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Renal Flashcards

0
Q

What is the composition of glomerular filtrate?

A

no blood cells no proteins all other substances in the same concentration as those in plasma

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1
Q

Pore size?

A

30 A

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2
Q

Describe the 3 things that restrict molecules from entering filtrate

A
  1. SIZE (30 A) -water, urea, electrolytes, glucose, amino acids can enter -Inulin freely filtered (98%) -assume no proteins -anything bound to protein is not filtered (40% calcium) 2. Shape ex) albumin has oblong shape 3. Charge -Negatively charged MACROmolecules are repelled by the negative podocytes/basement membrane *Cl- can still enter b/c it’s small enough -add positive charge and filtration increases
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3
Q

what 3 pressures act on the glomerular capillary?

A
  1. Hydrostatic pressure of the glomerular capillary favors filtration - stays constant across glomerular capillary because the efferent arteriole on the end of the GC has resistance 2. Oncotic pressure of the glomerular capillary = oppose filtration -Increases along the capillary as filtrate leaves the capillary, raising plasma protein concentration (*Protein from liver, not diet) 3. Hydrostatic pressure from Bowmans space =opposes filtration * Bowmans space oncotic pressure is 0 because there are no proteins in the Bowmans space, pulling fluid into it
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4
Q

What is the Starling equation for GFR

A

GFR = Kf * (HPgc - HPbs) - Onc-gc Kf = SA * Lp Net filtration pressure along enter glomerulus = 16 mmHg NFP along with Kf accounts for the high filtration of ~180 L/day

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5
Q

Effect on GFR if you increase the glomerular capillary HP?

A

If you increase hydrostatic pressure of the glomerular capillary, you push more fluid into the Bowmans space

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6
Q

Effect on GFR if you increase the Capillary oncotic pressure

A

Raise glomerular capillary oncotic pressure = more pressure pulling fluid back into the capillay = DECREASE GFR ex) increase protein in capillary

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7
Q

Effect on GFR if you increase the Bowmans Space hydrostatic pressure

A

More pressure opposing filtration = decrease GFR

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8
Q

Effect on GFR if you increase the Kf?

A

Increase Kf ex) Increase SA =More filtration can occur

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9
Q

Effect on GFR if you increase the RBF?

A

Increase RBF = faster = lower fraction of plasma is filtered out of the glomerular capillaries so there is a SLOWER rise in the glomerular capillary oncotic pressure that would opposite filtration Increase RBF = Increase GFR *also increase RPF = Increase GFR

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10
Q

Effect on GFR if you increase the AA resistance (constrict)

A

Lowers hydrostatic pressure of glomerular capillary Decreases RPF and decreases GFR

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11
Q

Effect on GFR if you increase the EA resistance (constrict)?

A

Increase hydrostatic pressure of glomerular capillary decreases RPF but increases GFR Increases Filtration Fraction

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12
Q

Effect on GFR if you increase the arterial BP?

A

Increases GFR

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13
Q

what happens to GFR in hemorrhage?

A

Drop in blood pressure Drop in GFR *protective to limit filtration when you’re trying to raise BP/CO dont want to pee when you’re losing blood!

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14
Q

what happens to GFR in hypertension?

A

Rise in BP Rise in GFR *dangerous b/c can cause hyperfiltration

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15
Q

what happens to GFR in liver failure?

A

Liver failure = less proteins made -less protein in glomerular capillary to create oncotic pressure opposing filtration -Higher filtration

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16
Q

list key regulators of GFR

A
  1. SA *Major cause of decreased GFR in renal disease is not a change in individual nephrons but a loss in the number of functioning nephrons. lower SA = lower Kf = lower GFR 2. Hydrostatic pressure in glomerular capillary -depends on 3 factors (perfusion pressure coming in, afferent arteriole Resistance and efferent arteriole resistance) –afferent arteriole resistance has a greater impact than efferent arteriole resistance
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17
Q

Describe the steps in the PT to move Na, water, and freely filtered solutes from the tubule lumen to the peritubular capillary

A
  1. Na/K ATPase on the basolteral side sets up a low Na+ intracellular concentration 2. Na+ then diffuses from the tubule lumen into the cell down its electrochemical gradient -chemical = less Na+ in cell -electrical = negative potential in the cell attracts Na+ *water follows transcellulary or paracellulary (thru tight junctions) 3. As Na+ diffuses down gradient into cell, it allows for Secondary Active Transport: a) of glucose,amino acids up their gradient into cell through luminal membrane b) Na/H antiport - where Na enters cell in exchange for H exit into lumen 4. Anions follow Na into cell to a) escape negative charge in lumen and b) preserve electroneutrality 5) bulk flow of Na/water/solutes from interstitium into plasma * glucose has to enter peritubular capillary via faciliated diffusion
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18
Q

PT vs CT?

A

PT: -bulk flow -low resistance -has brush border -high permeability -Leaky Epithelium with tight junctions that allow for paracellular movement -low concentration differences -low elec potential differnces CT: -fine tuning -high resistance to solute movement -no brush border -low permeability -TIGHT epithelium with NO paracellular transport -high concentration and electrical potential differences -still has Na/K ATPase *regulated by ADH

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19
Q

write equation for the rate of filtration units of filtration rate?

A

F = P * GFR mass/time

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20
Q

write equation for the rate of excretion

A

E = U * V

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21
Q

write equation for the rate of reabsoprtion

A

R = F - E

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22
Q

write equation for the rate of secretion

A

S = E - F

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23
Q

Difference between transport maximum vs. renal threshold of glucose

A

Transport Max = max rate of glucose reabsorption = Tm [a rate, mg/min]

  • filtered load < Tm = glucose reabsorbed, NONE in urine
  • filtered load > Tm = not all the glucose reabsorbed, excreted in urine ** NOT a kidney problem, just too much glucose**

Renal Threshold– plasma concentration at which the FIRST nephron maxes out

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24
Q

what is splayed curve? (Tm)

A
  • Graph of plasma glucose reabsop/secreted/filtered - reabsor/excretion graphs are curved to take into account nephron heterogeneity. Some will max out and reach Transport maximum bf others (Renal Threshold)
  • sharp reabsorbed/excreted curves would be for individual nephrons Tm
25
Q

what is the RLS of secretion?

A

anion exchanger on the basolateral side that captures solute

26
Q

write a starling equation that describes fluid uptake into the peritubular capillaries

A

Reabsoprtion = Kf [(HPi-HPpc) - (Onc-i - Onc-pc)] 1. hydrostatic pressure of peritubular capillary pushes fluid out of PC, opposes reabsorption 2. hydrostatic pressure of interstitium pushes fluid into the peritubular capillary, out of the interstitial, favors reabsoprtion 3. oncotic pressure of interstitium pulls fluid back into interstitium, opposes reabsoprtion 4. oncotic pressure of the peritubular capillary pulls fluid into the capillary ***Favors reabsorption

27
Q

renal handling of proteins and peptides?

A

Assume that no proteins are filtered and enter tubule Vanders says peptides and smaller proteins are filtered and get re-uptaken into the capillaries larger proteins are uptaken via endocytosis, degraded into AA, and those AA are returned to the blood Very small peptides are catabolized into AA and di/tri-pptides in tubular lumens by peptidases at the apical surface and reabsorbed as AA protein in urine = renal damage

28
Q

urea reabsorption? how much of the filtered load of urea is excreted?

A

Urea is passively reabsorbed from the tubule Steps: 1) PT will reabsorb 50% of the filtered load 2) LOH will secrete that same amount that was reabsorbed *higher urea concentration in the medullary interstitium favors secretion into the tubule 3) then as the urea concentration builds in the tubule (as fluid leaves), urea will be reabsorbed from the collecting duct to the blood Half of the filtered load of urea is excreted!

29
Q

urate ? how is it handled by kidneys? is most of urate reabsorbed or excreted?

A

urate is an anion base form of uric acid uric acid the product of nucleic acid metabolism! 1) almost all of the filtered load of urate is reabsorbed in the PT via antiporters (URAT1) 2) then further in the PT, urate undergoes active tubular secretion 3) urate is reabsorbed again in the straight portion of PT result = kidneys reabsorb most of the filtered load of urate

30
Q

how are organic anions reabsorbed and secreted by kidney

A

reabsorbed: as Na enters the cell down gradient, anions or neutral solutes enter via symporter secretion -active secretory pathway using alpha-keto-glutarate antiporter on the basolateral membrane -antiporter that moves alpha-keto-glutarate out of the cell into interstitium while anion is pumped into the cell for secretion

31
Q

organic actions reabsosrbed and secreted?

A

reabsorbed: cations leave lumen and enter cells via uniporters driven by negative membrane potential secreted: organic cations cross peritbular capillary basolateral membrane and enter cell via Organic Cation Transporter (uniporter) -cations secreted through apical membrane via cation/H antiporter -cations then excreted

32
Q

% of filtered load that is reabsorbed at the PT? Cl? H20, Na? HPO4-? K+ HCO3 amino acids glucose?

A

Cl: 65% H2O, Na, HPO4- = 70% K+ = 80% HCO3 = 85% amino acids/glucose = 100%

33
Q

what 6 factors help concentrate urine?

A
  1. anatomical characteristics of the LOH -longer = more concentrated urine 2. Different permeabilites in the descending vs ascending limbs descending = water permeable (+ solute) ascending = NOT permeable to water - only NaCl 3. Active NaCl transporters in the thick ascending limb create a concentration gradient 4. ADH 5. Urea 6. Low medullary blood flow
34
Q

Describe the steps of concentration and dilution from the PT to the collecting tubule

A
  1. Bowmans Space: 20% of plasma is filtered and enter BS 2. PT: about 60% solutes and water are reabsorbed in the PT -tubular fluid stays isosmotic to the interstitial b/c water can follow salt 3. Descending limb As you move down from cortex into medulla, there is an increasing concentration gradient in the interstitium from 300 to 1200. Water flows out Tubular fluid reaches equilibrum with the surrounding interstitium of the medulla which is very hypertonic 4. Ascending Limb NaCl will leave the ascending limb into the more dilute interstitium (gradient goes from 1200 to 300 as you ascend) now the tubular fluid is HYPO-tonic 5. Collecting tubule -tubular fluid is hypotonic and sine the CT is permeable to water now, water is reabsorbed -concentrates the urine -water diffuses out of the Collecting Duct until osmotic equilibrium is reached with the tubular fluid having the same concentration as the renal medullary interstitial (1200)
35
Q

Describe the countercurrent multiplier system for concentrating urine

A

Start with tubular fluid and interstitium with same osmolarity 1. Single Effect: Thick ascending limb has active NaCl transporters that pump out solute and generate a 200 mOsm gradient in the medullary interstitiuim 2. DL is permeabel to water so water flows into the interstitium until it’s iso-osmotic to interstitium 3. fluid continues to move around the loop from the DL and AL AL continues to pump out solutes This concentration gradient multiplies along the length of the LOH 4. process repeats and traps solute in the interstitium This makes it so you can superconcentrate the external space, and then reabsorb all the water on the way down the CD. Allows us to get our urine concentration up to 600 but we still need to get it to 1200 for maximal concentration

36
Q

explain urea recycling and how it helps concentrate urine

A
  1. PCT reabsorbs 50% of the filtered load of urea 2. In the LOH, that same amt that was reabsorbed is now secreted into the LOH 3. as NaCl and fluids leave the tubule, urea slowly builds up and cannot escape (impermeable to urea) 4. In the inner medullary collecting tubule, ADH allows water and urea to be reabsorbed *since urea was recycled into the thin ascending loop of Henle and cannot escape through tubule (until CD), it helps the urine become more concentrated. Then in the collecting ducts, when water can escape, it will because urine has raised the urine concentration *urea is reabosrbed in the inner medulla when ADH is present **without ADH, urea and water are NOT reabsorbed so urine concentration only reaches 600 instead of 1200
37
Q

how does low medullary blood flow help concentrate urine?

A

blood flow to medulla to keep it alive Need to make sure that the blood flow to the medulla is slow or it will wash away solutes/concentration gradient

38
Q

how does the Vasa Recta maintain a concentration gradient in the medulla?

A

Helps preserve the medulla concentration gradient while supplying medulla with necessary blood flow Come off the efferent arterioles and completely permeable to solute and water As blood descends into the medulla, solutes enter the vasa recta and blood leaves to enter interstitium (becomes more concentrated) As blood ascends from medulla, solutes leave blood and enter the interstitium (to then just load back into the descending vasa recta) and water enters vasa recta *makes sure the blood flow does not just carry solutes away *cycling of solutes

39
Q

what is the minimal and max concentration of the urine

A

min = 50 mOsm/L max = 1200 mOsm/L *requires ADH and hyperostmoic renal medulla interstitium which provides for the osmotic gradient necessary for water reabsorption to occur in the presence of ADH

40
Q

what is the osmolarity of each segment of the tubule? iso, hyper, hypo?

A

PCT: isomotic DL: water leaves until its isosmotic with the surroudning medulla interstitium which is very hyperotnic (1200) *fluid can leave which allows for osmotic equilibrium to be reached Al: hypotonic b/c water cannot follow DCT: hyptonic CT: tubular fluid equilibrates with hypertonic medulla until it is isosmotic water diffuses from the tubule into the interstitium until osmotic equilibrium is reached (1200)

41
Q

what % of CO do kidneys get? rate of blood flow?

A

20% of CO 20% of 5 L = 1 L/min

42
Q

explain relationship between RBF and GFR on renal O2 consumption

A

RPF = U * V / (Pa-Pv) like the Fick Principle CO = O2 consumption / (arterial - venous sample) More RPF = More GFR = more filtered so more O2 consumed for active transport

43
Q

define autoregulation of RBF and GFR

A

as arterial pressure increases, RPF remains stable to maintain a constnat GFR As pressure increases, myogenic mechanism kicks in and afferent arterioles vasoconstrict to prevent blood flow from increasing As pressure decreases, vessels dilate to maintain RPF and GFR

44
Q

what happens to RPF, GFR, FF and oncotic glomerular capillary pressure if you constrict AA?

A

RPF/GFR drop FF same (ratio same) oncotic pressure same (because FF same)

45
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you dilate AA

A

RPF and GFR increase FF and oncotic pressure same

46
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you constrict the EA?

A

RPF will decrease GFR will increase - pushing more out of the hole in hose FF will increase therefore onctoic pressure of the GC will increase - if you filter more of the plasma, the oncotic pressure rises

47
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you dilate EA?

A

RPF increases GFR decreases - relax hand and less will be pushed out of hole in hose FF decreases oncotic pressure drops

48
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you dilate AA and constrict EA?

A

no change in RPF increase GFR increase FF increase oncotic pressure ANP does this

49
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you constrict AA and dilate EA?

A

no change in RPF drop in GFR drop in FF and oncotic pressure

50
Q

what happens to RPF, GFR, FF and oncotic capillary pressure if you constrict BOTH the AA and EA

A

RPF drops a lot GFR drops (AA has more of an affect) increase in FF slightly so increase in oncotic pressure slightly

51
Q

what are some intrinsic vs. extrinsic mechanisms to regulate GFR?

A

Intrinsic -Myogenic mechanism -Tubuloglomerular feedback Extinrisc -SNS -catecholamines -Ang II -prostaglandsin

52
Q

Describe the myogenic mechanism of intrinsic GFR control

A

Increase in pressure = wall stretches = vasoconstrict arteriole to prevent blood flow and GFR from increasing

53
Q

what is the tubuloglomerular feedback mechanism of GFR?

A

Decreased blood flow = Macula dense sense thsi and dilate afferent arteriole to increase GFR in that nephron ** minute to minute regulation *local and weak (overcome by extrinsic mechanisms)

54
Q

how does SNS innervation control GFR?

A

SNS nerves innervate kidneys constrict both the AA and EA, but since the AA has more control, it will reduce RPF and GFR ex) hemorrahge

55
Q

how do catecholamines control GFR?

A

adrenals release NE and Epi reduce GFR

56
Q

how does Ang II decrease RPF and GFR

A

1) vasoconstrict the AA and EA which overall reduces RPF and GFR 2) causes the glomerulus to contract - decrease SA - decreases Kf - decrease GFR

57
Q

outline biochem of renin-ang system

A

1) reduced plasma volume 2) contract ECF 3) kidneys release renin 4) renin converts angiotensignoen from liver to ang I 5) ACE converts ang I to ang II

58
Q

what 3 things cause renin release?

A

1) renal baroreceptors sense s a drop in pressure/volume and release renin from juxtaglomerular cells 2) SNS directly innervates cells that release Renin 3) Macula densa- if there is a drop in flow past the macula densa cells, they will stimulate renin release

59
Q

how do prostaglandins affect GFR?

A

prostaglandins are not normally released by the kidneys If SNS and Ang II vasoconstricts are released and RPF drops, prostaglandins are released to buffer the effects of the vasoconstrictors so the kidneys dont shut down

Renal (14 decks)

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