NEPHROLOGI
NEPHROLOGIPWM Olly Indrajani
12-6-2012Nephrologi Batasan: ilmu yg mempelajari fungsi dan
patofisiologi ginjal dan saluran2 penunjangnya serta
penyakit2nya.Dasar2 yg perlu:1. Anatomi & histologi2. Fisiologi
& biokimia3. Patologi & laborat. 2Introduction:150gm: each
kidney1700 liters of blood filtered 180 L of G. filtrate 1.5 L of
urine / day.Kidney is a retro-peritoneal organBlood supply: Renal
Artery & VeinOne half of kidney is sufficient reservekidney
function: Filtration, Excretion, Secretion, Hormone
synthesis.STRUCTURE OF THE KIDNEYS
Kidney Anatomy:
STRUCTURE OF THE KIDNEYS
Kidney Anatomy:
8IntroductionFunctions of the kidney:excretion of waste
productsregulation of water/saltmaintenance of acid/base
balancesecretion of hormonesDiseases of the
kidneyglomerulitubulesinterstitiumvessels9Renal Pathology
OutlineGlomerular diseases: GlomerulonephritisTubular diseases:
Acute tubular necrosis Interstitial diseases:
PyelonephritisDiseases involving blood vessels:
NephrosclerosisCystic diseasesTumors10Pendekatan
klinis:AnamnesisPemeriksaan fisikLaboratoriumPem. Penunjang: a.
radiologis: - BOF - IVP - CT Scan - MRIb. biopsi
ginjal.1112Anamnesis: 1. Keluhan utama:a.
dysuria,polyuri,polakisuri,b. edemac. nyerid. penurunan fungsi
ginjale. hematuria 2. Penyakit terdahulu 3. Anamnesa
keluarga.Pemeriksaan fisik:inspeksiauskultasiperkusi
palpasi13Pem.laboratorium:1.Urinalisis: - pH, BJ, warna - albumin -
reduksi - bilirubin/urobilin - sedimen: eri,leko, kristal,silinder
epitel.2. Kimia darah: kreatinin plasma klirens kreatinin
konsentrasi ureum plasma.14 Azotemia: BUN, creatinine Uremia:
azotemia + more problems Acute renal failure: oliguria Chronic
renal failure: prolonged uremia
Abnormal findings15Clinical Syndromes:Nephritic
syndrome.Oliguria, Haematuria, Proteinuria, Oedema.Nephrotic
syndrome.Gross proteinuria, hyperlipidemia, Acute renal failure
Oliguria, loss of Kidney function - within weeksChronic renal
failure.Over months and years - Uremia Hematuria Oliguria Azotemia
HypertensionNephritic syndrome Massive proteinuria Hypoalbuminemia
Edema Hyperlipidemia/-uriaNephrotic syndrome17
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What are the possible causes of this appearance of the
kidneys?
22Glomerulopathy Proses inflamasi glomerulusTerjadi akibat
berbagai sebab yg berbeda etiologi, patofisiologi ataupun
patogenesanyaDulu dikenal dg istilah glomerulonephritisPeyebab
utama Gagal GinjalManifestasi klinis bisa tanpa gejala sampai
gejala yang berat Terpenting:menghambat progresifitas kerusakan
23Klasifikasi glomerulopathyKlasifikasi klinisKlasifikasi lesi
histopatologi Klasifikasi berdasar
etiologi&patogenesisKlasifikasi berdasar proses
imunologi24Klasifikasi klinis:Kelainan urine tanpa keluhanSindroma
nefrotikSindroma nefritik akutSindroma nefritik kronikSindroma RPGN
(Rapid Progressive Glomerulonephritis)
25Klasifikasi lesi histopatologisLesi minimalLesi
glomerulosklerosis fokal segmentalLesi mesangioproliferatif
(IgM)Lesi mesangioproliferatif (IgA) (penyakit Berger)Lesi
proliferatif akutLesi membranoproliferatifLesi membranosaLesi bulan
sabit (crescentic)Lesi glomerulosklerosis.26Klasif. Etiologi&
patogenesaKelainan imunologiKelainan metabolik:- nefropati
diabettik- nefropati as. Urat- amiloidosis primer/sekunderKelainan
vaskulerDisseminated Intravascular Coagulopathy (DIC)Kel.
Herediter: sindr.Alport, peny.FabryPatogenesis tak diketahui:
lipoid nefrosis27Klasifikasi. imunologiPeny. Kompleks immun:1.
Circulating immune complex:Nephropathy BergerHenoch-Schonlein
PurpuraNefritis Lohlein (endokar.bakteri)2. Pembentukan komplek
imun insitu:Glom. Post Streptococcus infectionGlom. Membranosa
b.Peny.AGBM: sindroma Goodpasteur.
28
Minimal change disease29Minimal change disease
Normal glumerular structure30
Normal glomerulus
Minimal change disease31Focal Segmental
GlomerulosclerosisPrimary or secondarySome (focal) glomeruli show
partial (segmental) hyalinizationUnknown pathogenesisPoor
prognosis32
Focal segmental glomerulosclerosis33Membranous
GlomerulonephritisAutoimmune reaction against unknown renal
antigenImmune complexesThickened GBMSubepithelial deposits34
Membranous glomerulonephritis
35
Post-infectious glomerulonephritis
36IgA NephropathyCommon!Child with hematuria after (URI) Upper
Respiratory Infection IgA in mesangiumVariable prognosis37
IgA nephropathy38Sindroma nefrotikBatasan: sindroma klinik
ok.berbagai penyakit yg ditandai dg meningkatnya perm.membran basal
glomerulus thd protein dg.G/ utama proteinuri > 3,5 gram/24
jam.
Patofisiologi:meningkatnya perm.GBM proteinuriBila loss
albumin> produksihipoalbuminemiHipoalbumin edema
anasarkaHiperlipidemia : patogenesanya belum jelasGgn.
Metab.lemaklipiduria: oval Fat Bodies 39Etiologi:Glomerulopati
primerGlomerulopati sekunder:a. infeksi: sifilis, malaria, TBC,
tifus,virusb. nefrotoksin: diuretik merkuri, bismuth, preparat
emasc. allergen: sengatan lebah, gigitan ular, tepung sari.d.
peny.kolagen: SLE, PAN,dermatomiositis, peny.Goodpastur, giant cell
arteritis.e. peny.lain: Hodgkin, mieloma, leukemi, DM,
feokromositoma, miksedema, gagal jantung kongestif, SBE,
perikarditis konstriktif, amiloidosis, trombosis vena renalis,
obstruksi vena cava inferior. 40Nephrotic SyndromeMassive
proteinuriaHypoalbuminemiaEdemaHyperlipidemiaLipiduria41Gejala
klinis:kencing berbuihSembab tungkai yg progresif s/d anasarkaSesak
nafas (bila ada cairan pleura)Sebah dan perut buncit (bila ada
asites)42Pemeriksaan & diagnosis1.urinalisis: - proteinuri +3
+4, lipiduria - torak eritrosit: khas utk SN prim - glukosuri: bila
ok DM.2.ekskresi protein 24 jam (Esbach)3.kadar albumin serum4.
Elektroforesa protein serum & protein urin5.kadar lipid
plasma6.tes imunologi7.pem.radiologi: BOF, IVP, foto thorax8.
Biopsi ginjal.43Diagnosis banding:Penyakit dg edema dan
hipoalbuminemi lain:Penyakit hati kronisMalnutrisiGagal
jantung44Penatalaksanaan Diet TKTP rendah garam.Obat: a. diuretikb.
antiagregasi platelet: dipiridamolc. infus albumind.
kortikosteroid:prednison 2mg/kg/hr 4 minggu lalu tapering offe.
imunosupresif: siklofosfamid 2 mg/ kg/hr atau klorambusil 0,2
mg/kg/hr selama 8 minggu.3. Koreksi penyakit primernya
45Komplikasi:Kelainan kardiovaskuler (atherosclerosis)Shock
hipovolemiMudah terserang infeksiGagal ginjal kronik.
46UTI
Identify the pathophysiology and clinical manifestations of
urinary tract infections.UTI (Cystitis):Evaluation:History and
physical examination includes queries about risk factors; s/s such
as pain, odor, hematuria, vital signs, temperature, U/A,
culture.Treatment:Antimicrobial therapy, pain medication.
Identify the pathophysiology and clinical manifestations of
urinary tract infections.Pyelonephritis:An infection of the renal
pelvis and interstitium. Causes include: kidney stones, reflux,
pregnancy, neurogenic bladder, instrumentation, female sexual
trauma.Pathophysiology: Can be spread by ascending microorganisms
along the ureters or blood borne pathogens. Inflammation affecting
the pelvis, calyces, medulla. Signs/Symptoms: Fever, chills, flank
or groin pain, frequency, dysuria. Evaluation: Urine culture, U/A,
clinical s/s, radiologic evaluation. Treatment: Antibiotic therapy,
pain management
Describe glomerulonephritis including etiology, pathophysiology,
and clinical manifestations.Glomerulonephritis: Inflammation of the
glomerulusGlomerular disease is the most common cause of chronic
and end-stage renal failure.Etiology (Varied):Immunological causes
(most common), drugs, toxins, vascular disorders, and systemic
diseasesTypes:Acute, rapidly progressive, chronic.
Describe glomerulonephritis including etiology, pathophysiology,
and clinical manifestations.Clinical Manifestations:UrineHematuria
w/red blood cell castsProteinuria exceeding 3-5 g/day (associated
w/nephrotic syndrome)Decrease in UOP/decrease in
GFREvaluationDefined by progressive development of clinical
manifestations and laboratory findings.Abnormal U/A w/ proteinuria,
RBC's, WBCs, and casts. Microscopic evaluation from renal biopsy
shows specific determination of renal injury and type of pathologic
condition.Treatment:Treating the primary disease, preventing or
minimizing immune responses, symptomatic treatment for edema,
hypertension, infections (antibiotics), corticosteroids (decrease
inflammatory response).
Describe nephrotic syndrome including etiology, pathophysiology,
and clinical manifestations.Nephrotic Syndrome:Excretion of 3.5 g
or more of protein/day, hypoproteinemia, edema.Characteristic of
glomerular injuryEtiology:Any condition causing increase in
glomerular membrane permeability: glomerulonephritis, diabetes,
infectious process, toxins, drugs,
malignancies.Pathophysiology:Plasma proteins (albumin,
immunoglobulins) cross the injured glomerular filtration membrane.
Basement membrane of the glomerulus looses negative charge.
Hypoalbuminemia ensues. Loss of albumin stimulates lipoprotein
synthesis by the liver and hyperlipidemia.
Describe nephrotic syndrome including etiology, pathophysiology,
and clinical manifestations.Signs/SymptomsProteinuria, edema,
hyperlipidemia, lipiduria, loss of vitamin D leading to
hypocalcemia.Evaluation:Protein level in urine is > 3.5 g. Serum
albumin decreases, and cholesterol, phospholipids, and
triglycerides increase. Pathologic condition is identified by
biopsy.Treatment:Diet (normal protein, low fat, salt restriction),
treat cause if known, diuretics, steroids, albumin IV. Monitor
closely for hypovolemia, hypokalemia or hyperkalemia secondary to
renal insufficiency. 54
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