NEPHROLOGI

PWM Olly Indrajani

12-6-2012

Nephrologi
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.

Introduction:

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.

STRUCTURE OF THE KIDNEYS

Kidney Anatomy:

STRUCTURE OF THE KIDNEYS

Kidney Anatomy:

Introduction
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

Renal Pathology Outline

Glomerular diseases:

Glomerulonephritis
Tubular diseases: Acute tubular

necrosis
Interstitial diseases: Pyelonephritis
Diseases involving blood vessels:

Nephrosclerosis
Cystic diseases

Pendekatan klinis:
1.
2.
3.
4.

Anamnesis
Pemeriksaan fisik
Laboratorium
Pem. Penunjang:
a. radiologis: - BOF
- IVP
- CT Scan
- MRI
b. biopsi ginjal.
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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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Pemeriksaan fisik:
inspeksi
auskultasi
perkusi
palpasi

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Pem.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.
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Abnormal findings
Azotemia: BUN, creatinine
Uremia: azotemia + more problems
Acute renal failure: oliguria
Chronic renal failure: prolonged uremia

Clinical Syndromes:
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

Nephrotic syndrome

Massive proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia/-uria

Nephritic syndrome

Hematuria
Oliguria
Azotemia
Hypertension

What are the possible causes of this appearance of the kidneys?

Glomerulopathy
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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Klasifikasi
glomerulopathy
1. Klasifikasi klinis
2. Klasifikasi lesi histopatologi
3. Klasifikasi berdasar

etiologi&patogenesis
4. Klasifikasi berdasar proses imunologi

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Klasifikasi klinis:
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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Klasifikasi lesi
histopatologis
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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Klasif. Etiologi&
patogenesa
a. Kelainan imunologi
b. Kelainan metabolik:

c.
d.
e.
f.

- 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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Klasifikasi. imunologi
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

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Minimal change disease

Minimal change disease

Normal glumerular structure

Minimal change
disease

Normal glomerulus

Focal Segmental
Glomerulosclerosis
Primary or secondary
Some (focal) glomeruli show

partial (segmental) hyalinization

Unknown pathogenesis
Poor prognosis

Focal segmental glomerulosclerosis

Membranous
Glomerulonephritis
Autoimmune reaction against unknown

renal antigen
Immune complexes
Thickened GBM
Subepithelial deposits

Membranous glomerulonephritis

Post-infectious
glomerulonephritis

IgA Nephropathy
Common!
Child with hematuria after (URI)

Upper Respiratory Infection

IgA in mesangium
Variable prognosis

IgA nephropathy

Sindroma nefrotik
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.
Patofisiologi:
meningkatnya perm.GBM proteinuri
Bila loss albumin>
produksihipoalbuminemi
Hipoalbumin edema anasarka
Hiperlipidemia : patogenesanya belum jelas
Ggn. Metab.lemaklipiduria: oval Fat Bodies
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Etiologi:
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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Nephrotic Syndrome
Massive proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria

Gejala klinis:
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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Pemeriksaan &
diagnosis
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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Diagnosis banding:
Penyakit dg edema dan hipoalbuminemi
lain:
1. Penyakit hati kronis
2. Malnutrisi
3. Gagal jantung

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Penatalaksanaan
1. Diet TKTP rendah garam.
2. Obat: a. diuretik

b. antiagregasi platelet: dipiridamol

c. infus albumin
d. kortikosteroid:prednison
2mg/kg/hr 4 minggu lalu tapering of
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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Komplikasi:
1. Kelainan kardiovaskuler

(atherosclerosis)
2. Shock hipovolemi
3. Mudah terserang infeksi
4. Gagal ginjal kronik.

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UTI

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 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.

Clinical Manifestations:

Urine

1.
2.
3.

Evaluation

Defined by progressive development of clinical

manifestations and laboratory findings.

Hematuria w/red blood cell casts

Proteinuria exceeding 3-5 g/day (associated w/nephrotic
syndrome)
Decrease in UOP/decrease in GFR

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 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.
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.

Terimakasih

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