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176 Cards in this Set

  • Front
  • Back
kidney location
between body wall and peritoneum
major functions of the kidney
1. rids body of wast
(from protein met. removes urea and creatine, and removes toxins/drugs)
2. maintain stable ICF and ECF by regulating excretion of solutes and water to balance intakes
3. during prolonges fasting kidney does gluconeogenisis from aa
4. make and release hormone
Failure of what function is most critical consequence of kidney failure
failure to maintain a stable ICF and ECF. Can cause hypo/hypercalcemia, acidosis, alkolosis, or dehydration
hormones made in the kidney
erythropoeitin stimulates RBC production

1,25 kihydroxy vitamin D3 allows Ca absorption in GI
amount of salt kidney filters per day
3 lbs or 1.5 kg
amount of plasma kidney filters per day
50 G/ day

or 2 G/hour
what must patient do if kidney fails?
change diet by resticting proteins, salts and monitor water consumption

dialysis so solutes excreted can move across membrane and down a conc. gradient
blood is removed from circulation through a tube to artifical membrane that is permeable to small solutes. blood is then returned to the body
pertioneal dialysis
fluid in injected and removed from the peritoneal cavity. the membranes are the natural membranes of the peritoneum.
outer layer of the kidney
functional unit of the kidney
blood supply to the nephron
afferent arteriole gives rise to the glomerular capillary. the glomerulus is drained by another cap called the efferent artiole
2 segement of the nephron
renal corpuscle and the renal tubule
renal corpuscle
segment of the nephron. composed of glomerulus, bowman' capsule, and bowmans space
renal tubule
segment of the nephron. composed of proximal tubule, thin descending limb of the loop of henle, thin ascending limb of the loop of henle, thick ascending limb of the loop of henle, distal convoluted tubule, and the collecting duct.
juxtaglomerular apparatus
occurs where the thick ascneding limb of the loop of henle at junction of distal convoluted tubule comes into close contact with the renal corpuscle and contacts the afferent arteriole
specialized cells in the nephron
cells in the tubule called macula densa

cells in afferent arteriole called jaxtaglomerular cells
What does the cortex, the outermost layer of the kidney contain?
renal corpuscles, proximal and distal convoluted tubules, superficial portions of the loop of henle and the Collecting ducts
what does the medulla, the deep layer of the kidney contain?
tad bit of the proximal tubule, deeper portions of the loop of henle and collectin duct.
are there renal corpuscles in the medulla?
No only in the cortex
describe cortical nephrons
v. superficial. renal corpuscle is near the kidney surface of the loop of henle does not penetrate into medulla
describe juxtamedullary nephron
renal corpuscle is v. close to the medulla and the loop of henle goes deep into the medulla
what does pelvis, innermost layer of kidney conain?
urine before it leaves to the ureter.
region where the ureter leaves the kidney
hilum. this is where bloodvessles, lymph, and nerves enter and exit the kidney too
amount of CO fro kidneys
bf from the renal arterie to the afferent arteriole
from larger to smaller: goes from renal a. to interlobar a. in medulla, then to arcutate a. in medulla, then to interlobular a. in cortex
How can BF to kidney be regulated?
by smooth muscle in the afferent and efferent arterioles.
what caps does the efferent arteriole give rise to?
peritubular caps. fluid reabsorbed from the nephron is returned to the peritubular caps.
caps the run parallel to the loop of henle
peritubular caps(vasa recta). so stuff from tube is reabsorbed into these caps. this helps make urine with hi solute conc.
Renal corpuscle physical adaptations for filtration
bowmans capsule is in an epithelial sac.

glomerulus is cap loops v. close to epithelial sac.

plasma is filtered into bowmans capsule.

filtered fluid goes into the renal tubule
how does the glomerular cap contrast with other cap. beds?
it is highly permeable due to fenestration that are 70-100 nm in diameter, therefore, solutes as large as plasma proteins can pass through
describe basement membrane between cap endothelium and bowmans capsule
gel like made from glycoproteins, proteoglycans like laminin.

v. thick

negative charge so repels negatively charged plasma proteins
what acts as a barrier to filtration of plasma protiens?
the basement membrane having a negative charge
describe epithelium on bowmans capsule
has podocytes that are elaborate thick foot like processes. there are filtration slits between the podocytes so larger molecules can be filtered
hydrostatic and osmotic forces that allow filtration from glomerular cap into bowmans capsule
cap hydrostatic pressure is 60 mmHg

cap protein osmotic pressure is 29 mmHg

Bowmans hydrostatic pressure is 15 mmHg

Bowmans osmotic pressure is 0 mmHg

(60-29)-(15-0)= 16 mmHg
net force favors filtration
why is glomerular cap. protein osmotic pressure high compared to other caps?
bc of filtration of fluid filtered but proteins are left behind so hi solute conc.
Why is bowmans space protein osmotic pressure 0?
bc no proteins are filtered
glomerular filtration rate (GFR) per day
125 mL/min or 180 L/day
typcial plasma flow to the nephrons
600 ml/min or 900 L/day
% of plasma flow to the nephrons that is filtered
Amount of time it takes to filter all the plama in the body
less than 30 min so plasma filters approx. 50 times a day
ohms law

if pressure increases and flow does not change, then resistance must have also increased
the ability of nephrons to regualte blood flow to a constant value at different levels of arterial pressure
what pressure does kidney regulate blood flow?
between 80-180 mmHg
myogenic hypothesis of autoregulation
as pressure rises the afferent arteriolar smooth muscle contracts and increases arteriolar resistance. this keeps blood flow and hydrostatic pressure in glomeruli from increasing
tubulogomerular feedback
increase in GFR due to increase in pressure with increase delivery of solute to juxtaglomerular apparatus and macula densa. the macula densa secretes a mediator (arachadonic acid or ATP) to cause afferent arteriole constriction to increase resistance to bring GFR back down
what does constriction of afferent arteriole cause?
decrease in pressure in glomerular caps. so for any given pressure, GFR is decreased and flow is reduced.
what does constrictio of the efferent arteriole cause?
increase in pressure in glomerular caps. For any given pressure, GFR is increased since net filtration pressure is increased but BF is decreased
what causes constriction of afferent and efferent arterioles?
sympathetic nerve activity. the increase in resistance causes reduction in blood flow, even if pressure increases.
besides symp NS what other vasoconstrictors affect afferent and/or efferent arterioles?
angiotensin II, ADH, cortisol
How is GFR reduced with angiotensin II?
mesangial cells which support glomerular capilllary loops can contract and reduce GFR
vasodilators to the kidney
prostaglandins increase BF during intense symp vasoconstriction so GFR wont shut down
Effect of moderate increase in symp activity
decrease blood flow but does not change GFR bc of constriction of both afferent and efferent arterioles
effect of severe increase in symp activity
reduces BF and GFR
amount of Na+ and water reabsorbed in the proximal tubule
67% or 2/3
amount of filtered K+ that is reabsorbed in the proximal tubule
4 main things that occur in proximal tubule
1. reabsorbs 67% of filtered Na+ and H2O and 60% of filtered K+

2. reabsorbs all glucose & aa

3. secretes metabolic end products and toxins

4. preferential reabsorbtion of HCO3-; Cl- conc. rises
structure of tubular epithelium
luminal membrane, basolateral membrane, tight junctions between cells, interstial fluid surrounds the tubule (peritubular fluid)
How is Na+ reabsorbed in proximal tubule?
Na+ in tube moves into tubular epithelial cells through luminal membrane down conc and electrical gradient (passive transport)
tube lumin conc of Na?

promial tubular epithelial cell Na conc?
luminal conc of Na is 140 mM/L and inside cell is 20mM/L. so Na want to move into the tubular epithelial cells.
How does Na+ get from proximal tubular epithelial cell to the interstial fluid then into the peritubular cap. for reabsorbtion?
Na+/K+ ATPase paump is on basolateral membrane of proximal tube epithelial cell. So Na+ are pumped into ISF and K+ are pumped into cell causing decrease of Na+ osmolarity in cell and increase in Na+ osmolarity in ISF. this causes water to move to ISF too through aquaporin channels and tight junctions. ISF moves into caps bc hydrostatic pressure is hi in ISF and lo in caps which promotes reabsorbtion of water and Na+.
Na+conc by the end of the proximal tubule
Na+ conc is the same as in the orginally filtered plasma by the end of the proximal tubule due to Na+ being isosmotically reabsorbed
volume of fluid at end of proximal tubule
1/3 less volume by the end of proximal tubule due to H2O and Na+ reabsorbtion
How is K+ reabsorbed in the proximal tubule?
K+ is NOT actively reabsorbed

As fluit leaves the tube, K+ is in the tube and it is concentrated in the tube.

K+ then moves across tight junctions and into the ISF and into peritubular caps
How are glucose and aa reabsorbed in the proximal tubule?
passive movement of Na+ across the lumin and into the epithelial cell uses cotransporter to bring glucose and aa with it. Once these solutes enter the cell, specific transporters extrude theses substances at basolateral membrane into ISF. the substances then enter peritubular cap.
describe glucose reabsorbtion with diabetes
glucose is higher than 200mg/dL a day so cotransporters are saturated and glucose cannot be reabsorbed so glucose is excreted in the urine (more glucose filtered than reabsorbed)
What happens when certain drugs are secreted by the kidney to rapidly?
an inhibitor of secretion like probenicid can be given to hel p maintain the plasma level
How is H+ secreted into proximal tube?
When Na+ passively moves out of lumen and into the cell it is coupled with H+ secretion into the lumen (Na+/H+ contransporter)

This allows H+ removal from plasma and HCO3- reabsorbtion
What increases H+ secretion in proximal tubule?
peptide angitensin II bc it increases Na+ and H2O reabsorbtion by proximal tubule which is coupled with H+ secretion
PAH in proximal tubule
filtered and secreted. almost completely cleared from peritubular caps and into tube
inulin in proximal tubule
only filtered. so remains in tube to be excreted
creatine in prxoimal tubule
just filtered
sodium in proximal tubule
reabsorbed with water
What remains in the tube at the end of the proximal tubule?
33% of filtered Na+
33% of filtered H2O
40% of filtered K+
0% glucose
amount of Na+ and K+ orginally filtered that is reabsorbed in the loop of henle
25% Na+ and 25% K+
only part of loop of henle that allows H2O reabsorbtion
thin descending limb is v. permeable to water
What part of the loop of henle is v. permeable to Na+ and Cl-?
the ascending limb is not permeabel to water but is v. permeable to Na+ and Cl-. this aids in concentrating and diluting the urine
What does thick ascending loop of henle do?
creates a hypoosmotic tubular fluid bc it is impermeable to water but Na+, K+, and Cl- are reabsorbed. So salts leave and water remains.
What does amount of water reabsorbtion in the thin descending limb of the loop of henle depend on?
its location. whether it is among juxtamedually and superfical nephrons.

Juxtamedullary reabsorbs over 20% while superficial reabsorbe less than 10%
How are Na, Cl, and K reabsorbed in the thick ascending loop of henle?
on luminal membrane Na+ movement is coupled with cotransporter that carries 1 K+ and 2 Cl-. A tad K+ leaks back into lumen. since water is not reabsorbed but solutes leave, the tube conc. decreases.

From cell to ISF. Na gets into ISF from Na/K ATPase. Cl-, and K+ diffuse through.
conc of tube by end of the thick ascending loop of henle
150 mOsm/L which is hypoosmotic bc solutes are leaving the tube and water is remaining
most typical mechanism of action of diuretics
normally reabsorbed solutes remain in tubule bc solute reabsorbtion is inhibited. leading to increased solute and water excretion
how does alchol act like a diuretic?
it interferes with water reabsorbtion
how does mannitol act like a diuretic?
bc it cannot be reabsorbed
Loop diuretics
work in the thick ascending limp of the loop of henle by blockin Cl- binding site on the cotransporter so normal reabsorption of Na+, K+, and Cl- in thick ascending limb of the loop of henle isdecreased with a loop diuretic and these solutes will be excreted
by the time tubular fluid leaves the distal convoluted tubule and collecting duct as urine, how much filtered Na+ and Water has been reabsorbed?
99% or Na+ and 99% of water has been reabsorbed
amount of Na reabsorbed in Distal convoluted tubule and colecting duct
after the loop of henle, where is most water reabsorbed?
well the distal convoluted tubule is impermeable to water so the collecting ducts reabsorb most water remaining in the tube
How is Na+ reabsorbed in the distal convoluted tubule
Na+ and Cl- cotransporter to get Na and Cl from tube into cell. At cell requires the Na+/K+ ATPase pump at the basolateral membrane to get Na into ISF and K into cell. Cl- isreabsorbed throught tight junctions between cells

tube fluid becomes hypoosmotic bc solutes are leaving and water remains
Thiazide diuretics
block the NaCl cotransporter at DCT. So excretion of Na+, Cl-, K+, and Water are increased
Amiloride and triamterene
block the luminal membrane Na+ channels (called K+ sparing) so Na+ not reabsorbed and K+ is not secreted at DCT. More water is elminated in the urine as NaCl excretion is increased. these diuretics spare K+ bc K+ is not secreted into lumen
When is K+ reabsorbed?
K+ can be reabsorbed by intercalated cells in the collecting duct when K+ is low. There is a K+/H+ exchanger on the luminal membrane so K+ will come into cell aa H+ leaves cell and goes into tube. K+ will diffuse out of intercalated cell at the basolateral membrane
Purpose of aldosterone
steriod hormone that is released from the adrenal cortex when the body needs to retain sodium. Aldosterone binds to receptor and causes signal to nucleus which activates receptors which promote protein synthesis. Mainly acts on principle cells and increases Na reabsorbtion.

Increases luminal Na channels

increase Na/K ATPase on baloateral side

increase citric acid cycle enzymes so more ATP for Na/K

Activate luminal K+channels

More Na reabsorbed and more K+secreted
prevnets aldosterone from entering the cell nucleus
what is in the tube at the end of the loop of henle/
8% of filtered Na
10% of filtered K
16-% of filtered water
what is in tube at the end of the collecting tube (in urine)?
<1% filtered Na
1-80% K (variable)
<1% filtered water
if urine is hypoosmotic, what does this mean?
hi water intake w/ hyposmotic urine and lo wate intake with hyperosmotic urine
when is tubular fluid concentrated?
as it flows through collecting duct into the renal medulla
How does urine become hyperosmotic in the collecting ducts into the renal medulla?
tube fluid enters the collecting ducts as very hypoosmotic w/ respect to plasma.

osmolarity of ISF in the medulla around collecting ducts is hi (1200 mOsm/L)

permeability of collecting duct to water is hi so water leaves tube and goes into ISF
This increases tube conc.

when tube fluid reaches the pelvis ist is hyperosmotic and excreted as urine
How is hyperosmotic condition of ISF created?
by loop of henle
how does loop of henle concentrate the ISF?
thick ascending limb reabsorbs NaCl by juxtamedullary nephrons to increase NaCL conc in the ISF by 150-200 mOsm/L above level in tube. tube has lo permeability to water so NaCl conc decreases wi tube and increases in ISF

thin descending loop is close to ascending limb and is permeable to water but not NaCl so water leaves tube and solutes remain.

thin ascending limb is permeable to NaCl but impermeable to water so NaCl goes into ISF.
where is NaCl conc highest in the ISF?
inner medulla
where is NaCl conc lowest in the ISF?
renal cortex
besides help from the loop of henle, how is ISF osmolarity further increased?
by urea in ISF in inner medulla
Max osmolarity of inner medulla
over 1200 mOsm/L
What keeps the solute gradient from being washedout of the ISF by peritubular cap?
Caps are unusually arranged in that they are parrallel to the loop of henle (vasa recta loops) This minimezes the loss of solute throught cap blood

also the lo level of blood throgh the vasa recta (5% of kidney blood flow) reduces chance of cap washing out gradient
made by PP. increasing plasma ADH increases permeabilty of collecting ducts to water so water will leave tube and enter ISF to conserve water. Without ADH the colllecting ducts are impermeable to water
How is water reabsorbed from collecting duct?
ADH signals receptor (V2) it is coupled with G protein receptors cAMP is made by activating adenyl cyclase to activate protein kinase A. proteins are phosphorylated causing insertion of water channels into luminal membrane. water flows out of collecting duct bc of large conc gradient and into ISF
What does ADH do to NaCL?
ADH increases NaCl reabsorption in the thick ascending loop of henle to icrease osmolarity of ISF in inner medulla to help with gradient so water will flow from CD into ISF
Absence of ADH at Collecting ducts
water permeability v. low from thick ascending loop of henle to CD so water trapped in tube but NaCl can be reabsorbed so tube fluid becomes progressively hypoosmotic
diabetes insipidus
extreme circumstances when ADH cant be released into the circulation there is no collect duct reabsorption of water

NaCL reabsorbtion causes lowere osmolarity in CD lumen

ISF in medulla is less concentrated

urin v. hypoosmotic with hi volume
When looking at kidney performance what should be looked at?
BF to kidney tubules
substances in urine
clearance equals plasma flow through kidney
means substance is entirely removed from plasma. filtered and secreted so volume equla to entire plasma flow through the kidney has been cleared of that substance
clearance equals GFR
substance only filtered not secreted not reabsorbed. vol equal to GFR has been cleared
What does the amount of substance entireely cleared from a volume of plasma over time equal to?
plasma vol eintirely cleared of that substance
clearance calculation
amount of substance lost from plasma is same as amount of substance in urin

C= Urine conc x urine vol/[P]
using inulin to check clearnace
inulin is filtered but not reabsorbed or secreted by kidney so allows dr to check GFR.

using C=UxV/P
C should be .125 l/min=GFR
using creatine to check clearance
creatine is filtered (secreted a tad) and made by body.

normal plasma conc is 1 mg/dl
what does it mean if plasma creatine is 3 mg/dl?
well plasma creatine should only be 1 mg/dl so that means plasma is higher and GFR is lower by 1/3
using PAH to check clearance
PAH is filtered by glomerulus and secreted into tube so almost all PAH is removed from plasma
glucose clearance
0 bc filtered amount is entirely reabsorbed by proximal tubule
sodium clearance
99% of filtered is reabsorbed so plasma vol cleared is v. low
where are osmoreceptors in brain?
suproptic and paraventricula nuclei in hypothalmus and they activate the PP to release ADH
Normal range of plasma osmolality
280-290 mOsm/Kg differ from osmolarity which is 300 mOsm/L
When does ADH secretion increase?
when plasma osmolalities are above 275 mOsm/Kg
When is ADH secretion surpressed?
when plasma osmolality is below 275 mOsm/Kg
flow chart: drink excess water
decrease body fluid osmolarity bc hi water conc.

decrease firing of hypothalmic osmolrecetors

decrease ADH release from PP

Decrease plasma ADH

Decrease permeablity to water at CD

increase water excretion
(urine hypoosmotic)
Flow chart with dehydration
increase body osmolarity

increase firing of osmoreceptors in hypothalmus

increase ADH release by PP

Increase plasma ADH

Increase CD permeabilty to water

Increase water reabsorbtion

decrease water excretion (urine is hyperosmotic)
How does kidney maintain extracellular vol ie blood vol?
by regulating Na conc in vascualr component of ECM bc Na is major cation so increase or decreasing Na changes vol.
What happens when kidney dectects low Na+ vol?
sensors dectrect lo Na in extracellular space which means low water vol so effects of osmoreceptors bring plasma osmolality back up to normal
high pressure arterial baroreceptors
carotid and aortic

stimulated by stretch, when stretched, means hi Na+ and carotid stretch receptor releases ANP
Low pressure baroreceptors
in great veins of chest or atria of heart. they are stimulated by increased stretch
neural signal pathway to CNS from high pressure arterial barorecptors
carotid-glossopharyangeal n.

aortic uses vagas n.
What happens when pressure is reduced in kidney?
barorecptors in afferent arteriole of nephron produces a humoral signal resulting in release of renin
How does juxtaglomerular apparatus ajust to lo NaCl levels?
humoral signal causes release of renin
where are osmoreceptors for juxtaglomerular apparatus?
in macula densa
Where does juxtaglomerular apparatus respond to delivery of NaCl?
at ascending limb of loop of henle before junction with distal convoluted tubule
What happens to GFR with hi vascular pressure?
decrease symp NS to kidney

arteriolar constriction is decreased causing increase in GFR with increase excretion of Na+ and water
What happens to GFR with lo vascular pressure?
arteriolar constriction is increased so decrease in GFR and decrease excretion of Na+ and water
describe activation of renin-angiotensin system that leads to secretion of aldosterone
juxtaglomerular cells of juxtaglomerular apparatus secrete renin which splits angiotensinogin to angiotensin I. In lungs, angiotensin I is converted to angionstensin II by angiontensin converting enzyme. Angiotensin II stimulates secretion of aldosterone from the adrenal cortex
Function of aldosterone
increase Na+ reabsorbtion and K+ secretion by collectin duct cells

so less Na+ is excreted and more in conserved
what stimulates juxtaglomerular apparatus to release renin?
decrease in BP or blood vol.

decrease perfustion of baroreceptors
3 ways renin release from juxtaglomerular apparatus is stimulated
1. increase in symp outflow to kidny is decreased causing beta adrengeric stimulation of juxtaglomerular cells

2.decrease in GFR, decreases NaCl to macula densa of ascending limb of loop so increases renin secretion in juxtaglomerular apparatus bc macula densa signal jux. cell through prostaglandins

3. barorecptors in jux. cells in afferent arteriole of nephron produces singan for increased renin as vascular pressure falls
how does angiotensin II directly promote Na+ and water reabsorbtion?
by activating Na+/H+ exchanger in proximal tubule
so Na+ and Water are retained in the body
What causes ADH to be releasedd?
decrease in barorectors stimulation with reduction in BP and vol cause PP to release ADH
ADH function
increase permeabilty of collecting duct to water and water reabsorbtion will be increased
When Is ANP released?
with hi stretch to atria due to BP and vol increased
ANP functions
increases GFR by dialating afferent arteriole and constricting efferent arteriole

decreases renin secretion by juxtaglomerular cells so this will decrease aldosterone and reduce Na+ reabsorbtion

promotes Na+ excretion
amount of Ca in plasma
10 mg/dl 40% is bound to protein
where is most Extracellular Ca?
99% in bone
Ca functions
deposition and maintainance of bone

second messenger intracellular signaling
ionized Ca levels too low so get muscle spasms and bone reabsorbtion
inonized Ca levels too hi so get cardiac arrgythmias and reduced neuromuscular excitability
what does plasma Ca regulation depend on?
GI tract
endocrine systems
Ca in bone
most critical regulation of Ca in plasma
Parathyroid glands which makes PTH
When is PTH secreted?
when Ca plasma levels are low
What does PTH act on?
PTH effects on bone
stimulates osteoclast activity indirectly through actions on osteoblasts

bone reabsorbtion increases conc of plasma Ca
What does bone consist of?
collagon matrix which is mineralized and demineralized by osteocytes, osteoblasts, and osteoclasts
what other hormones increase bone reabsorbtion other than PTH?
cortisol and thyroid hormone
PTH effects on Ca absorbtion in GI
indirect effect PTH causes enzymatic conversion of Vit D to active form 1,25 OhD3 in proximal tubule of kidney

1,25 OHD3 promotes GI absorbtion of Ca and P
PTH effects on renal handling of Ca
only 1% of filtered Ca is excreted

the entire renal tubule reabsorbs Ca with 2/3 of Ca reabsorbed in proximal tube and 25% reabsorbed in loop of henle
How is Ca reabsorbed in kidney?
Ca enter kidney tube cell at luminal membrane by moving down electrochem gradient. Ca gets out of cell and into ISF by either Ca ATPase or by Ca/Na exchanger (one Ca out for 3 Na in cell)
PTH effect on kidney
increaes reabsorbtion of Ca in thick ascending limb of loop of henle and distal convoluted tubule.

It promotes excretion of Phosphate through actions on proximal tubule the suppress phosphate reabsorbtion
Where is calcitonin secreted?
by parafollicular cells of thyroid when plasma Ca conc is HI
calcitonin function
increases mineralization of bone by inhibitying osteoclasts
hormones that increase bone mineralization
calcitonin, insulin, GH, estrogen, testosterone
mineralization of bone matrix is decreased to point that bone easily fractures
ostoporosis risk factors
post menopausal
small frame
lo weight
low Ca intake
Treatment of osteoporosis
biphosphonates to kill osteoclasts



primary hyperparathyroidism
parathyroid tumor cause excessive PTH releae so increse bone reabsorbtion, incease Ca uptake by gut, and increase renal reabsorbtion of Ca. Cause hypercalcemia
main causes of hypocalcemia
primary cause is by removal of parathyroid glands

secondary cause by malabsorption of vit D by gut, kidney disease which reduces D3 conversion
what does mechanism to reabsorb filtered bicarbonate depend on?
conversion of CO2 and water wi tube cells into H+ and HCO3-

H+ is seceted into tube

H+ combines with HCO3- in tube to make CO2

CO2 returns to cell
How is HCO3- reabsorbed?
by contransport with Na+ or by exchange for Cl-
2 mechanisms to add new HCO3- to plasma and make net excretion of H+ by kidney
1. depends on H+ and HCO3- made in tube cells from intracellular CO2 after all HCO3- is reabsorbed. The H+ secreted into the tube combines with another anion like PO4- so the H+ is excreted. the HCO3- is reabsorbed (new bc made in cell)

2. glutamine is reabsorbed with Na into cell. Glutamine is broken down into ammonia and aKG. ammonia gets H+ to make ammonium which is secreted. HCO3- is reabsorbed (this is new)
How do kidneys maintian pH
H+ made as result of metabolism is excreted

HCO3- reabsorbed and made by kidney to raise pH

CO2 is eliminated by lungs