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Renal Exam > GFR & Renal Hemodynamics > Flashcards

GFR & Renal Hemodynamics Flashcards

1
Q

kidney morphology

A

*nephron = subunit of kidney
*1-1.3 million nephrons per kidney
*lengths of loops of Henle vary (short in the outer cortex, long in juxtamedullary)

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2
Q

renal plasma flow (RPF) - definition & formula

A

*amount of plasma delivered to both kidneys per unit time
*RPF = (Upah x V) / Ppah
*normal = 625 ml/min

note - PAH (para-aminohippuric acid) clearance is used to estimate renal plasma flow b/c it is almost completely excreted by the kidney

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3
Q

renal blood flow - definition & formula

A

*amount of blood delivered to both kidneys per unit time
*renal blood flow = RPF / (1 - hematocrit)
*normal = 1.2 L/min

note - RPF is renal plasma flow (calculated by: Upah x V / Ppah)

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4
Q

glomerular filtration rate (GFR) - definition

A

*flow rate of filtered fluid through the kidneys (ml/min)
*normal = 125 ml/min
*helps us define and stratify loss of kidney function due to disease

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5
Q

filtration fraction - definition & formula

A

*fiiltration fraction (FF) is the fraction of plasma that enters the kidney that is actually filtered
*filtration fraction = GFR / RPF
*normal = 20% (or 0.2)

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6
Q

clearance - definition

A

*amount of plasma cleared of a substance per unit time (ml/min)
*any substance (including creatinine, urea, or infused substances such as inulin)
*can be an estimate of GFR
*creatinine clearance long used to define safe drug dosing for decreased kidney function

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7
Q

clearance equation

A

Cx = (Ux x V) / Px

Cx: clearance of substance X (in mL/min)
Ux: urine concentration of substance X
V: urine flow rate → (urine volume / time)
Px: plasma concentration of substance X

recall: clearance is the volume of plasma completely cleared of a substance per unit time (unit = mL/min)

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8
Q

clearance vs. GFR

A

*clearance is measuring the amount in the final product (urine)
*glomerular filtration rate (GFR) is measuring the flow rate of the filtrate
*clearance may be different from GFR

*if substance X is freely filtered at the glomerulus AND:
-unaltered in the tubules: Cx = GFR
-partially reabsorbed in the tubules: Cx < GFR
-secreted by the tubules: Cx > GFR

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9
Q

3 outcomes of the relationship between clearance (Cx) and GFR

A

*if substance X is freely filtered at the glomerulus AND:
-unaltered in the tubules: Cx = GFR
-partially reabsorbed in the tubules: Cx < GFR
-secreted by the tubules: Cx > GFR

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10
Q

if clearance of substance X (Cx) < GFR…

A

net tubular reabsorption and/or not freely filtered

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11
Q

if clearance of substance X (Cx) > GFR…

A

net tubular secretion of X

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12
Q

if clearance of substance X (Cx) = GFR…

A

no net secretion or reabsorption

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13
Q

inulin clearance

A

*inulin = a fructose polymer
*inulin is freely filtered and is not secreted or reabsorbed in the tubules
*therefore, inulin clearance is good for estimating GFR

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14
Q

using inulin clearance to determine properties of other substances

A

for any substance, X:
*Cx / Cinulin = 1, the Cx is a good estimate of GFR
*Cx / Cinulin > 1, then X is filtered and secreted in the tubules (ex. creatinine)
*Cx / Cinulin < 1, then either:
-substance is not freely filtered (ex. albumin)
-substance is filtered but then is reabsorbed in the tubule (ex. glucose, urea, amino acids, Na+)

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15
Q

techniques for measurement of renal blood flow & renal plasma flow

A

*electromagnetic flow meter (lab only)
*doppler / ultrasonic flow meter
*analysis of an appropriate marker

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16
Q

PAH clearance for estimating renal plasma flow

A

*para-aminohippuric acid (PAH)
*PAH clearance:
-freely filtered
-remainder leaving the glomerulus is completely secreted
-between filtration and secretion, 90% is cleared on the first pass through the kidneys
-clearance of PAH is thus good for estimating renal plasma flow

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17
Q

effective renal plasma flow (ERPF)

A

*ERPF = clearance of PAH (Cpah) = Upah x V / Ppah

*true RPF = Cpah / 0.9

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18
Q

estimating renal blood flow (RBF) using cardiac output

A

*the kidneys tend to receive approximately 25% of the cardiac output, so we can estimate RBF by taking 25% of the known cardiac output

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19
Q

factors that affect GFR

A
  1. arteriolar resistance (afferent & efferent arterioles)
  2. forces across glomerular filtration barrier (oncotic & hydraulic forces)
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20
Q

relationship between arteriolar resistance & renal plasma flow (RPF)

A

*changes in afferent and efferent arteriole diameter result in changes in overall RPF
*resistance to flow across arterioles = 85% of total vascular resistance
*peritubular capillaries & renal veins: remaining 15% of total vascular resistance

*constriction of afferent arteriole → decreased total RPF and decreases GFR
*constriction of efferent arteriole → decreased total RPF but increases GFR

21
Q

changes in RPF & GFR due to constriction of afferent arteriole

A

*decreased total RPF
*decreased GFR
*decreased Pgc (hydraulic pressure in glomerular capillary)

22
Q

changes in RPF & GFR due to constriction of efferent arteriole

A

*decreased total RPF
*INCREASED GFR
*increased Pgc (hydraulic pressure in glomerular capillary)

23
Q

3 systems for governing arteriolar resistance

A
  1. renin-angiotensin-aldosterone system (RAAS)
  2. autoregulation
  3. tubuloglomerular feedback
24
Q

renin-angiotensin-aldosterone (RAAS) system - overview

A

*the afferent arteriole contains specialized juxtoglomerular (JG) cells:
-renin is stored & released from secretory granules

*stimuli for renin release:
1. renal hypoperfusion: hypotension or volume depletion
2. decreased NaCl delivery to macula densa
3. increased sympathetic activity

25
Q

renin-angiotensin-aldosterone (RAAS) system - pathway

A

hypotension / hypovolemia → renal hypoperfusion → decreased afferent arteriolar stretch, decreased NaCl delivery to macula densa, & increased sympathetic tone → renin release → conversion of angiotensinogen to Angiotensin I → conversion to Angiotensin II (by the ACE enzyme, located in lung, endothelium, and glomerulus) →
1. increased aldosterone secretion → increased renal Na+ reabsorption → extracellular volume expansion
2. increased systemic blood pressure

26
Q

angiotensin II - 2 major effects

A

*Ang II has 2 major effects:
1. systemic vasoconstriction / constriction of efferent arteriole → increased GFR, decreased RPF
2. sodium & water retention

27
Q

angiotensin II → Na+/water reabsorption

A

*2 mechanisms by which angiotensin II → Na+/water reabsorption:
1. direct stimulation of proximal tubule → increased activity of Na+/H+ antiporter
2. increased secretion of aldosterone from the adrenal cortex → enhances Na+ transport in the cortical collecting tubule

28
Q

angiotensin II - effects on GFR

A

*Ang II causes constriction of afferent & efferent arterioles, plus interlobular arteries
*net effect: reduction in renal blood flow & maintenance (increase) of GFR, even if there is a drop in systemic BP

note - vasoconstrictive effects of Ang II is balanced by vasodilatory prostaglandins, which preferentially dilate the afferent arteriole

29
Q

effects of NSAIDs on GFR in presence of Ang II

A

*NSAIDs inhibit production of prostaglandins
*prostaglandins are usually helping to attenuate the vasoconstrictive effects of Ang II
*in patients with high Ang II (such as very low salt intake), NSAIDs cause an acute decline in GFR (due to inability to vasodilate afferent arteriole)
*note - NSAIDs produce minimal effects on renal function in normo-volemic subjects with low prostaglandin production

30
Q

autoregulation

A

*ability to keep GFR & RPF constant over a wide range of arterial pressures
*myogenic stretch receptors in the afferent arteriole play an important role:
-afferent arteriole constricts or dilates in response to stretch to keep intra-glomerular pressure stable
*system is impaired below MAP of 70 mmHg (increased risk of acute kidney injury)

31
Q

tubuloglomerular feedback (TGF)

A

*macula densa cells sense increased NaCl delivery → signaling through the JG apparatus → afferent arteriole constriction → decreased GFR
*helps prevent excessive salt & water losses

32
Q

glomerular filtration barrier - overview

A

*responsible for filtration of plasma according to size & charge selectivity (smaller & more cationic molecules more likely to be filtered)
*3 layers:
1. fenestrated endothelial cell
2. glomerular basement membrane
3. epithelial cell (attached to the GBM by discrete foot processes)
*pores between foot processes (slit pores) are closed by a slit diaphragm

33
Q

glomerular filtration barrier - CHARGE barrier

A

*contains negatively charged glycoproteins (heparan sulfate) in GBM that prevent entry of negatively charged molecules (ex. albumin)
*adhesion properties between layers

34
Q

glomerular filtration barrier - components of the SIZE barrier

A

*combination of:
1. fenestrated capillary endothelium (prevents entry of large molecules & blood cells)
2. effective pore size in GBM
3. slit diaphragm in epithelium (prevents entry of medium-sized molecules)

35
Q

glomerular filtration barrier - results of the SIZE barrier

A

*allows passage of small molecules (sodium, urea)
*solutes up to size of inulin (MW 5200) are freely filtered
*myoglobin (MW 17000) less completely
*albumin (MW 69000) should not be in the urine

36
Q

4 components that determine whether a filtrate is formed

A
  1. Pgc = hydraulic pressure in glomerular capillary (pressure pushing across glomerular barrier from capillary into bowman’s space)
  2. Pbs = hydraulic pressure in bowman’s space (pressure pushing from bowman’s space backwards)
  3. Πp = oncotic pressure in plasma (pressure from proteins in the plasma that draws water across the semipermeable membrane)
  4. Πbs = oncotic pressure in bowman’s space (effectively ZERO)
37
Q

glomerular filtration rate (GFR) - equation

A

GFR = Kf x (Pgc - Pbs - Πp)

Kf: filtration coefficient
Pgc: hydraulic pressure in glomerular capillary
Pbs: hydraulic pressure in bowman’s space
Πp: oncotic pressure in plasma

*changes in GFR result from:
-anything that changes these values
-change in renal plasma flow (RPF)

38
Q

GFR in normal physiology

A

*hydraulic pressures remain constant
*capillary oncotic pressure progressively rises as we progress through the capillary bed due to filtration of protein-free fluid
*gradient starts around 13 mmHg and falls to zero

39
Q

examples of how the GFR can change based on changes in pressures

A

*reduction in surface area available in glomerulonephritis → decreased GFR
*increased Pbs in obstruction → decreased GFR
*increased Πp in volume depletion → decreased GFR
*increased Πp in multiple myeloma (high levels of Ig light chains) → decreased GFR
*decreased Πp in nephrotic syndrome → increased GFR

40
Q

intraglomerular hypertension (hyperfiltration)

A

*starts with nephron loss (due to any kidney disease)
*compensatory rise in filtration in other nephrons, driven by afferent dilation
*plays a major role in diabetic nephropathy

41
Q

ACE inhibitors / ARBs in chronic kidney disease

A

*reduces angiotensin II effects
*helps dilate afferent & efferent arterioles, but more so the efferent
*reduces glomerular capillary hydraulic pressure

42
Q

SGLT2 inhibitors in chronic kidney disease

A

*block sodium glucose transporter
*sends sodium to the macula densa
*may result in increased afferent constriction and long term decreased Pgc

43
Q

plasma creatinine & GFR

A

*plasma creatinine should vary inversely (exponential) with GFR (ex: creatinine 1.5 = GFR 67; creatinine 2 = GFR 50; creatinine 4 = GFR 25)
*limitations: loss of nephrons leads to compensatory hyperfiltration; when GFR begins to fall, tubular secretion of creatinine increases
*result: creatinine remains stable despite a drop in true GFR
*a stable creatinine does not necessarily mean stable GFR

44
Q

urine clearances for estimating GFR

A

*inulin clearance is the gold standard for GFR measurement, but is only used in experiments due to expense & difficulty
*another option: check 24 hour urine for expected creatinine excretion

*urine creatinine clearance tends to OVERestimate GFR
*urine urea clearance tends to UNDERestimate GFR
*therefore, we can take the average of creatinine clearance and urea clearance

45
Q

eGFR

A

*estimated GFR
*equations predict better at low GFR than at high GFR

46
Q

cystatin C

A

*low molecular weight protein produced by all nucleated cells
*not altered in the tubules to a large extent
*great for boosting accuracy of creatinine-based equations
*great for low muscle mass situations

47
Q

stages of CKD

A

stage 1: eGFR 90+ (with other sign of kidney damage)
stage 2: eGFR 60-89
stage 3a: eGFR 45-59
stage 3b: eGFR 30-44
stage 4: eGFR 15-29
stage 5: eGFR < 15

also - take into account albuminuria

48
Q

what “equation” provides the best estimate of GFR

A

non-race based creatinine + cystatin C CKD-EPI eGFR equation

Renal Exam (44 decks)

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