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Summary Chapter 27; Glomerular Filtration, Renal Blood Flow, and Their Control
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Chapter 27; Glomerular Filtration, Renal BloodFlow, and Their Control
The GFR is 125 ml/min (or 180 L/day), and the RPF (renal plasma flow) is 625 ml/min,
which means 20% of the RPF is filtered.
Filtration fraction = GFR/RPF, so 125/625 = 0.2
The REAB (reabsorption rate) is 124 ml/min, and so: Urinary excretion rate = 125-124
=1 ml/min
The glomerular membrane consists of the endothelium of the capillaries, the
basement membrane, and podocytes lining the outer surface of the basement
membrane. These membranes prevent large molecules such as proteins from passing
through. In addition, all 3 of these membranes have negatively charged substances
(such as proteoglycans) and so repel negatively charged plasma proteins.
In minimal change nephropathy, these negative charges are absent, and so the
proteins aren’t repelled, and end up in the filtrate. The proteins, such as albumin,
show up in the urine, a condition known as albuminuria or proteinuria. This condition
is most common in young children.
Determinants of GFR:
The GFR depends on the sum of colloid osmotic and hydrostatic forces across its
capillary membrane (the net filtration pressure), and the Kf, or capillary coefficient
(which further depends on the permeability and surface area of the capillaries).
GFR = Kf x Net filtration pressure
Net filtration pressure = Glomerular hydrostatic pressure – Bowman’s capsule
pressure – Glomerular colloid osmotic pressure + Bowman’s colloid osmotic pressure.
, Net filtration pressure= 60 – 18 – 32 + 0 = +10 mmHg
GFR = 125 ml/min
Therefore, Kf = GFR/NFP = 125/10 = 12.5 ml/min/mmHg
Increasing the Kf increases the GFR. And since it is a product of the permeability and
surface area of the capillaries, it is decreased by conditions like uncontrolled
hypertension and diabetes mellitus, which increase the thickness of the basement
membrane, reducing the GFR.
Obstruction of the urinary tract (for example by stones) can cause fluid to accumulate
in the tubules and increase the Bowman’s capsule pressure, decreasing the GFR. This
can lead to hydronephrosis, in which the pelvis is dilated.
Increasing the glomerular colloid osmotic pressure (πG) decreases the GFR. Two things
determine the πG. The arterial colloid osmotic pressure, which is 28 mmHg (increasing
this increases the πG), and the filtration fraction (FF). As seen above, this fraction
depends on the RPF. If the RPF is decreased, the blood doesn’t just pass by quickly
and so more plasma is filtered. So, initially the GFR increases. However, as plasma
proteins aren’t filtered, their concentration in the plasma increases. Therefore, this
increases the πG, causing the GFR to decrease overall. The opposite happens when the
RPF increases, and leads to an increased GFR.
↓RPF, so ↑FF, so ↑πG, so ↓GFR.
Out of these forces, the GFR is mainly controlled by the glomerular hydrostatic
pressure (Pg). The Pg depends on 3 things. The arterial pressure (which it increases
with), the afferent arteriolar resistance (which it decreases with), and the efferent
arteriolar resistance.
If the efferent arterioles constrict moderately, the ↑Pg, so the ↑GFR.
However, if the efferent arterioles constrict severely, then the ↓RPF, so ↑FF, so ↑πG,
so ↓GFR.
The afferent arteriolar resistance could increase by sympathetic vasoconstrictor
activity, such as by epinephrine and norepinephrine.
The efferent arteriolar resistance is affected by angiotensin II, and so angiotensin II
blockers reduce it.
RPF determinants:
RPF depends on the renal pressure gradient and the renal vascular resistance.
RPF = (Renal artery pressure – Renal vein pressure)/ Renal vascular resistance
This resistance mainly comes from interlobular arteries, afferent and the efferent
arterioles.
Sympathetic stimulation of the renal vessels through epinephrine and norepinephrine
causes vasoconstriction and reduce GFR. Their function is important during periods
when blood pressure drops severely low, such as during hemorrhage or brain
ischemia.
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