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Renal blood flow
Parameter  Value 

renal blood flow  RBF=1000 ml/min 
hematocrit  HCT=40% 
renal plasma flow  RPF=600 ml/min 
filtration fraction  FF=20% 
glomerular filtration rate  GFR=120 ml/min 
urine flow rate  V=1 mL/min 
Sodium  Inulin  Creatinine  PAH 

S_{Na}=150 mEq/L  S_{In}=1 mg/mL  S_{Cr}=0.01 mg/ml  S_{PAH}= 
U_{Na}=710 mEq/L  U_{In}=150 mg/mL  U_{Cr}=1.25 mg/mL  U_{PAH}= 
C_{Na}=5 mL/min  C_{In}=150 ml/min  C_{Cr}=125 mL/min  C_{PAH}=420 ml/min 
ER=90%  
ERPF=540 ml/min 
Contents
Introduction
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 22% of cardiac output, amounting to 1.1 L/min in a 70kg adult male. 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 RBF_{a}, RBF_{v}, RPF_{a}, and RPF_{v}. 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 is the volume of plasma that reaches the kidneys per unit time. Renal plasma flow is given by the Fick principle:
 <math>RPF = \frac{U_x V}{P_a  P_v}</math>
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 nonmetabolizable 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:
 <math>RPF_a \times P_a = RPF_v \times P_v + U_x \times V</math>
where P_{a} is the arterial plasma concentration of the substance, P_{v} is its venous plasma concentration, U_{x} 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 RPF_{a} is assumed to be equal to RPF_{v}, thus
 <math>RPF \times P_a = RPF \times P_v + U_x V</math>
Rearranging yields the previous equation for RPF:
 <math>RPF = \frac{U_x V}{P_a  P_v}</math>
Measuring
Values of P_{v} are difficult to obtain in patients. In practice, PAH clearance is used instead to calculate the effective renal plasma flow (eRPF). PAH (paraaminohippurate) is freely filtered and it is not reabsorbed within the nephron. Although freely filtered not all PAH crosses into the primary urine within Bowman's capsule. PAH remaining in the vasa recta or peritubular capillaries is taken up actively by epithelial cells of the proximal convoluted tubule and secreted into the tubular lumen. In this way PAH, at low doses, is completely cleared from the blood during a single pass through the kidney. Accordingly, the venous plasma concentration of PAH is approximately zero. Setting P_{v} to zero in the equation for RPF yields
 <math>eRPF = \frac{U_x}{P_a} V</math>
which is the equation for renal clearance. For PAH, this is commonly represented as
 <math>eRPF = \frac{U_{PAH}}{P_{PAH}} V</math>
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 RPF and hematocrit using the following equation:
 <math>RBF = \frac{RPF}{1Hct} </math>
Autoregulation and Renal Failure
If the kidney is methodologically perfused at moderate pressures (90220 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.^{[1]} Patients with poor renal perfusion caused by drugs that inhibit angiotensinconverting enzyme face Renal failure.^{[2]}
References
 ^ Ganong. Ganong's Review of Medical Physioloy (24 ed.). TATA McGRAW HILL. p. 678. ISBN 9781259027536.
 ^ Ganong. Ganong's Review of Medical Physioloy (24 ed.). TATA McGRAW HILL. p. 678. ISBN 9781259027536.
 Bibliography
 Boron, Walter F., Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1416023283.
 Eaton, Douglas C., Pooler, John P. (2004). Vander's Renal Physiology (8th edition ed.). Lange Medical Books/McGrawHill. ISBN 0071357289.
External links
