Renal Physiology

Front 1

Principle Cells of Distal tubule

Back 1

- ADH causes aquaporins to reabsorb H20
-Enac - Na reabsorption, stimulated by aldosterone, inhibited by ANP
-K secretion, stimulated by aldosterone
- urea reabsorption via UT1 and UT4

Front 2

alpha intercalated cells of distal tubule

Back 2

-reabsorb K via H/K atpase
-secrete H by H atpase and H/K atpase; stimulated by aldosterone

Front 3

Renin
-stimulated/inhibited by
-action, origin

Back 3

from: JG cells of afferent arteriole
stimulated by:
-low BP
-low Na (in macula densa)
- norepinephrine (symp)
inhibited by:
-aliskiren
-increased afferent pressure
-ANP
-AII (negative feedback)
turns angiotensiogen to AI

Front 4

ACE
-inhibited by

Back 4

turns AI --> AII
inhibited by: enalapril, captopril
-inhibits bradykinin

Front 5

AII

Back 5

binds A1TR
- vasoconstricts efferent arterioles to maintain glomerular pressure and GFR
-stimulates aldosterone production
-stimulates Na/H exchanger in prox tubule, increase Na reabsorption
-vasoconstricts peripheral vasculature
-thirst
-increase norep production/ SNS tone
- can inhibit renin secretion/ stimulate angiotensinogen expression (can modulate RAS expression)

Front 6

ADH
- origin, stimulated by
-function

Back 6

- from the posterior pituitary
- stimulated by hyperosmolarity
causes:
- increase H2O reabrosption, aquaporin expression in principle cells of distal tubule
- increased Na reabsorption - stimulates Enac in principal cells

Front 7

Diabetes Insipidus

Back 7

insensitivity to ADH
- dilute urine (losing H2O), low bp - volume depleted
- increased thirst
- hyperosmolarity
- ions may follow water - maybe hypo or hyper nutremic

Front 8

SIADH

Back 8

increased ADH production
-retain lots of H20
- hyponutremia (diluted)
-hypoosmolarity, causes cellular swelling
-concentrated urine
-generally euvolemic (distributed H20)

Front 9

ANP
-stimulated by
-produced by
-function

Back 9

- stimulated by increased rt atrial pressure
-produced by rt atrium
-vasodilates afferent and efferent arterioles - increases RBF and GFR
-inhibits Enac, decreasing Na reabsorption
- inhibits renin secretion

Front 10

Norepi
- different receptors and effects

Back 10

alpha 1 receptors in afferent and efferent arterioles --> vasoconstriction, decrases GFR and RBF
Beta 2 receptors stimulate renin secretion and ADH secretion
-kick in immediately after volume depletion

Front 11

Aldosterone
-from
-stimulated by
-function
-escape

Back 11

from the adrenal cortex - zona glomerulosa
- stimulated by AII and hyperkalemia
-stimulates Enac causing Na reabsorption (principal cells), H2O follows
-stimulates K secretion in principal cells (possibly by ROMK or just by Na+ gradient & na/k pump)
-stimulates H secretion in alpha intercalated cells
- stimulates na/k pump
- escape: pressure naturesis - increase GFR due to increased volume (K+/Na+ excretion)

Front 12

Hypoaldosteronism

Back 12

mass excretion of Na and H20
obvious as an infant

Front 13

hyperaldosteronism

Back 13

- hypokalemia
-near normal Na due to pressure naturesis
-hypertension
-metabolic alkalosis
-kaliuresis

Front 14

Calcitrol
-origin
-stimulated by
-function

Back 14

- produced by kidney tubular cells
- stimulated by PTH & low phosphate
- formed from Vitamin D
- stimulates Ca reabsorption from the distal tubule
- blocks PO4 excretion
-stimulates SI to reabsorb Ca and Po4
-induces bone breakdown aka reabsorption
- blocks PTH secretion

Front 15

PTH

Back 15

- secreted in the parathyroid gland
-secretion is stimulated by low Ca++
-stimulates Ca++ reabsorption from the distal tubule
-inhibits PO4 reabsorption in the proximal tubule
- mobilizes Ca++ from bone
- stimulates calcitrol production

Front 16

secondary hyperparathyroidism = increased bone turnover renal osteodystrophy

Back 16

- chronic renal disease causes decreased Ca++ because it can't be reabsorbed, which causes PTH production
-calitrol is produced in the kidneys, so in damaged kidneys, it can't be produced to "help" PTH or to turn off PTH
- PTH stimulates bone reabsorption -->release of Ca++
- hyperphosphatemia since kidney disease does not allow the secretion of PO4 - causes even more PTH release

Front 17

hypo PTH

Back 17

low Ca++, high PO4, low urinary Ca++
t/x low/ normal range of Ca++ by giving vitamin D

Front 18

effective osmolarity

Back 18

depends on sodium (mostly) and glucose

Front 19

renal clearance
- definition
- eqn

Back 19

- volume of blood that can be 100% cleared of a solute per unit time
- C=U*V/Plasma
-PAH is used to measure clearance since it is filtered and secreted but not reabsorbed

Front 20

filtered load

Back 20

amt of solute filtered into bowman's capsule per unit time

Front 21

fractional excretion

Back 21

the amount of what gets filtered that actually gets excreted

Front 22

Autoregulation

Back 22

stretch induced activation system of cation channels --> depolarization--> Ca++mobilization and contraction

Front 23

tubular glomerular feedback

Back 23

increased GFR, increased NaCl in urine, increased NaCl transverse the macula densa (in the TAL), macula densa cells produce ATP/adenosine to vasoconstrict the afferent arteriole to lower glomerular pressure and GFR
- decreased sensitivity of this response in volume expansion (pressure naturesis), since concentration of Na isn't that high, this allows volume to return to normal

Front 24

pressure natriuresis

Back 24

increased pressure/ increased GFR causes increased H2O and Na+ filtration

Front 25

Atenolol, metoprolol

Back 25

beta blockers, sympathetics can't stimulate increased HR/ contractility
effect: lower CO and BP

Front 26

enalapril/captopril

Back 26

ACE inhibitors, stop AI-->AII, can't vasoconstrict or cause Na reabsorption
effect: lower BP
ACE escape: there is some other way to form AII that isn't via ACE, so ACE inhibitors don't always work/ stop working

Front 27

aliskiren

Back 27

renin blocker, can't activate RAS
effect: lower BP

Front 28

Losartan, irbesartan

Back 28

ARB - blocks AII receptors (AT1)

Front 29

Prostaglandins
- effects
-inhibitors

Back 29

-Prostaglandins are vasodilatory
- save the kidney from hypoperfusion
-inhibited by NSAIDs and COX-2 inhibitors

Front 30

Signs of renal hypoperfusion (prerenal azotemia)

Back 30

- increased urine specific gravity
- decreased urinary Na and urea
- elevated plasma BUN/creatinine ratio

Front 31

Proximal Tubule

Back 31

apical
- na/ gulcose cotransporter - SGLT
-Na/H exchanger -NHE (AII +)
-UT2 secretes urea
-Na/PO4 cotransporter (PTH inhibits, Calcitrol stimulates)
Basolateral
- Na/HCO3- cotransporter

Front 32

TAL

Back 32

apical:
-Na,Cl,K cotransporter (NKCC2) - loop diuretics
-Na/H exchanger
-K secretion - ROMk
basolateral:
Cl/HCO3- excahnger

Front 33

Distal convoluted tubule

Back 33

-Na/Cl cotransporter (NCC) inhibited by thiazides
- Ca reabsorption (stimulated by calcitrol & PTH), on basolateral side - na/Ca exchanger (allows Ca++ reabsorb)
- ENaC, Na reabsorption

Front 34

Urea
-where it comes from
-how the kidney deals with it

Back 34

- generated from NH4; end product of protein metabolism
- filtered and reabsorbed and secreted; reabsorbed urea gets trapped in interstitium and maintains the hyperosmotic gradient, aiding in the production of concentrated urine
-secreted via UT2 in thin ascending and descending
-reabsorbed in collecting ducts (UT1,4)

Front 35

Kidney and Glucose
- insulin - how its dealt w/ in kidney

Back 35

- 20% of gluconeogenisis occurs in the kidney and can therefore partially compensate after hepatic failure
-insulin allows renal glucose uptake
-insulin is metabolized by the kidney (renal failure - often accompanied by hypoglycemia)

Front 36

spironolactone

Back 36

aldosterone antagonist; K+ sparing diuretic