PWM Olly Indrajani
12-6-2012

Batasan: ilmu yg mempelajari fungsi dan patofisiologi ginjal dan saluran2 penunjangnya serta penyakit2nya.
Dasar2 yg perlu:
1. Anatomi & histologi
2. Fisiologi & biokimia
3. Patologi & laborat.
2

 150gm: each kidney
 1700 liters of blood filtered  180 L of G. filtrate
 1.5 L of urine / day.
 Kidney is a retro-peritoneal organ
 Blood supply: Renal Artery & Vein
 One half of kidney is sufficient – reserve
 kidney function: Filtration, Excretion, Secretion,
Hormone synthesis.

 Functions of the kidney:
 excretion of waste products
 regulation of water/salt
 maintenance of acid/base balance
 secretion of hormones
 Diseases of the kidney
 glomeruli
 tubules
 interstitium
 vessels

 Glomerular diseases: Glomerulonephritis
 Tubular diseases: Acute tubular necrosis
 Interstitial diseases: Pyelonephritis
 Diseases involving blood vessels:
Nephrosclerosis
 Cystic diseases
 Tumors

1.
2.
3.
4.
Anamnesis
Pemeriksaan fisik
Laboratorium
Pem. Penunjang: a. radiologis: - BOF
- IVP
- CT Scan b. biopsi ginjal.
- MRI
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Anamnesis : 1. Keluhan utama: a. dysuria,polyuri,polakisuri, b. edema c. nyeri d. penurunan fungsi ginjal e. hematuria
2. Penyakit terdahulu
3. Anamnesa keluarga.
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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.
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• Azotemia :

BUN, creatinine
•
Uremia: azotemia + more problems
•
Acute renal failure: oliguria
•
Chronic renal failure: prolonged uremia

 Nephritic syndrome.
 Oliguria, Haematuria, Proteinuria, Oedema.
 Nephrotic syndrome.
 Gross proteinuria, hyperlipidemia,
 Acute renal failure
 Oliguria, loss of Kidney function - within weeks
 Chronic renal failure.
 Over months and years - Uremia

• Massive proteinuria
• Hypoalbuminemia
• Edema
• Hyperlipidemia/-uria
• Hematuria
• Oliguria
• Azotemia
• Hypertension

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-
-
-
-
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Proses inflamasi glomerulus
Terjadi akibat berbagai sebab yg berbeda etiologi, patofisiologi ataupun patogenesanya
Dulu dikenal dg istilah glomerulonephritis
Peyebab utama Gagal Ginjal
Manifestasi klinis bisa tanpa gejala sampai gejala yang berat
Terpenting:menghambat progresifitas kerusakan
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1.
2.
3.
4.
Klasifikasi klinis
Klasifikasi lesi histopatologi
Klasifikasi berdasar etiologi&patogenesis
Klasifikasi berdasar proses imunologi
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1.
2.
3.
4.
5.
Kelainan urine tanpa keluhan
Sindroma nefrotik
Sindroma nefritik akut
Sindroma nefritik kronik
Sindroma RPGN (Rapid Progressive
Glomerulonephritis)
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a.
b.
c.
d.
e.
f.
g.
h.
i.
Lesi minimal
Lesi glomerulosklerosis fokal segmental
Lesi mesangioproliferatif (IgM)
Lesi mesangioproliferatif (IgA) (penyakit
Berger)
Lesi proliferatif akut
Lesi membranoproliferatif
Lesi membranosa
Lesi bulan sabit (crescentic)
Lesi glomerulosklerosis.
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a.
b.
c.
d.
e.
f.
Kelainan imunologi
Kelainan metabolik:
- nefropati diabettik
- nefropati as. Urat
- amiloidosis primer/sekunder
Kelainan vaskuler
Disseminated Intravascular Coagulopathy
(DIC)
Kel. Herediter: sindr.Alport, peny.Fabry
Patogenesis tak diketahui: lipoid nefrosis
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a.
Peny. Kompleks immun:
1. Circulating immune complex:
Nephropathy Berger
Henoch-Schonlein Purpura
Nefritis Lohlein (endokar.bakteri)
2. Pembentukan komplek imun insitu:
Glom. Post Streptococcus infection
Glom. Membranosa b. Peny.AGBM: sindroma Goodpasteur.
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Minimal change disease

Minimal change disease
Normal glumerular structure

Minimal change disease
Normal glomerulus

 Primary or secondary
 Some (focal) glomeruli show partial
(segmental) hyalinization
 Unknown pathogenesis
 Poor prognosis

Focal segmental glomerulosclerosis

 Autoimmune reaction against unknown renal antigen
 Immune complexes
 Thickened GBM
 Subepithelial deposits

Membranous glomerulonephritis

Post-infectious glomerulonephritis

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



IgA nephropathy

Batasan: sindroma klinik ok.berbagai penyakit yg ditandai dg meningkatnya perm.membran basal glomerulus thd protein dg.G/ utama proteinuri
> 3,5 gram/24 jam .
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-
-
-
-
Patofisiologi: meningkatnya perm.GBM  proteinuri
Bila loss albumin> produksi  hipoalbuminemi
Hipoalbumin  edema anasarka
Hiperlipidemia : patogenesanya belum jelas
Ggn. Metab.lemak
 lipiduria: oval Fat Bodies
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1.
2.
Glomerulopati primer
Glomerulopati sekunder:
a. infeksi: sifilis, malaria, TBC, tifus,virus
b. nefrotoksin: diuretik merkuri, bismuth, preparat emas
c. 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.
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 Massive proteinuria
 Hypoalbuminemia
 Edema
 Hyperlipidemia
 Lipiduria

-
-
-
kencing berbuih
Sembab tungkai yg progresif s/d anasarka
Sesak nafas (bila ada cairan pleura)
Sebah dan perut buncit (bila ada asites)
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1.urinalisis: - proteinuri +3  +4, lipiduria
- torak eritrosit: khas utk SN prim
- glukosuri: bila ok DM.
2.ekskresi protein 24 jam (Esbach)
3.kadar albumin serum
4. Elektroforesa protein serum & protein urin
5.kadar lipid plasma
6.tes imunologi
7.pem.radiologi: BOF, IVP, foto thorax
8. Biopsi ginjal.
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Penyakit dg edema dan hipoalbuminemi lain:
1.
Penyakit hati kronis
2.
3.
Malnutrisi
Gagal jantung
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1.
2.
Diet TKTP rendah garam.
Obat: a. diuretik b. antiagregasi platelet: dipiridamol c. infus albumin d. kortikosteroid:prednison
2mg/kg/hr 4 minggu lalu tapering off e. imunosupresif: siklofosfamid 2 mg/ kg/hr atau klorambusil 0,2 mg/kg/hr selama 8 minggu.
3. Koreksi penyakit primernya
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1.
2.
3.
4.
Kelainan kardiovaskuler (atherosclerosis)
Shock hipovolemi
Mudah terserang infeksi
Gagal ginjal kronik.
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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.




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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 glomerulus



Glomerular 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 diseases
Types:
 Acute, rapidly progressive, chronic.

Describe glomerulonephritis including etiology, pathophysiology, and clinical manifestations.
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

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Clinical Manifestations:
1.
Urine
Hematuria w/red blood cell casts
2.
3.
Proteinuria exceeding 3-5 g/day (associated w/nephrotic syndrome)
Decrease in UOP/decrease in GFR

Evaluation

Defined by progressive development of clinical manifestations and laboratory findings.
Abnormal U/A w/ proteinuria, RBC's, WBC’s, 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 injury
Etiology:
 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.
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

Signs/Symptoms
 Proteinuria, 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.

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