, a dog), then, there is a proportionate increase of:

-Renal Vascular Resistance

Along with the increase in pressure. At low perfusion pressures, Angiotensin II may act by constricting the efferent arterioles, thus mainlining the GFR and playing a role in autoregulation of renal blood flow.[2] People with poor blood flow to the kidneys caused by medications that inhibit angiotensin-converting enzyme may face kidney failure.[3]

References

  1. ↑ Barrett, Kim E.; Brooks, Heddwen L.; Boitano, Scott; Barman, Susan M. (2010). Ganong's Review of Medical Physiology (23rd ed.). McGraw-Hill Medical. pp. 643–644. ISBN 978-0-07-160568-7. OCLC 430823856.
  2. ↑ Ganong. Ganong's Review of Medical Physiology (24 ed.). TATA McGRAW HILL. pp. 644–645. ISBN 978-1-25-902753-6.
  3. ↑ Ganong. Ganong's Review of Medical Physiology (24 ed.). TATA McGRAW HILL. pp. 644–645. ISBN 978-1-25-902753-6.
Bibliography
  • Boron, Walter F., Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1-4160-2328-3.{{cite book}}: CS1 maint: multiple names: authors list (link)
  • Eaton, Douglas C., Pooler, John P. (2004). Vander's Renal Physiology (8th ed.). Lange Medical Books/McGraw-Hill. ISBN 0-07-135728-9.{{cite book}}: CS1 maint: multiple names: authors list (link)
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