Glomerular Disease

Naifah Luthfiyah Putri

1510211009
Glomerular Disease
 many forms of glomerular disease with
pathogenesis variably linked to :
 presence of genetic mutations,
 infection,
 toxin exposure,
 autoimmunity,
 atherosclerosis, Mostly
idiopatik
 hypertension,
 emboli,
 thrombosis, or
 diabetes mellitus.
MOST OF GLOMERULAR DISEASE
ARE IMMUNOLOGICALLY
MEDIATED, WHEREAS TUBULAR
AND INTERSTITIAL DISORDERS
ARE FREQUENTLY CAUSED BY
TOXIC / INFECTIOUS AGENT
Epidemiologi
GLOMERULONEPHRITIS IS DIAGNOSED
IN CLINICAL SCENARIOS IN WHICH
THERE IS EVIDENCE OF GLOMERULAR
INFLAMMATION AS EVIDENCED BY
THE PRESENCE OF HEMATURIA,
PROTEINURIA, DECREASED GFR,
AND/OR
HYPERTENSION.
Hematuria, Proteinuria, and Pyuria
 Microscopic hematuria may appear with
the onset of benign prostatic hypertrophy,
interstitial nephritis, papillary necrosis,
hypercalciuria, renal stones, cystic kidney
diseases, or renal vascular injury.
However, when red blood cell casts or
dysmorphic red blood cells are found in
the sediment, glomerulonephritis is likely
Hematuria, Proteinuria, and Pyuria
 Sustained proteinuria >1–2 g/24 h is also
commonly associated with glomerular
disease.
 Patients often will not know they have
proteinuria unless they become edematous
or notice foaming urine on voiding.
 Some patients with inflammatory
glomerular disease (acute poststreptococcal
glomerulonephritis/MPGN), have pyuria
characterized by the presence of
considerable numbers of leukocytes.
Diagnosis
 Several simple assessments and questions
can help narrow the differential diagnosis
and assist in decision
 How old is the patient?
 Is this an acute issue or is there evidence of
long-standing disease?
 Basic investigations (hemoglobin, renal
ultrasonography)  are the kidneys large, indicating
an acute process? or small, indicating a chronic
progressive process?) & parathyroid hormone (PTH)
(assessing for evidence of renal osteodystrophy)
 hypertension, hematuria, and edema can occur
in any of these disorders and are not indicative
of a specific diagnosis
Diagnosis
 Several simple assessments and questions
can help narrow the differential diagnosis
and assist in decision
 How old is the patient?
 Is this an acute issue or is there evidence of
long-standing disease?
 Has the patient had recurrent asymptomatic
gross hematuria?
 Is there any evidence of extrarenal
involvement?
 Is significant hypertension or renal insufficiency
present?
 Sindrom Nefrotik
Tanda patognomik peny. Glomerular yg
ditandai dengan edema, protenuria
masif > dr 3,5g/hari,
hipoalbuminemia < dr 3,5g/hari,
hiperkolesterolemia,dan lipiduria
Sindrom Nefrotik
 Dapat disebabkan
o/ GN primer &
sekunder akibat
infeksi, keganasan,
penyakit jaringan
ikat, obat/toksin
dan akibat
peny.sistemik
 Glomerulonefritis
Penyakit inflamasi/non inflamasi
pada glomerulus yang
menyebabkan perubahan
permeabilitas, perubahan
struktur dan fungsi glomerulus
 Glomerulonefritis
 Etiologi?  Faktor presipitasi?
• sebagian besar etiologi
GN tidak diketahui
 Infeksi
• Kecuali yg disebabkan o/  Pengaruh
infeksi beta obat/pajanan toksin
streptokokus pd GN yg menginisiasi
pasca infeksi tjdnya respon imun
streptokokus/akibat
virus hepatitis C serupa
Sign & Symptoms
 Protenuria
 Hematuria
 Penurunan fungsi ginjal
 Urin berwarna kecoklatan
 Perubahan ekskresi garam dengan akibat
edema
 Edema tungkai
Gejala klinik awal GN
 Edema periorbita
Glomerulo Nefritis Akut Pasca
Streptokokus
 GNAPS adalah suatu bentuk peradangan glomerulus
yang secara histopatologi menunjukkan proliferasi &
Inflamasi glomeruli yang didahului oleh infeksi group A
β-hemolytic streptococci (GABHS) dan ditandai dengan
gejala nefritik seperti hematuria, edema, hipertensi,
oliguria yang terjadi secara akut.
Epidemiology
 Children between the ages of 2 and 14 years
(Harrison’s)
 Most common in children aged 3–10 years (Smith
and Tanagho’s)
 It is more common in males, and the familial or
cohabitant incidence is as high as 40%
 Poststreptococcal glomerulonephritis
due to impetigo develops 2–6 weeks after skin
infection
1–3 weeks after streptococcal pharyngitis
Etiology
 By far the most common cause is an antecedent
infection of the pharynx and tonsils or of the skin
with group A beta-hemolytic streptococci, certain
strains of which are nephritogenic
 Skin and throat infections
 M types of streptococci (nephritogenic strains)
antedate glomerular disease
 M types 47, 49, 55, 2, 60, and 57 Impetigo
 M types 1, 2, 4, 3, 25, 49, and 12 
Pharyngitis
 Etiologi
Streptococcus β-hemolytic
group A
 Identifikasi
Bentuk : bulat
Susunan : berantai
Warna: ungu
Sifat : gram positif
Metoda: pewarnaan gram
 Membentuk zona bening
disekeliling koloni
 Membentuk 2 macam
hemolisin: streptolisin O dan
streptolisin S
Nephritogenic Streptococci
 Streptococcus pyogenes
Bentuk: coccus
Susunan: berantai
Warna: ungu
Sifat: Gram Positif
Metode: Pewarnaan Gram
 Transmission
saliva or nasal
secretions from an
infected person
facilitate transmission
foodborne
 Incubation period
10 days
 Streptococcal pyogenik exotoxin B (SPEB)
 Nephritis-Associated Plasmin Receptor
(NAPlr)
antigen nefritogenik ini dapat ditemukan
pda jaringan hasil biospsi ginjal
dapat meningkatkan proses inflamasi yg
dapat merusak membran basilis glomerulus
 M protein
infection, avoiding human immune cells
ability to resist phagocytosis by
polymorphonuclear leukocytes in the
Clinical Manifestation
 Headache
 Malaise,
 Mild fever
 Puffiness around the eyes and face
Edema (often pronounced facial and orbital edema,
especially on arising in the morning)
 Flank pain
 Oliguria
 Hematuria
usually noted as “bloody” or, if the urine is acid, as
“brown” or “coca-cola colored”
 There may be moderate tachycardia, dyspnea, and
moderate to marked elevation of blood pressure
 Tenderness in the costovertebral angle
Gejala Klinis
Gejala Klinis
 Periode laten
 Edema
 Hematuria
 Hipertensi
 Oliguria
 Gejala lain: pucat, malaise,
letargi, dan anoreksia
 Gejala Klinis
Makroskopik Mikroskopik
 Ginjal membesar  Gelung glomerolus
 Sinusoid dan membesar, simpai
simpai tidak jelas Bowman menyempit
 Permukaan licin  Glomerolus
hiperseluler krn
 Terdapat bercak
proliferasi endotel
hemoragik dan sel mesangial
 Serbukan PMN dan
limfosit
 Lumen kapiler
menyempit kadang
obliterasi
Diagnosis
 Anamnesis  ditemukan gejala klinis yang khas
 Pemeriksaan fisik  edema palpebral/ tangan /
kaki,
 Pemeriksaan urin  proteinuria (biasanya < 2
gr/m2 LPB/ 24 jam), hematuria
 Pemeriksaan darah
• Serologis: Antistreptolisin O (ASO) ↑
• Aktivitas komplemen serum: komplemen C3 ↓
• LED: umumnya ↑ pada fase akut, dan ↓
setelah gejala klinik menghilang
Komplikasi
Komplikasi terjadi karena hipertensi dan disfungsi
ginjal akut yaitu:
 Hipertensi (60% pasien)  hypertensive
encephalopathy (10%), gangguan neurologis,
seperti pendarahan intrakranial
 Potensi komplikasi lainnya adalah gagal jantung,
hiperkalemia, hiperfosfatemia, hipokalsemia,
asidosis, kejang, uremia
Prognosis
 Dubia ad Bonam
 5–20% show progressive renal damage
 Tata laksana
 Non- Farmakologi
• Istirahat  perawatan 10-14 hari dengan syarat tidak ada komplikasi
• Diet  makanan rendah garam 0,5 – 1 gr/hari
 protein dibatasi jika kadar ureum ↑ (0,5 – 1
gr/KgBB/hari

 Farmakologi
• Antibiotik (gol. Penisilin)
 Amoksisilin 30 mg/KgBB/hari (3 dosis) selama 10 hari
Mekanisme: hambat sintesis dinding sel bakteri. Sangat kuat untuk
bakteri gram positf
ESO: hipersensitivitas, alergi, kulit kemerahan
Tata laksana
 Farmakologi
• Kalau alergi amoksisilin
 Eritromisin 50 mg/KgBB/hari (3 dosis)
selama 10 hari
Mekanisme: berikatan dengan ribosomal RNA
30s untuk hambat sintesis protein bakteri
ESO: gangguan GIT, toksisitas hepar
• Edema  diuretic  FUROSEMID 1-2
mg/KgBB/kali, PO/IV, prn
Mekanisme: hambat reabsorbsi elektrolit (Na, Cl,
K) pada ansa henle asenden
ESO: hiperurisemia, hipokalemia
• Hipertensi  ACI + ARB
Tata laksana
 Follow up  cek proteinuria
 Indikasi Rawat Inap:
• Masa inkubasi pendek (< 1 mgg)
• Usia < 2 th
• Hematuria makroskopis > 3 bln
• Hematuria mikrokopis > 12 bln
• Proteinuria > 6 bln
• C3 ↓ > 3 bln
 Edukasi
Proteinuria hilang dalam 6 bulan, hematuria
hilang dalam 12 bulan.
Kontrol ke dokter lagi
Referensi
 Konsensus Glomerulonefritis Akut Pasca Streptokokus
IDAI
 Christopher R Kelly, Jaime Landman-The Netter
Collection of Medical Illustrations - Urinary System_
Volume 5. 5-Saunders (2012)
 J. Jameson, Joseph Loscalzo-Harrison's Nephrology
and Acid-Base Disorders, 2e-McGraw-Hill Education _
Medical (2013)
 Jack W. McAninch, Tom F. Lue-Smith and Tanagho's
General Urology-McGraw-Hill Medical (2012)
 ILMU PENYAKIT DALAM FKUI JILID II EDISI VI