“Mapping

the Nephron”

Cellular Templates

9/26/19

Clinical Small Group #: 9

Group Members: Gina Brock Christina Bartoni Lana Amerie Bryce

Perry Nicholas Scapini John

Beale QamarKhan

Daniel Shin


PCT
Lumen urine Interstitium blood

SGLTZ basolateral
Normal Physiology:
apical Nat

3Nat

CT

Proximal Tubule Gue

catikfvajeouTA.t.cl o
Nat ATP
2kt
brushborder urea NHE3
Contains

AngTt fat 1
Reabsorbs all glucose A A t Ht HCOs

Heo Ht 0
most

1h05Nat Cr Pop Kt Witt Ht
wits Nat

H2O uric acid

Haq CA Azcoz uneaI

CO2 H2O CAT Guest phosphatecitrate
isotonic

absorphois CT Lactate
Generates

t secretes NHz O_ coat A At
H 2O

which 4 Htsecretor's Base
PTH

inhibits Natypoy3cotranstransport 94043excreta's PTIstraight

stimulates NatlHtexchange 9NotHz0 t Haz

AngI

secretionto c
resorption

contractors alkalosis PAH reabsorption

458070Nat reabsorbed oforganic

Highlypermeable towater acidslbases

includinguric

Clinical Small Group #:

9 acid must
diuretics t PAH


Proximal Tubule +

diuretic

Diuretic(s) with activity at this site: i
i e y

Inhibition of carbonicanhydrasede intracellular n

It

Haz Ht f nitz

d
basolateralNAHH
Htt
cos symporter t apical
Natankporteractivity
9 1

urinary NatlHaz
in Acetazola
water

follows solutes opp cannotbe

q delivery of solutes to macula densa Mannitolglycerin reabsorded

9 TG feedback 9 afferent arterior filteredfreely

resistance RBF Gfr abodyvolume

Hyperchlonemic metabolicacidosis big osmotic

Muricemia because it competesNHS c uric acidsecretor pressure

9encephalopathy hypernatremia

Alkaline urine turns Mtytinto

Ktwastingdue to 9 Notpresented in collectingduct
hyperkalemia
postdiuresis

9
Clinical Small Group #:

Lumen urine Interstitium bloo

apical
Normal Physiology:
basolateral

Natt CNkor 3Nat

Thick Ascending Limb 0

let
24
OATP
2kt

Resorbs Nat Kt CT
t

cellularresorption t
Indirectly la para 1

of
Mg2t t cart via lumen potential
co 2 kt

Kt backleak
trunk

generated by ftp.D kt t

Impermeable to H2O t

Cl
Makes urine less concentrated as

it ascends mgst

to 20 Natreabsorbed

9
Clinical Small Group #:


Thick Ascending Limb apical basolateral

+ Diuretic Meck

Blockade
Diuretic(s) with activity at this site:

of NKC.cz
1
Furosemide
Torsemide

d reabsorption of Nat c Bumetanide

Trans

epithelialvoltage d Ethacrynic
Romy

acid
paracellularresorpbo's 4h20

ofmg2t Carty

can mimic Barter syndrome

4COX Z T PGE2 Tdilation of X

afferentarteriole AGFR
alkalosis

Hypokalemia metabolic

A Natdelivery to collecting ducts 9

secretion

of Kt Ht in collectingducts

Hyponatremia Hyperuricemia Hypercalcemia hypomagnesemia

Clinical Small Group #:

9

men urine cos Interstitiumblood

Normal Physiology: apical

04 basolateral

Distal Convoluted 9 NatNCC

I CT
3
AtP

Tubule e
2kt

EE
Reabsorbs Nat Cl to Get

Impermeable to H2O
EYE f Nat

Makes urine fully dilute hypotonic cast

caztonca

t.PH
9Cat1Nut exchange a cartreabsorption MO Ht

S 10 Notreabsorbed t a
Ki

e
mga is absorbed by unknown mechanism Mg e

0mV
10mV

Clinical Small Group #:

Distal Convoluted Tubule

+ Diuretic Hotz
Chlorothiazide
Chlorthalidone

Diuretic(s) with activity at this site:
hlorthalidone

retainssignificant CA
activity

intracellular Natdrives basolateral

Naticaltexchanger

Rarely coursehypercalcemia butmay

unmasked previous hypercalcemia condition ft

unknown

Tresorphin Mgk

4 absorption
of calcium to risk of osteoporotic fxs

Nephvolithiasis due to idiopathic hypercalcemia

i
Hypokalemia metabolic alkalosis

hyperglycemia offtargeteffects B cells

Hyponatremia hyperuricemia

Ityperlipidemed
Clinical Small Group #:

9

Lumenunine a intercalated Interslium blood

apical Nat basolateral

Normal Physiology: µzO_atp

Cortical Collecting Duct AP
Ht I

Aldosterone T Htatpase activity I
go ite

THTsecretion 9 1

HozICI exchanger In let 1 Has

U TOAD L 0
exchange for

Reabsorbs Natin

E
E Ift a

secreting Kt 2 Ht regulated by

aldosterone
Kt 2

t

Reasorb Kt F E
8
a

Hz Poy t NHytexcretion

Hoop Ht
ATP

It

11
Koz 203

Clinical Small Group #: Bintercalated

9


Cortical Collecting

Duct + Diuretic A

Diuretic(s) with activity at this site:

17

kt searing diuretics antagonize effects of spironolactone

adolstenone in collectingduct 1 Aldactone

u n l

Htsecretor hyperchloremic
metabolic

acidosis

Hyperkalemia

Spironolactone gynecomastomia

Clinical Small Group #:

9

principal cell
Lumenurine interstitiumblood

Normal Physiology: apical basolateral

Medullary Collecting H2O o V2

1 o ES c

Duct Aqua
pains

SecreteKt Kt

CF 3nat
Addaquaponins
Topical Kt conductance
O atp
Aldosterone
ENaC 1
I
Nat1kt pump 9 epithelia watchannel
i
µ
t m
ENac activity mRNAsyn from aldosterone
A
Ktsecretion a
ADH acts at Uz receptor insertion
of aguaporin H2O channels on apical
side
3 5 Nat reabsorbed secretion
Ktexcreted Cl absorbed drivels Ht
Clinical Small Group #:
9
ADH 9H2O reabsorption
 Medullary Collecting
Duct + Diuretic
Diuretic(s) with activity at this site: discussed
later
4 sparing ANP
Amioride
Amiluride blocks ENac inhibiting triatnteremT
transepithelial potential
fitt secretion intercalatedcells i
q Spironalac
typerchloremic metabolic Acidosis Aldactone
Amiloride mimics Liddlesyndrome
4 Nat reabsorption

Clinical Small Group #:

9