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Renal organ system
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Cortical andjuxtamedull
arynephrons
2
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Renal corpuscle
3
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Normal glomeruli
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The glomerular fltration barrier
1. Capillaryendothelium
2. Basementmembrane
3. pithelial layer
!. "iltration slits o#the podocytes
$
%
%
%
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Tubularcell
&nterstitial'uidTubul
ar
lumen
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(istribution o# body )2*
&ntracellular 'uid
xtracellular 'uid
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&ntracellular 'uid +&C",
&s 2-3 o# TB
The major cations o# &C" are /0 andg00
The major anions o# &C" are proteinand organic phosphates
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xtracellular 'uid
&s 1-3 o# TB
Composed o# interstitial 'uid andplasma
The major cation o# C" is Na0
The major anions are Cl and )C*3
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lasma
1-! o# C"
1-12 o# TB +1-! 4 1-3,
The major plasma proteins arealbumin and globulins
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&nterstitial 'uid
&s 3-! o# C"
is 1-! o# TB
&ts composition 5 plasma exceptthat has a little protein
&nterstitial 'uid is an ultrafltrate o#plasma
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$6!626 rule
TB is $67 o# body 8eight
&C" is !67 o# body 8eight
C" is 267 o# body 8eight
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easuring the 9olumes o# the 'uidcompartments
(ilution method: a /no8n amount o#substance is gi9en 8hose 9olume o#distribution is the body 'uid
compartment o# interest
1. Tritiated 8ater: mar/er #or TB
2. annitol; inulin: mar/ers #or C"
3. Radiolabeled albumin mar/er #orplasma 9olume
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xercise
< patient is injected 8ith =66 mg o#mannitol. uilibration period;the ?mannitol@ in plasma is 3.2 mg-166 mA.
(uring the e>uilibration period; 167 o# themannitol is excreted in urine. hat is thepatients C" 9olume
Dolume 5 amount-concentration 5
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Clearance
Dolume o# plasma cleared o# asubstance per unit time +mA-2! hrs,
C 5 FD- +mA-min or mA-2! hr,
here:
F 5 Frine concentration +mg-mA,
D 5 Frine 9olume-time +mA-min, 5 lasma concentration+mg-mA,
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xercise
plasma ?Na0@ is 1!6 m>-A; theurine ?Na0@ is G66 m>-A; and theurine 'o8 rate is 1 mA-min; 8hat is
the clearance o# Na0
CNa05 ?F@Na0 x D-?@Na0 5
G66 m>-A x 1 mA-min E 1!6 m>-A
5
= mA-min
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Clearance; reabsorption;secretion
Cx H I"R: net tubular reabsorption o#J
Cx K I"R: net tubular secretion o# J
C 5 I"R: no net secretion orreabsorption
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easurement o# I"R: clearance o# inulin
&nulin is #reely fltered
Not reabsorbed or secreted by renaltubules
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I"R calculation
I"R 5 Cinulin5 ?F@inulinx D-?@inulin+mA-min,
?F@inulin5 urine concentration o#inulin +mg-mA,
D 5 urine 'o8 rate +mA-min,
?@inulin5 plasma concentration o#inulin +mg-mA,
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xercise
&nulin is in#used in a patient to achie9e asteadystate plasma concentration o# 1 mg-mA.< urine sample collected during 1 hour has a9olume o# $6 mA and a inulin concentration o#126 mg-mA. hat is the patients I"R
I"R 5 ?F@inulin x D-?@inulin 5
126 mg-mA x $6 mA-hr E 1 mg-mA 5 126 mg-mA x 1 mA-min E 1 mg-mA 5 126
mA-min
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stimates o# I"R 8ith BFN
and serum ?creatinine@ Both BFN and serum ?creatinine@
increase 8hen I"R decreases
&n prerenal aLotemia BFN increasesK serum creatinine
&n prerenal aLotemia BFN-creatinine
ratio increases +K 26:1,
t # R"
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easurement o# R":clearance o# para
aminohippuric acid +
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R" calculation
R" 5 C
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easurement o# Renal blood 'o8+RB",
RB" 5 R"-1 %hematocrit
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"iltration #raction
&s the #raction o# RB" fltered acrossthe glomerular capillaries
"iltration #raction 5 I"R-RB"
Normally about 6.26 +267 o# the R"is fltered,
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&ncreases in the fltration#raction &ncrease the ?protein@ in the tubular
capillary blood
&ncrease reabsorption in the proximaltubule
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(ecreases in the fltration#raction (ecrease the ?protein@ o# peritubular
capillary blood
(ecrease reabsorption in theproximal tubule
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(etermining I"R: Otarling#orces
2P
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Changes in glomerulardynamics: I"R; RB"; ""
1. Constriction o#aMerent arteriole
2. Constriction o#
eMerent arteriole3. &ncreased plasma
?protein@
!. (ecreased plasma?protein@
=. Freteral obstruction
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Oummary o# changes in glomerulardynamics
Efect RFP GFR Filtrationraction
(FF)
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Tubuloglomerular #eedbac/
&ncreased renal arterial pressureleads to increased deli9ery o# 'uid tothe macula densa
The macula densa senses theincreased load and causesconstriction o# nearby aMerent
arteriole Resistance increases to maintain
constant blood 'o8
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Renal 9ascular disease
(ecrease renal blood 'o8
&ncrease the release o# renin
Renal artery fbromuscular dysplasia+hyperplasia,
Renal artery atherosclerosis
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"ree8ater clearance
&s used to estimate the ability toconcentrate or dilute the urine
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"ree 8ater
roduced in the diluting segment+thic/ ascending loop o# )enle, o# the/idney
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Calculation C)2*
C)2*5DC*O
here:
C)2* 5 #ree%8ater clearance+mA-min,
D 5 urine 'o8 rate +mA-min,
C*O
5 osmolar clearance+F*OD-*O, ?mA-min@
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xample
the urine 'o8 rate is 16 mA-min; urineosmolarity is 166 m*sm-A and plasmaosmolarity is 366 m*sm-A; 8hat is the #ree
8ater clearance
C)2* 5D % C*O
C)2* 5 16 mA-min % +C*O 5 166 m*sm-A J16 mA-min E 366 m*sm-A,
C)2* 5 16 mA-min % 3.33 mA-min 5 0$.G
mA-min
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C)2* and
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Reabsorption and secretionrates
"iltered load: I"R x x
xcretion rate: D x Fx
Reabsorption: fltered % excreted
Oecretion: excreted % fltered
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Ilucose clearance
Ilucose at a normal plasma le9el iscompletely reabsorbed in proximaltubule
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Reninagiotensinaldosteronesystem
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Renin
Otimuli #or release
1. (ecreased blood pressure in SI cells
2. (ecreased Na0 deli9ery to maculadensa cells
3. &ncreased sympathetic tone +1receptors,
. "unction
Con9ert angiotensinogen intoangiotensin
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1
1 1
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echanism o# aldosterone
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echanism o# action o#
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rythropoietin
Released in response to hypoxia#rom endothelial cells o# peritubularcapillaries
&ncreases erythropoiesis
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rostaglandins
aracrine secretion 9asodilatesaMerent arterioles to increase I"R
&n9ol9ed in
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V0 shi#ts out o# cells: hyper/alemia
&nsulin defciency: Q Na0-V0
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V0 shi#ts into cells:hypo/alemia
&nsulin: Na0-V0
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Renal )0 handling; acid basephysiology
xcretion o# )0 as titratable
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xcretion o# )0 as titratableacid
(epends on the amount o# urinarybuMer present +)2*!,
&n urine the )0 combines 8ith
fltered )*!W to #orm )2*!
)2*! is excreted as titratable acid
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xcretion o# )0 as N)!0
The amount o# )0 excreted as N)!0depends on:
1.The amount o# N)3 produced by renal
cells2. Frine p)
. )0 excretion as N)!0 increases as the
p) o# tubular 'uid decreases.
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)0 excretion as N)!0
$6
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Oerum anion gap
?Na0@ % +?Cl@ 0 ?)C*3@,
Normal range is X1$ m>-A
Represents unmeasured anions inserum
1. hosphate
2. Citrate
3. Oul#ate
!. rotein
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Normal anion gap alteration
hen the ?Cl@ is increased to replace)C*3
&ncreased anion gap
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&ncreased anion gapalteration
hen the ?@ o# an unmeasured anionis increased to replace )C*3
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etabolic acidosis
&ncreased ?)0@
(ue to o9erproduction or ingestion o#a fxed acid or loss o# base
)C*3 decreases as it is used as abuMer
"eatures o# metabolic
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"eatures o# metabolicacidosis
)C*3: decreased
C*2: decreased
?)0@: increased
Causes o# normal anion gap
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Causes o# normal anion gapmetabolic acidosis
(iarrhea ; glue sniYng
Type & +distal, renal tubular acidosis
1. (e#ect in collecting tubules ability to excrete )0
2. )ypo/alemia; ris/ #or Ca00 /idney stones.Type && +proximal, renal tubular acidosis
1. (e#ect in proximal tubule )C*3 reabsorption
2. )ypo/alemia; hypophosphatemic ric/ets
.Type &D +hyper/alemic, renal tubular acidosis
1. )ypoaldosteronism-lac/ o# response toaldosterone
2. )yper/alemia;QN)! excretion in proximal tubule
Causes o# high anion gap metabolic
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Causes o# high anion gap metabolicacidosis
Vetoacidosis
Aactic acidosis
Chronic renal #ailure +uremia,
Oalicylate intoxication
ethanol-#ormaldehyde intoxication
thylene glycol intoxication &ron tablets; &N)
Compensation #or metabolic
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Compensation #or metabolicacidosis
)yper9entilation
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etabolic al/alosis
(ecreased arterial )0
(ue to loss o# fxed )0 or gain o#base
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"eatures o# metabolical/alosis
)C*3: increased
C*2: &ncreased
)0: decreased
Causes o# metabolic
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Causes o# metabolical/alosis
Domiting
)yperaldosteronism
Aoop and thiaLide diuretics
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Compensation #or metabolical/alosis
)ypo9entilation
Opecial situation: 9olume contraction
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Opecial situation: 9olume contractionmetabolic al/alosis
The reninangiotensin &&aldosteronesystem acti9ates
The reabsorption o# )C*3 increases
The metabolic al/alosis 8orsens
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Respiratory acidosis
Caused by a decrease in respiratoryrate and retention o# C*2
C*2increases
)0 and )C*3 &ncrease
Causes o# respiratory
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Causes o# respiratoryacidosis
Oedati9ehypnotics; generalanesthetics
Neurologic diseases +IBO;
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Compensation #or respiratoryacidosis
&ncreased excretion o# )2*! andN)!0
&ncreased reabsorption o# ne8 )C*3
&ncreased C*2supplies more )0 tothe renal cells #or secretion
&ncreased )C*3 normaliLes p)
i l/ l i
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Respiratory al/alosis
Caused by an increased respiratory rate
(ecreased C*2results in a decrease in)0 and )C*3
"eatures:1. C*2: decreased
2. )0: decreased
3. )C*3: decreased!. )ypocalcemia
Causes o# respiratory
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Causes o# respiratoryal/alosis
neumonia and pulmonary embolus
)igh altitude
sychogenic
Oalicylate intoxication
Compensation #or respiratory
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Compensation #or respiratoryal/alosis
(ecreased excretion o# )2*! andN)!0
(ecreased C*2causes a defcit o#
)0 in the renal cells #or secretion (ecreased reabsorption o# ne8 )C*3
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C t i i
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Casts in urine
&ndicate renal disease
RBC t
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RBC casts
Ilomerulonephritis
&schemia
alignant hypertension
hit bl d ll t
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hite blood cell casts
Tubulointerstitial in'ammation
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Iranular casts
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axy casts
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)yaline casts
Non specifc
" tt t
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"atty casts
Nephrotic syndrome
Ilomerular disorders
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Ilomerular disorders
Nephrotic syndrome
Nephritic syndrome
Rapidly progressi9e
glomerulonephritis
Normal glomerulus
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Normal glomerulus
Nephritic syndrome
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Nephritic syndrome
&n'ammatory process hen it in9ol9es glomeruli:
Aeads to hematuria and RBCs casts in
urine
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p pglomerulonephritis
ost #re>uently seen in children eripheral and periorbital edema
Resol9es spontaneously
Aight microscope:1. nlarged; hypercellular glomeruli 8ith
neutrophils
2. Zlumpybumpy[ appearance
. lectron microscope: subepithelial immunecomplexes; humps
. &mmuno'uorescence: granular pattern
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pithelial
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pimmunocomplexes
Iranular appearance on
7/25/2019 Renal Organ System
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ppimmuno'uorescence +&",
Rapidly progressi9e +crescentic,
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p y p gglomerulonephritis
oor prognosis tiology:
1. Ioodpasture syndrome: linear &"
2. egener granulomatosis: c
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p ypIoodpastures syndrome
Crescent proli#eration
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Crescent proli#eration
Crescent appearance on &"
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Crescent appearance on &"
(iMuse proli#erati9e
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glomerulonephritis
tiology:1. Aupus +CC o# death,
2. embranous proli#erati9e glomerulonephritis
3. Can present as nephrotic syndrome. icroscopy:
1. Oubendothelial (N
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deposits
Bergers disease +&g
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glomerulonephropahty,
*#ten presents 8ith a FR& or acutegastroenteritis
&ncreased synthesis o# &gue stones
Tx: al/aliniLation o# urine
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/idney disease
ultiple; large; bilateral cysts destroyingparenchyma
nlarged /idneys
utation in
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/idney disease
&n#antile presentation in parenchyma uence
)ypertension; portal hypertension;
progressi9e renal insuYciency
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Renal cell carcinoma
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Renal cell carcinoma
C renal malignancy &n9ades &DC and spreads 9ia the blood
etastasiLes to lung and bone
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Clinical #eatures
)ematuria alpable mass
Oecondary polycythemia
"lan/ pain "e9er; 8eight loss
reneoplastic syndromes:
1. ctopic erythropoietin
2. ctopic
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a s o a ce ca c o a
C tumor o# urinary tract system ainless hematuria suggests bladder
cancer
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C renal malignancy o# early childhood )uge palpable 'an/ mass and hematuria
ay be associated 8ith hemihypertrophy
syndromes +Bec/8ithiedemannsyndrome,
mbryonic glomerular structures
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py p
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py p
Coarse; asymmetric corticomedullaryscarring
Blunted calyx
Tubules can contain eosinophiliccasts +thyroidiLation,
(ruginduced interstitialnephritis
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nephritis
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CC o# acute renal #ailure in hospital Oel#re9ersible but #atal i# le#t untreated
Cause: ischemia; myoglobinuria +crush injury,;toxins
hases: initiating e9ent; maintenance +lo8 urine,;reco9ery +23 8ee/s,
(eath C occurs during initial oliguric phase
athology:
1. Aoss o# cell polarity
2. pithelial cell detachment
3. Necrosis
! Iranular casts
Renal papillary necrosis
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p p y
Oloughing o# renal papillae Iross hematuria; proteinuria
ay be triggered by recent in#ection or
immune stimulus tiology:
1. (
2.
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Nephrosclerosis
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p
C renal disease in essentialhypertension
)yaline arteriolosclerosis o# cortical
arterioles Tubular atrophy; interstitial fbrosis;
glomerular sclerosis
Omall /idneys 8ith a fnely granularcortical sur#ace
Aab: proteinuria; hematuria +no
casts, aLotemia
Renal in#arction
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Causes: emboli #rom le#t heartthrombi; atheroembolic renaldisease; 9asculitis
&rregular; 8edgeshaped palein#arctions in cortex
Oudden onset o# 'an/ pain and
hematuria
(iMuse cortical necrosis
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Complication o# obstetricemergencies and septic shoc/
(ue to (&C limited to renal cortex 0
9asospasm "ibrin clots in arterioles and
glomeruli
Bilateral; diMuse; pale in#arct o# renalcortex
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y
(ecreased proximal tubule transporto# amino acids; glucose; phosphate;uric acid
Can be congenital or ac>uired tiology:
1. ilsons disease
2. Ilycogen storage diseases3. Cisplatin; expired tetracycline
"eatures o# "anconissyndrome
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syndrome (ecreased phosphate reabsorption:
ric/ets
(ecreased bicarbonate reabsorption:
metabolic acidosis; type && RT< (ecreased early Na0 reabsorption:
increased distal Na0 reabsorption;
hypo/alemia
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(ecreased RB" leads to decreased I"R Na; )2* and urea are retained by /idney
BFN-creatinine ratio increases to
conser9e 9olume Frine osmolarity K =66
Frine Na0 H 16
"eNa0H 17 Oerum BFN-Cr K 26
&ntrinsic renal aLotemia
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(ue to acute tubular necrosis; ischemia; toxins Aess commonly due to glomerulonephritis
atchy necrosis leads to debris
(ebris obstruct tubules and there is 'uid bac/'o8
across necrotic tubules I"R decreases; BFN reabsorption is impaired
BFN-creatinine ratio decreases
Frine has epithelial-granular casts
Frine osmolarity H 3=6 Frine Na0 K 26
"eNa0: K 27
Oerum BFN-Cr H 1=
ostrenal aLotemia
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*ut'o8 obstruction: stones; B);neoplasia; congenital anomalies
(e9elops only 8ith bilateral
obstruction Frine osmolarity H 3=6
Frine Na0 K !6
"eNa0 K !7 Oerum BFN-Cr K 1=
Conse>uences o# renal#ailure
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#ailure &nability to ma/e urine and excrete
nitrogenous 8astes
Na0 and )2* retention: hypertension;pulmonary edema; C)"
)yper/alemia etabolic acidosis
Fremia
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&ncreased BFN and creatinine Nausea and anorexia
ericarditis
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lectrolyte disturbances
Na0
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Ao8: disorientation; stupor; coma )igh: irritability; delirium; coma
Cl
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Ao8: 2dary to metabolic al/alosis;hypo/alemia; hyperaldosteronism
)igh: 2dary to nonanion gap
acidosis
V0
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Ao8: F 8a9es on CI; 'attened T8a9es; arrhythmias; paralysis
)igh: pea/ed T 8a9es; 8ide ]RO;
arrhythmias
Ca00
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Ao8: tetany; neuromuscularirritability
)igh: delirium; renal stones;
abdominal pain
g00
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Ao8: neuromuscular irritability;arrhythmias
)igh: delirium; hyporre'exia;
cardiopulmonary arrest
hosphate
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Ao8: bone loss; osteomalacia )igh: renal stones; metastatic
calcifcation
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(iuretics
annitol
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*smotic diuretic &ncreases tubular 'uid osmolarity; increasing
urine 'o8
Fses: drug o9erdose; shoc/;
intracranial-intraocular hypertension;rhabdomyolysis
Toxicity:
1. Aung edema2. (ehydration
3. C& in anuria and C)"
Carbonic anhydraseinhibitors
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inhibitors
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Oite o# action: thic/ ascending limb o#loop o# )enle
echanism: inhibition o# Na0; V0;
2Cl symport ajor eMects:
1. &ncrease Na0; Cl; V0 and Ca00
excretion2. &mpair ability to concentrate urine
3. &mpair ability to dilute urine
"urosemide
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Oul#onamide loop diuretic &ncreases Ca00 excretion
Fses: edematous states; hypertension;hypercalcemia
Toxicity:1. *totoxicity
2. )ypo/alemia; hypocalcemia; hypomagnesemia
3. (ehydration
!. Oul#a allergy
=. &nterstitial nephritis
$. )yperuricemia; gout
thacrynic acid
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ssentially same action as#urosemide
Not a sul#a drug
Fse: diuresis in patients allergic tosul#a drugs
Toxicity:
1. Oimilar to #urosemide2. (oesnt cause hyperuricemia
ThiaLide diuretics
7/25/2019 Renal Organ System
158/161
Oite o# action: early distal tubule echanism: inhibition o# Na0 % Cl
symport
ajor eMects:1. &ncrease Na0; Cl; V0 excretion
2. (ecrease Ca00 excretion
3. &mpair ability to dilute urine +not ?@,
)ydrochlorothiaLide
7/25/2019 Renal Organ System
159/161
Fses: hypertension; C)"; idiopathichypercalciuria; nephrogenic diabetesinsipidus
Toxicity:
1. )ypo/alemic metabolic al/alosis
2. )yponatremia
3. )yperglycemia
!. )yperlipidemia +gi9e indapamide,=. )yperuricemia
$. )ypercalcemia
G Oul#a allergy
V0 sparing diuretics
7/25/2019 Renal Organ System
160/161
Oite o# action: late distal tubule and collectingduct
echanism:
1. Triamterene; amiloride; eplerenone: inhibition
o# Na0 reabsorption and V0 secretion in CCT2. Opironolactone: aldosterone antagonist in CCT
. ajor eMects:
1. &ncrease Na0 excretion
2. (ecrease V0 excretion
3. (ecrease )0 excretion
Fses and toxicity o# V0 sparingdiuretics
7/25/2019 Renal Organ System
161/161
Fses: hyperaldosteronism; V0depletion; C)"
Toxicity:
1. )yper/alemia2.