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Flashcards in Renal I- Physiology Review Deck (26)
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General kidney info:


% of CO?

innervation of kidney?

Innervation of bladder and ureters?

  • Located retroperitoneal at L2
  • Receives 25% of CO
    • very low O2 extration ratio
  • Innervation of kidney:
    • SNS via preganglionic fibers (T8-L1
    • Pain (SNS) T10-L1
    • PSNS CN X
  • Innervation of bladder and ureters
    • motor: PSNS S2-S4
    • sensory: SNS T11-L2


How does blood flow through the kidney?

  • Renal artery ->Arcuate arteries-> interlobular arteries
  • Afferent arterioles (leading to glomerular tuft)
  • Glomerular capillaries and bowman's capsule->
  • efferent arteriole-> peritubular capillaries/vasa Recta ->
  • venous system


How do the arterioles affect GFR?

How do vasoconstricting medications affect the GFR?

  • contraction of efferent arteriole = increased GFR
  • contraction of afferent arteriole = decreased GFR
  • Vasoconstricting medications:
    • mild/moderate causes preferential constriction of efferent, causing increase in GFR
    • very high causes afferent constriction (decreases GFR in shock situations)


Cortex of the kidney:

What are the anatomical parts?

How much blood flow?

How is blood flow regulated through the cortex?

  • Anatomical parts:
    • glomerulus
    • proximal tubule
    • distal tubule
    • portion of the collecting duct
  • Receives 94% of the total blood flow (approx 5 ml/L/g
  • Regulated by vasoactive compounds
    • adenosine induces vasoconstriction (opposite of usual effect) by stimulating the adenosine A1 receptor
    • stress-> SNS -> renal cortical constriction and potential tubular ischemia
    • **Kidney has no B2 receptors! Epi=vasoconstrict


What is the PO2 in the cortex?

What is the extraction ratio of the cortex?

  • 50 mmHg with an 18% extraction ratio


Medulla of the Kidney:

What is the functional part of the kidney in the medulla?

How much blood flow does it receive?

How is the blood flow regulated?


  • Contains the loop of Henle
  • Receives 6% of total blood flow (approx 0.03mL/min/g)
  • Regulated by:
    • Prostaglandins (PGs) and NO, promoting vasodilation
    • PGs and NO + adenosine A1 in cortex work to shunt blood into the medulla
    • NSAIDS disrupt this compensatory mechanism and can cause medullary ischemia by inhibiting PGs


What is the PO2 in the madulla?

What is the extraction ratio?

  • PO2 = 8 mmHg with an 80% extraction ratio
  • Severe hypoxia can develop in the medulla despite relatively adequate RBF
  • High extraction ratio b/c this area is highly metabolically actively


What happens with medullary ischemia in hemodynamically-mediated renal injury?

  • First response is to increase active NaCL absorption
    • this increases metabolic activity and O2 demand, decreasing O2 delivery
  • compensation attempted via cortical vasoconstriction and flow redistribution
    • ultimately ATP becomes depleted and NaCl reqbsorption decreases
    • causes increased NaCl in tubular fluid
    • renin is released from macula densa and afferent arteriole is constricted


What are the different types of nephrons?

  • Cortical nephrons (recieve 85% of RBF and make up majority of the nephrons)
    • found in outer/middle cortex
    • short loop of henle
    • efferent arterioles drain into peritubular capillaries
  • Justamedullary nephrons (recieve 10% of RBF)
    • found in inner renal cortex
    • longer loop of henle to reach inner medulla
    • efferent arterioles drain into specialized peritubular capillaries (vasa recta)
      • countercurrent mechanism


What is the glomerulus?

What are the 5 components?

  • Glomerulus: capillary network that originates from an afferent arteriole and are surrounded by dilated blind end of the nephron (bowman's capsule)
  • 5 components:
    • capillary endothelium- produces NO and endothelin-1 which vasodilate and constrict
    • glomerular basement membrane, and visceral epithelium- make up the filtration barrier
    • parietal epithelium (bowman's capsule)
    • mesangium (interstitial cells)- contract in response to angiotensin II and other vasoconstrictors to decreasesflow and GFR


What happens in the proximal convoluted tubule?

(5 actions)

  • Reabsorption
    • PCT is a direct continuation of bowman's capsule
      • the higher the peritubular pressure, the less reabsorption occurs
  • Actions:
    • 65% of H20, Na, K, Cl reabsorpion (ATP req for Na)
    • almst 100% reabsorption of glucose, lactate, AA
      • glucose max is 375 mg/dL
    • H+ exchanged for bicarb
    • Ca reabsorbed under influence of PTH
    • waste products actively excreted ( bile salts, urea, Cr, dopamine, drugs)


What happens in the loops of Henle?

  • Ultrafiltration- interstitial osm increases from 300 to 1500
  • Continuation of PCT
  • Descending loop of Henle:
    • permeable to H20, thus it passively leaves the tubule
  • Ascending loop of henle
    • impermeable to H2O, but d/t highly concentrated ultrafiltrate, NaCl passively diffuses out into the interstitial
  • Thick ascending loop of henle
    • thickness caused by active transport channels in the epithelium layer
    • high metabolic activity, susceptible to ischemia
    • Na/K/2Cl cotransporter to increase osm of interstitial and dilute urine


What is the vasa recta?



  • network of capillaries surrounding the loop of henle that take up and/or release Na, Cl, and H2o passively along the gradient


What is the Juxtaglomerular apparatus?

What is the function?

How is this achieved?

  • made of of the distal convoluted tubule and the afferent arteriole.
  • main function is to control BP and filtration rate
    • mesangial (sm muscle) cells contract, decreasing surface area of glomerulus and decreasing GFR (in response to vasoconstrictors)
    • granular cells secrete renin in response to:
      • Beta 1 stimulation
      • decreased RBF which leads to decreased GFR


What happens in the distal convoluted tubule?

  • electrolyte, H2O, and pH fine tuning
  • High metabolic activity
  • 10% of Na/H2O reabsorption, also Cl reabsorption d/t
    • ADH mediated V2 receptors
    • aldosterone


What is aldosterone?

When is it released?

What does it do?

  • Aldosterone is a steroid released by the zona glomerulosa of the adrenal cortex 
  • Released in response to:
    • angiotensisn II
    • ACTH
    • SNS stimulation
    • low Na
    • high K
  • Aldosterone increases active Na reabsorption via K exchange (this takes a few hours to work)
    • excessive aldosterone causes hypokalemic acidosis


Where is ADH released from?

When is it released?

What is the E1/2t of ADH/AVP?

Antidiuretic hormone (ADH)= Vasopressin (AVP)


  • ADH is released from the posterior pituitary gland in response to:
    • chemoreceptors (increased ECF Na levels or osm >280
    • baroreceptors (atrial, aortic, carotid)
      • hypotension is most potent trigger for ADH release
    • Angiotensin II
    • stress via cortical input
    • surgical stimulation (for 2-3 days afterward) and hypotension d/t anesthesia (not directly the anesthetics)
  • E1/2t ADH/AVP = 5-15 min


What does the release of ADH result in?

  • V2 receptor stimulation
    • increased cAMP->PK activation, causing migration and fusion of pre-formed vesicles containing aquaporin-2 water channels
    • thus increasing H2O permeability
  • with high amts of ADH can cause V1 receptor stimulation
    • causes renal cortical vasoconstriction (primarily efferent arteriole)
  • Stimulates thirst


What happens in the collecting ducts?

  • Electrolyte, H2O, and pH fine tuning
  • 10% of Na and H2O reabsorption
    • under influence of ADH
    • principle cells reabsorb Na (and water) in exchange for K
    • capable of secreting H+
      • intercalated cells secrete H+ and reabsorb bicarb


Summary of the four major kidney functions

  • Control of fluid and inorganic ion balance
  • removal of metabolic wastes and chemicals from the circulation (via filtration or secretion)
  • gluconeogenesis
  • endocrine function/hormone secretion
    • fluid balance (renin, PGs, kinins)
    • RBC production (EPO in response to decreased renal PO2)
    • bone health (1,25-dihydroxyvitamin D3)


Summary of urine production when hypovolemic

With hypervolemia?

  • Hypovolemia:
    • SNS and angiotensin II = vasoconstriction = decreased GFR and increased Na reabsorption
    • aldosterone = increased Na reabsorption
    • vasopressin (ADH) = increased H2o reabsorption in collecting ducts
  • Hypervolemia
    • ANP= vasodilation = increased GFR
    • decreases SNS and angiotensis II = vasodilation = increased filtered Na
    • increased capillary hydrostatic pressure = decreased reabsorption of Na
    • decreased aldosterone = decreased Na reabsorption in DCT and CD
    • decreased ADH = decreased H2O reabsorbed in CD


What are the mechanisms of autoregulation?


  • myogenic (local feedback)
    • arteriole stretch or lack of stretch causes reflex vasoactivity of the afferent arteriole
  • first response to renal ischemia = increase Na/Cl reabsorption in TALOH
  • SNS (esp Alpha 1) and angtiotensin II
    • first efferent vasoconstriction
    • effects seen on afferent arteriole when levels are really high
  • AVP/ADH causes reabsorption of H2O + efferent vasoconstriction
  • Adenosine: decreases renin w/high NaCl + redistributes RBF
    • afferent vasoconstriction + selective vasodilation of deep cortical vasculature
  • tubuloglomerular feedback
    • high Cl sensed in macula densa of JA indicates high GFR, causing release of adenosine, decreased renin release, and NO synthatase inhibition
  • PGs: produced via ang II activation d/t renal ischemia, hypotension, or physiologic stress and cause renal vasodilation
  • Natriuretic peptides in response to stretch
    • block reabsorption of Na in DT and CD and increases GFR, decreases renin/aldosterone release
  • NO: opposes vasoconstrictive effects of SNS/angiotensin, promotes Na/H2O excretion, influences tubuloglomerular feedback


What is normal RBF?

What is autoregulation maintained between?

What impairs autoregulation?

  • RBF is 1200 ml/min (25% of CO)
    • 2/3 is to the cortex
  • Autoregulated btwn MAP 80-180
  • Autoregulation maintained with most anesthetics
  • Autoregulation impaired by:
    • CCB
    • sepsis
    • ARF
    • CPB
    • NO


What is normal GFR?

What directly impacts GFR?

Why does GFR matter?

  • GFR is approx 90-140 ml/min (180 L/day)
  • Autoregulation of GFR directly impacted by RBF
    • b/c blasma hydrostatic pressure is the easiest and most realistic variable to manipulate
  • Why does it matter?
    • too slow = tubular fluid would pass through too slowly, causing complete reabsorption and no UOP
    • too fast = passes too fast and unable to reabsorb the substances that need to be conserved


What makes GFR?

What can affect each component?

  • GFR = permeability of filtration barrier = difference b/t hydrostatic pressures - oncotic pressure of plasma
  • Glomerular hydrostatic pressure affected by:
    • efferent/afferent arteriole tone
    • hyper/hypovolemia
    • MAP outside the auto regulation range
  • Filtrate hydrostatic pressure affected by:
    • Bowman's capsule pressure
  • Plasma oncotic pressure affected by:
    • alterations in protein
    • anemia
  • permeability of filtration barrier affected by:
    • integrity of the endothelial glycocalyx


What are some methods of renal protection?

  • Low dose dopamine- does NOT decrease incidence of ARF, dialysis, or mortality despite having diuretic activity
  • Fenoldopam- DA-1 specific agonist
    • may help preserve post-op renal function in high risk patients
  • Research ongoing for:
    • PGE-1
    • Natriuretic peptide
  • Renal protection in shock:
    • vasopressors
    • NE (if MAP increased to >60 it will improve RBF more than the vasoconstriction will decrease it
    • vasopressin (increased renal perfustion pressure and preferentially the efferent arteriole)