Facts Flashcards
renal cortex
90% of renal blood
glomeruli, PCT and DCT
renal medulla
10% of renal blood: prevents washing out hypertonic medulla
tubules and vasa recta
cortical nephrons
85% of nephrons
small; short LoH
lower arterial perfusion and filtration rate
reserve capacity
juxtamedullary nephrons
15%
large; long LoH
higher arterial perfusion and filtration rate
operate at full capacity
concentration of urine: conserve water and Na conservation to produce hypertonic medulla
mesangium
support capillary loops
can alter capillary SA (actin and myosin)
ingest and remove circulating immune complexes (only fenestrated endothelial cells between it and blood; no BM)
podocytes
visceral epithelial cells
heavy proteinuria: podocyte problem
macula densa
cortical thick ascending limb
senses Cl and syn. and releases renin (systemic) and Na-K-2Cl cotransporter releases ATP or Ca for smooth muscle contraction (auto regulation)
low delivery: vasodilate afferent
high delivery: constrict afferent
proximal tubule
cortex (PST descends to corticomedullary junction)
bulk reabsorption (2/3 of filtrate): iso-osmotic
reabsorption:
50-55%: Na (active) and H2O
90% (active): HCO3
100% (active): glucose, amino acids
PO4, urate, organic anions
urea, K (passive)
production: NH3
secretion (mostly active cotransporters): organic acids and bases (cations, anions)
passive Cl paracellular reabsorption (Na reabsorption creates a neg. lumen driving Cl and HCO3 reabsorption; maintains electroneutrality)
Na/K- ATPase
all cells primary active transport basolateral: interstitial 3 Na out of cell (into capillary) 2 K into cell creates Na electrochemical potential gradient
Na/X cotransport
proximal tubule
luminal
active: coupled to Na electrochemical potential gradient
X: glucose or amino acids or PO4
Cl-/anion exchanger
proximal tubule passive luminal Cl- into cell anion into tubule lumen
Na/H exchanger
proximal tubule
luminal
Na into cell
H into tubule lumen
HCO3 reabsorption
proximal tubule
active: driven by H secretion
1. H in lumen (due to Na/H exchanger) binds filtered HCO3
2. lumen: CA converts carbonic acid to CO2 + H2O that move into cell
3. cell: CA converts CO2 + H2O to H + HCO3
4. HCO3 moves into interstitium (HCO3/Na cotransporter) creating a negative charge on interstitial side of cell
5. negative charge drives paracellular reabsorption of Na, Ca, Mg
Thin descending limb
cortex to outer medulla passive: osmotic gradient reabsorption: H2O, urea impermeable: Na concentrates tubular fluid
Thin ascending limb
passive: osmotic gradient
reabsorption: NaCl
impermeable: H2O, urea
decrease tubular fluid osmolarity
Thick ascending limb
between medulla and cortex
active
reabsorption: NaCl (20-25%), Ca, Mg
impermeable: H2O, urea
recycle: NH4
requires O2 to operate N/K-ATPase that maintains ion gradient for Na/K/2Cl
other: basolateral Cl (into interstitium), basolateral K/Cl cotransporter (into interstitium), apical K channel (into tubular fluid)
Na/K/2Cl transporter
thick ascending limb
luminal
Na/K/2Cl into cell from tubular lumen
driven by: electrochemical gradient
ROMK
thick ascending limb
K from cell into tubular lumen that makes it more positive
drives Mg, Ca into interstitium (paracellular)
active Na reabsorption in thick ascending limb
DCT and CD
- Na/K ATPase creates concentration gradient by pumping Na out of the cell into the interstitium
- Na/K/2Cl transporter needs all ions to work
- K must be supplied to tubule by ROMK for Na/K/2Cl to work
- Cl leaves cell via basolateral Cl channels
- K in tubular lumen causes paracellular reabsorption of Na, Ca, Mg
affarent arteriole
baroreceptor
myogenic sensor: release renin from JG cells in response to low flow or inhibit renin release in high flow (systemic)
distal convoluted tubule
cortex reabsorption: Na (5-8%), Cl impermeable: H2O, urea major site of Ca reabsorption/regulation dilution of tubular fluid
Na/Cl cotransporter (NCCT)
DCT
luminal
electroneutral
Na and Cl into cell
Ca dependent protein (TRPV5)
DCT: responds to PTH
luminal
Ca into cell
Ca/Na countertransporter
DCT
basolateral
3 Na into cell
1 Ca into interstitium
collecting duct
6-8 DT form 1 CD
cortex through medulla
reabsorption: Na (2-3%), Cl
secretion: K (ONLY place)
impermeable: H2O, urea
more Na reabsorption than K secretion: Cl reabsorbed
*water deprivation: ADH causes high water permeability: reabsorb water
principal cells
cortical CD and inner medullary CD
reabsorption: Na/H2O
secretion: K
alpha-intercalated cells
cortical CD and outer medullary CD active normal pH: secretion: H alkalosis: reabsorb H H-ATPase or H-K ATPase
beta-intercalated cells
CD
normal pH: reabsorb HCO3
secrete: HCO3 under alkalosis
Cl-HCO3 exchanger
epithelial sodium channel (ENac)
CD
luminal
Na into cell due to negative cell interior created by ATPase
now negatively charged lumen favors secretion of K
cortical collecting duct
concentrates urine
medullary collecting duct
urea concentration in urine increases
What does the kidney do during fasting?
gluconeogenesis
ECF
1/3 TBW
Na, Cl, HCO3
slightly more Na and less Cl in plasma (Gibbs Donnan: Pr-)
plasma
1/4 ECF
Pr
interstitial fluid
3/4 ECF
ICF
2/3 TBW
K, Mg, PO4, Pr
NO Ca
TBW
60% body weight in males
50% females
inversely related to fat
mMol/L vs. mOsm/L
Osm counts each particle that a molecule can ionize into
Mol counts each molecule
low PNa, high urea
iso-osmotic: hypoosmotic NaCl with added urea to make iso-osmotic
cell swells: urea gets into ICF and ECF becomes hypo-osmotic
normal PNa, elevated urea
hyperosmotic
no change in cell volume
low PNa, high glycerol
shrink initially, then swell
driving force for Na reabsorption
active through length of nephron driving forces: decrease in intracellular Na increase in membrane potential
HCO3/Na cotransporter
PT
luminal
3 HCO3 and 1 Na into interstitium from cell
water reabsorption
PT
facilitated by mass solute reabsorption in PT
osmotic gradient drives water reabsorption by leaky epithelium with high hydraulic conductivity (high Kf)
protein and peptide reabsorption
PCT
large proteins not filtered
peptides have greater filtration and are reabsorbed by transporters
PO4 reabsorption
PCT
Na/PO4 cotransporter
low threshold (poised at plasma concentration), partially excreted in urine
PTH: decreases transport maximum
Cl reabsorption
PCT
passive
driven by: concentration gradient created by water reabsorption, Na electrochemical potential gradient
less reabsorbed because of HCO3 active transport
K reabsorption
PCT
passive transport along concentration gradient though claudins
reabsorption of urea
PCT
passive: slow
only 50% reabsorbed
increase in urine flow increase urea clearance
mannitol
poorly permeant
freely filtered, not reabsorbed: increase osmolarity and cause diuresis
Tx: cerebral edema; reduce intracranial and intraocular pressure, promote excretion of toxins, edema
Na channels
PT
luminal
passive
What maintains net filtration in glomerular capillary bed 50-100x greater than other capillary beds?
glomerular capillary bed is separated by the afferent and efferent arterioles (resistance arterioles) that cause arterio-venous pressure drops that occur in two steps maintaining high hydrostatic pressure
What happens to plasma hydrostatic pressure and oncotic pressure from afferent to efferent arteriole? How does this effect the peritubular capillary?
hydrostatic pressure drops in afferent and efferent arteriole: increase in oncotic pressure from afferent to efferent arteriole
resulting in a low hydrostatic pressure in peritubular capillary and an increase in peritubular oncotic pressure allowing for reabsorption
B1 adrenergic nerves
SNS response stimulates renin release from JG cells (systemic)
renin-angiotensin system
decrease BP or perfusion decreases ECFV
1. increased SNS firing
2. JG cells release renin
3. renin converts alpha2 globulin to angiotensin I
4. angiotensin converting enzyme converts angiotensin I to angiotensin II
5. angiotensin II
importent regulatory system in intact system
NOT part of kidney autoregulation
SNS activation effects on kidney
constrict afferent and efferent arterioles causing reduced RPF and PG and therefore GFR
stimulates renin secretion and increase Na reabsorption
ONLY important under severe ECFV loss: overrides auto regulation
decrease Kf by stimulating mesangial cells
determinants of GFR
Kf and net filtration pressure:
hydraulic conductivity, glomerular SA, capillary hydrostatic pressure, capillary oncotic pressure, bowman’s space hydrostatic pressure
duct of Bellini
CDs join in medulla
drain into minor calyx
K secretion
CD
driven: high intracellular K and negative lumen
regulated by:
increase: increase Na delivery of Na to CD: change in lumen-negative voltage: aldosterone, vomiting, diuretics, Barrter’s, Gitelman’s
decreased: renal failure, distal tubular disfunction, decreased distal tubular flow, hypoaldosteronism
H-ATPase
DCT and CD luminal active H secretion alkalosis: basolateral: H into interstitium
HCO3-Cl exchanger
DCT and CD? basolateral HCO3 into interstitium Cl into cell alkalosis: luminal: HCO3 into lumen, Cl into cell
H/K- ATPase
electroneutral transport
expressed under high acidosis condition
HCO3 secretion
*under alkalosis condition
H-ATPase and HCO3-Cl exchanger switches direction
activate alpha and B intercalated cells
bicarbonate buffer system
CO2 + H2O …. H2CO3…. H + HCO3
What is going on if Na concentration stays constant but Cl concentration changes?
acid-base disorder
How do acid base disorders affect serum K?
alkalosis: hypokalemia
acidosis: hyperkalemia
How does plasma tonicity affect K serum?
solvent drag: K moves in direction of water
hyperosmolarity: hyperkalemia
hypoosmolarity: hypokalemia
How do cell lysis and cell proliferation affect K?
lysis: hyperkalemia
proliferation: take up K: hypokalemia
osmoreceptor
hypothalamus: senses changes in osmolarity
1. supraoptic and paraventricular nuclei stimulates posterior pituitary: increase intracellular Ca causes fusion of AVP vesicles at nerve terminal and secretion of AVP
2. lateral preoptic nucleus: regulate thirst
positive CH2O
Uosm less than Posm
dilute urine: increase plasma osmolarity
negative CH2O
Uosm greater than Posm
concentrate urine: decrease plasma osmolarity
factors responsible for medullary hyperosmolarity
- arrangement of loop of Henlee and vasa recta
- active transport of Na and co transport of K and Cl out of TALH into medullary ISF
- active transport of Na out of CD into ISF
- passive diffusion of urea from inner medially CD into medullary ISF
- only small amount of water from medullary tissues into medullary interstitium
- low medullary blood flow
components of GBM
perlecan, entactin, laminin, type IV collagen
When do ECV and ECFV not move in the same direction?
Liver disease, CHF, nephrotic syndrome, pregnancy and anaphylaxis
ECV decreased
ECFV increased
ECV decrease is due to either decreased CO or arterial vasodilation causing secondary ECFV increase
