All contents are copyrighted.
No unauthorized distribution allowed.

Renal Hemodynamics IV

Chris Baylis, PhD

Learning Objectives:
To learn and understand:

• The mechanisms of renal autoregulation
• How events at the glomerulus control

peritubular capillary reabsorption.
• The relationship between renal

metabolism and renal oxygen extraction
• Clinical assessment of RBF
• How renal hemodynamics are deranged in

kidney disease.

PHYSIOLOGIC SITUATIONS IN WHICH RENAL HEMODYNAMICS ARE
ALTERED

Volume depletion/overload

Volume depletion: Renal vasoconstriction; decreased RPF and GFR;
suppression of vasodilatory systems; activation of vasoconstrictors, ANG II
and SNS

(reverse occurs in volume expansion)

GENERALLY GFR STAYS FAIRLY CONSTANT IN HEALTHY, “VOLUME
REPLETE” ADULTS.

EXCEPTIONS:
High Dietary protein
Vasodilation of both afferent and efferent resistance; increased RPF and GFR.
Pregnancy
Vasodilation of both afferent and efferent resistance; increased RPF and GFR.
Exercise
Vasoconstriction of afferent and efferent resistance; decreased RPF and GFR.

Renal Hemodynamics can change dramatically in disease.

Maintaining a constant GFR as BP changes
RENAL AUTOREGULATION

Renal perfusion pressure (RPP)
(mm Hg)

0 40 80 120 160 200 240

R
en

al
p

la
sm

a
flo

w
(R

PF
)

gl
om

er
ul

ar
B

P
(P

G
C

) a
nd

G
FR

Autoregulatory range

Afferent glomerulus efferent
arteriole PGC arteriole

BP No change in RPF

HIDDEN SLIDE
Renal Autoregulation means constant renal blood

flow (and RPF) over a range of systemic blood pressure
(BP) (remember BP is changing constantly).

RPF= pressure drop (BP – renal vein P)
renal vascular resistance

Constancy of RPF during changes in BP must involve
parallel changes in renal resistance. Only the afferent
arteriole (RA) participates.

An increase in BP (RPP) leads to constriction of RA,
resulting in ~ constant RPF and PGC. This leads to
excellent autoregulation of GFR.

2 MECHANISMS OF RENAL AUTOREGULATION

1. Myogenic (immediate, msec) general autoregulatory
mechanism.

2. Tubuloglomerular feedback (delayed,sec to min)
specific to kidney

HIDDEN SLIDE
Occurs at juxtaglomerular apparatus, JGA.
Signal : rate of delivery of fluid to the macula

densa
Feedback response to change resistance in the

afferent arteriole.
 BP  Transient   flow and PGC 
SNGFR  distal delivery of fluid  signal at
macula densa  vasoconstriction of afferent
arteriole  restoration of flow and PGC.

NOTE 1: Autoregulation means constant RPF and
GFR during a change in BP.
Hormones/drugs/nerve traffic can act directly on
kidney vasculature and alter RPF, GFR.

NOTE 2: Autoregulation of PGC is very important
for long term kidney health.

Events at the glomerulus determine the reabsorptive
pressure in the peritubular capillaries

As glomerular filtrate is
formed:

1). Protein concentration
increases in glomerular
blood ( GC).

2). Postglomerular blood flow
decreases (because some
volume is filtered out of the
glomerular blood).

The peritubular capillaries need
to reabsorb most of the
filtrate.

Pressure profile through the
renal microcirculation

P 

P
 

P

FILTRATION NO FLUID FLUX REABSORPTION

Glomerular capillary efferent arteriole peritubular
capillaries

HIDDEN SLIDE
The PGC is ~ 55mmHg and P is ~ 40 mmHg at the

beginning and ~38 mmHg at the end of the glomerulus.
As water leaves by filtration, plasma protein
concentration and therefore  increases.

When blood leaves the glomerulus it enters RE. There is
no fluid movement across the wall of RE so  stays
high. RE is a resistance vessel so blood pressure
must fall significantly during forward flow of blood.

Therefore, when blood enters the peritubular capillaries
(PTC) it has a low hydrostatic pressure (P,
~20mmHg) and a high colloid osmotic pressure (, ~
40 mmHg) which creates a net reabsorbtive pressure.

Other Functions
Peritubular blood flow supports tubular secretion of organic anions

and cations, drugs.
Sensing the circulating red cell mass in control of erythropoietin

release, which is synthesized by interstitial cells of the renal
cortex

RBF supplies oxygen for metabolism.
Renal O2 uptake regulated according to energy requirement.

Main energy requiring process is active sodium reabsorption in
the tubules.

RBF, GFR and sodium reabsorption usually change in proportion
to each other. Therefore, when RBF increases, sodium
reabsorption increases and O2 utilization increases so that the
O2 extraction across the kidney stays constant.

Clinical Measurement of Renal
Perfusion

Quantitative methods to measure RPF
(CPAH), used for research.

Quantitative assessment of renal perfusion
is not necessary for most renal patients.

Commonly used clinical measures are semi-
quantitative
doppler ultrasonography
imaging methods (contrast).

Renal Blood Flow Values

Renal perfusion ~ 20-25% of the cardiac
output.

~4 mL/min/g kidney tissue weight
4 times more than blood flow rate to

exercising muscle
RPF > men vs women, irrespective of size

increases with size
increases with maturation
decreases with aging, after ~40 in men.

Renal Hemodynamics in Kidney
Disease

ACUTE KIDNEY INJURY (AKI)
An abrupt loss of kidney function due to compromised

hemodynamics.
Sometimes due to severe systemic hypotension, to below the

autoregulatory range.
Sometimes due to intense renal vasoconstriction.
Always reductions in RPF and GFR in AKI.

Afferent glomerulus efferent
arteriole  PGC arteriole

Afferent glomerulus efferent
arteriole  PGC arteriole

BP

Chronic Kidney Disease (CKD)
Chronic kidney disease can develop from many causes.
Irrespective of the cause, renal disease tends to be
progressive. When GFR falls, control of body fluid and
composition is deranged.
When patients reach end stage kidney disease (ESKD)
they require dialysis or a renal transplant to survive.

There are several primary
causes of CKD (eg. diabetes 1
and 2); hypertension; immune
and autoimmune diseases,
etc. The renal hemodynamic
pattern as each disease
evolves often includes
increases in PGC.

200

150

100

50

0

Glomerular filtration rate
(GFR)

(ml / min)

0 25 50 75 100 125
0

5

10

15

20

Plasma creatinine
concentration

(Pcr)
(mg / dl)

Blood urea
nitrogen

(BUN)
(mg / dl)

Many potential Mechanisms of Progressive
Glomerular Injury

Hemodynamic
Glomerular capillary Hypertension

Preferential efferent arteriolar vasoconstriction lead to
increased glomerular blood pressure. This directly damages
the glomerular capillary.

Inappropriate activation of intrarenal ANGII raises PGC.
Also promotes expansion of mesangium and vascular
smooth muscle cells; fibrosis and oxidative stress.
Angiotensin converting enzyme (ACE) inhibitors slow down
progression of diabetic renal disease.
They lower BP. They give superior renal protection over
other antihypertensive treatments. Brenner et al.

Summary of key concepts.
• Renal autoregulation, achieved by the myogenic response

and tubuloglomerular feedback (TGF) maintain constant
GFR over a wide range of BP, by control of RA.

• Filtration of fluid at the glomerulus leads to high colloid
osmotic and low blood pressure in the peritubular
capillaries, which favor reabsorption.

• When RBF increases, renal oxygen utilization increases
(due increased tubular reabsorption of sodium). Although
absolute oxygen uptake is increased, the oxygen extraction
(A-V difference) remains fairly constant.

• In AKI, falls in RPF and PGC lead to falls in GFR, either
due to large falls in systemic BP or to increased RA.

• In CKD, increased PGC often contributes to progression of
the disease. Elevated intrarenal ANGII activity contributes
to the pathogenesis.