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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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