(slide tahun lalu)pkd gus
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Policystic Kidney DiseasesAcute Tubular Necrosis
( ATN )
Tubulo Interstitial Nephritis
Lecture : Genito-urinary system.
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Kidney Disorders
CONGENITAL
C!TIC
GLO"E#$LA#
T$%$LE!&INTE#!TITI$"
%LOOD 'E!!EL!
O%!T#$CTION
T$"O#!
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Cystic #enal Dysplasia
AutosoalDoinant (Adult)
Polycystic Autosoal#ecessi*e (Childhood)
Polycystic
#enal "edulla Cystic Diseases Ac+uired (Dialysis) Cystic Disease
,!iple- Cysts
#enal cysts
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Autosomal-Dominant (Adult) Polycystic
ADPKD
Autosomal dominant polycystic kidney disease
( adult polycystic disease )
Autosomal dominant inheritance
PKD-1 gene disorder inchromosom 1!"echanism o# cysts #ormation unclear
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Grossly: huge kidneys (1-$ kg)! cysts up to %& mm
"icro : cysts #rom all parts o# nephron (#lat
epithelium)! atrophy o# renal parenchyma
'linical course: %thdecade! #lank pain!
hypertension! hematuria! renal #ailure (end stage
kidney) intracystic leeding! in#lammation! tumorAccompanied y lier * pancreatic cysts!
aneurysms o# cereral arteries!
Autosomal-Dominant (Adult) Polycystic
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Grossly: large kidneys (ilateral)
ith multiple tiny cysts (1- mm) - huge adomen!pulmonary hypoplasia! oligohydramnion
/istology: elongated cysts #rom collecting tuules
'linical course: stillorn or die ery soon
(pulmonary or renal #ailure)ho surie in#ancy - disordered concentration
aility! uremia! congenital hepatic #irosis!
Autosomal-Resessive Polycystic
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Polycystic Kidney Diseases
ARPKD Kidney
AutosomalRecessive PKD
ARPKD
Infantile Polycystic Disease
0ephromegaly
Pulmonary hypoplasia
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Polycystic Kidney Disease Slowly progressive irreversible
replacement of normal kidney tissue with
multiple grape-like cysts. S&S-Lumbar pain hematuria infections
calculi hypertension dilated palpablekidneys upon physical e!am.
"tiology-inherited but isn#t seen untiladolescence or adulthood. $an be acomplication of kidney disease or dialysis.
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Polycystic Kidney Disease D!-clinical %ndings renal function
tests !-rays 'P.
(!-cannot be cured dialysis and
kidney transplant.
Prognosis no cure
Prevention either inherited orac)uired cannot be prevented
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*"+,L "DLL,
$/S($ DS",S"S
"edullary !pon.e Kidney ("!K)
Nephrolithiasis"edullary CysticDisease
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Medullary Sponge Kidney (MSK)
Small cystic dilatation involving the
medullary colecting ductsongenital ectasia of distal collecting
tu!ules"
Its pathogenesis is not clear
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AC/$I#ED #ENAL C!TIC
DI!EA!E
#he development of cysts in the patients $ith
long standing chronic R% or maintenancedialysis"
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SIMP&' S#S
#he prevalence increases $ith age in general
population
"* + of those aged more than ,
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Acute #u!ular .ecrosis ( A#. )
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#/0/&AR1I.#'RS#I#IA& DIS'AS'S
Acute #u!ular .ecrosis (A#.) #u!ulointerstitial .ephritis
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$auses of ,*0 in 1ospitali2ed
Patients012 ATN
schemia +ephroto!ins
345 Prerenal$10 volume depletion
sepsis
465 rinary obstruction
75 8lomerulonephritis or vasculitis
32 Acute Interstitial Nephritis
45 ,theroemboli
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A/#' #/0/&AR .'R2SIS ( A#. )
Pathogenesis
Morphology linical ourse
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Acute Tubuler Necrosis(ATN) is an abruptDecrease of GFR caused
By tubular damage from:-renal hypoperfusion-nephrotoic in!ury-Tubulointerstitial nephritis
Rapidly re"ersible decrease#n GFR caused by renal$ypoperfusion%
&auses ' of ARF
Rapidly re"ersible decrease#n GFR caused by obstructi#n renal or *retero+uretheral+"esico urinary
(,B-TR*&T#./ *R,0AT$1)
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auses of acute Renal %ailure
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auses of AR% in a 3ospital Setting
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Intrinsic A4oteia
Acute tubular necrosis schemia9 as for prerenal a2otemia obstetrical
complication :abruptio plancentae postpartum
hemorrhage;
+ephroto!ic damage9 contrast media antibiotics :e.g.aminoglycosides amphotericin
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IntrinsicA4oteia
nterstitial nephritis ,llergic9 antibiotics :e.g. beta-lactams
sulfonamides trimethoprime rifampicin; $ycloo!ygenase inhibitors diuretics captopril
nfection9 bacterial :e.g. acute pyelonephritisleptospirosis; viral :e.g. $'; fungal
n%ltration9 lymphoma leukemia sarcoidosis
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#/0/&2I.#'RS#I#IA&
.'P3RI#IS
Pyelonephritis
Reflu4 .ephropathy Drugs1#o4ins
/rate .ephropathy
.ephrocalcinosis
Multiple Myeloma
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PELONEP5#ITI!
AC$TE
C5#ONIC #E6L$7 NEP5#OPAT5
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DR/5S1#26I.S
Anal.esic Nephropathy
N!AID! Others
Chinese 5erbs Nephropathy
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Symptoms and Signs of Renal %ailure
*etention of potassium >eakness lassitude paralysis "K8
changes with tenting ( waves wideningof
?*S comple! increased P* interval sinewave pattern cardiac arrest '(
*etention of acid Kussmaul respiration hyperre@e!ia
hypotension
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"ana.eent
Prevention
"tiology treatment
Prevention additional inAury
"stablish diuresis
(reatment of complication $onservative measurement
*enal replacement therapy
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Pre*ention
denti%cation of high-risk patients for
pharmacologic agents-induced nephroto!icity iodinated radiocontrast medium +S,Ds
,ggressive surveillance for nephroto!in-inducedrenal dysfunction
cisplatin amphotericin
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'sta!lish Diuresis
'olume e!pansionBhydration
Csmotic diuretics and loop diuretics9mannitol furosemide
*enal vasodilators9 dopamine :4-3ugBkgBmin; atrial natriuretic peptid
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onservative Measurement
0luid balance $areful monitoring of BC and body weight
0luid restriction :usually less than 4 LBday in oliguric ,*0; (otal intake urine output Ee!trarenal losses
"lectrolytes and acid -base balance hyperkalemia hyponatremia Keep serum bicarbonate F4G hyperphosphatemia (reat hypocalcemia only if symptomatic
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Dietary
modi%cation total caloric intakeH IGJ G6
kcalBkgBday
to avoid catabolism
Salt restrictionH 3J7 gBday
Potassium intakeH 76 me)Bday
Phosphorus intakeH 66 mgBday
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remia-nutrition *estriction protein but maintain caloric
intake $arbohydrate 466gmBdayto minimi2e
ketosis and protein catabolism
Drug *eview all medication Stop
magnesium-containing medication ,dAusted dosage for renal failure
*eadAust with improvement of 80*
onservative Measurement
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