Renal Circulation Flashcards
How much of the body mass do the kidneys make up?
Percentage of Cardiac Output? How does this compare to other organs?
1% of TBM (150g)
25% of CO (~1.25L/min, 1800L/day)
4x the blood flow of the liver
4x more blood than striated muscle during exercise
8x coronary blood flow
What are the consequences and causes of blocked renal arteries?
Ischemic kidney can cause mesenteric angina
Segmental arteries are end arteries so if arteries are occluded that part of the kidney is necrosed and lost
Atrial fibrillation can cause embolus into main renal artery, occluded kidney. Superior segment artery occlusion would cause necrosis of this section.
Causes flank pain, hematuria, and increase in LDH.
Renal vessel hypertension and stenosis
Renal HTN: lesion in main artery with stenosis
Stenosis can occur distal to main renal artery or in segmental arteries.
If hypertension in a more distal segment there can be stenosis without total occlusion but still causes hypertension.
Responsds to Renin-Angiotensin system
Renal vascular pathway
Main renal artery –> Segmental Artery –> Interlobar arteries –> Arcuate artery –> Interlobular arteries –> (90’ angle) affarent arterioles –> Glomerular tufts –> Efferent Arteriole –> Peritubular capillary network (surrounds tubules) –> lobular vein –> arcuate vein –> lobar vein –> renal vein
Structural components of the glomerulus
- Capillaries
Feed and drain kidney with blood - Mesangium
- Visceral layer of Bowman’s epithelium
- The parietal surface of Bowman’s epithelium
Glomerular Capillary Wall components
- Fenestrated endothelium
- Glomerular basement membrane
- Visceral epithelial cell - Podocyte
Peritubular circulation properties and components
Capillaries outside the glomerulus in renal circulation.
Purpose is filtration process and reabsorption, regulating what reaches urine.
Hypovolemic, hyponatremic, hypoeverything.
Post-glomerular microcirculation is made up of efferent arterioles: peritubular capillary network. Absorbs water and solutes from PCT and DCT into circulation.
Starling’s Law for fluid removal from tubules into capillaries (peritubular capillary hemodynamics)
Jv=k[(Pcap- Pis)-ð(pcap- pis)]
Under normal conditions:
Pis = 0 pis = 0 ð= 1 (capillaries impermeable to proteins)
Jv=k[Pcap- pcap]
Oncotic P is much higher than hydraulic so Jv < 0.
Jv is flux of fluids, negative value means fluid flows into capillaries.
k = hydraulic permeability or porosity of the capillary wall
Pcap - Pis = hydraulic pressures of the capillary and interstitium
pcap, pis (pi) = colloid osmotic (oncotic) pressures of the capillary and interstitium
ð = permeability to proteins (1 is impermeable and 0 is totally permeable)
How is renal plasma flow measured? (Which indicator substance, etc.?)
PAH (para-amino-hippuric acid)
70-90% of PAH excreted into urine, 10-30% through renal vein (for calculation, 100% excreted)
Rate at which substance enters the kidney
[arterial plasma flow x arterial concentration]
RPF x [PAH]A
Rate at which substance exits the kidney
[urine flow x urine concentration]
VU x [PAH]U
Clearance = effective RPF =([PAH]U x VU)/ [PAH]A
Renal blood flow (RBF) can be estimated from RPF = RPF / 1-hematocrit (Ht)
Lower in females
How is blood distributed and regulated amongst different parts of the kidney? How is this reflected in hydraulic pressure?
Most goes to superficial layer (120mmHg in renal artery)
80% of blood flow goes into superficial cortex
Afferent and efferent arterioles main role in regulating pressure
10-15% into deep cortex
5-10% into medulla
The deeper in, the less blood flow (0 hydrostatic pressure in small renal veins)
Redistribution: Situations like sepsis (cytokines and chemokines) in which GFR declines and filtration decreases, blood flow in superficial cortex declines and is shunted into the deep cortex. Prevents damage to the kidney.
Renal perfusion pressure and RVR (renal vascular resistance) and autoregulation
Kidney perfusion proportional to systemic BP
Perfusion of the kidney is inversely proportional to RVR
RVR is determined by the combined resistances of the AE and EA. As BP rises, AA constricts.
The higher (or lower) the perfusion pressure, the higher (or lower) the resistance; consequently, RBF and GFR remain constant
Instrinsic Autoregulation: occurs in denervated and in vitro kidneys.
Effferent arterioles NOT a player in autoregulation (though they are in total resistance)
Mechanisms not known but hypothesized:
Myogenic: Arterial smooth muscle contracts and relaxes in response to increases and decreases in vascular wall tension
Humoral: Angiotensin II may play a role when BP is reduced by increasing efferent arteriolar R
Under MAP of 70mmHg GFR decreases and efferent arteriole may constrict to increase flow. Under 40mmHg GFR ceases (need to increase volume or give adrenaline).
Tubuloglomerular Feedback (TGF)
What does it regulate, how and why?
Alterations in GFR that are induced by changes in rate of tubular flow, principally by the macula densa: Highly specialized epithelium located at onset of DCT, between AA and EA.
As GFR increases from increased perfusion pressure (increased Pgc), flow at macula densa increases, sensed by an increased in chloride delivery.
Signa (mostly with adenosine) causes AA vasoconstriction returning renal pressure to normal. GFR returns to normal (lowers) as does flow at macula densa.
If macula densa senses decreased chloride, it releases prostaglandins to dilate the AA and raise GFR.
Prevents excess loss of salt and water
