GLOMERULONEFRITIS AKUT

Hipertensi
Hematuria
Silinder eritrosit
Piuria
Proteinuria ringan-sedang
 ETIOLOGI
INFEKSI (GNAPS)
NON-INFEKSI (RPGN, SLE)
 PATOGENESIS
Pembentukan kompleks imun yang
terdeposisi di glomerulus
Pencetus pasti belum diketahui,
kecuali pada GNAPS
GNAPS
 Usually affects children between 2-14
y.o.
Most common in male
Familial incidence 40%
2-6 weeks after skin infection
(impetigo) M types streptococcus :
47, 49, 55, 2, 60, 57
1-3 weeks after pharingitis M types
streptococcus : 1, 2, 3, 4, 25, 49, 12
 Diagnosis
C3
Anti-DNAse (70%)
Titer ASO (30%)
Tata laksana
Antibiotics (amoksisilin 50 mg/KgBB/hari
dibagi 3 dosis selama 10 hari / eritromisin
30mg/KgBB/hari dibagi 3 dosis 10 hari)
Suportif (diet rendah garam dan protein)
LUPUS NEFRITIS
 Common and serious complication of
SLE (30-50% when diagnosed, 60-
80% in the course of their disease)
Hypocomplementemia (70-90%)
 Patogenesis
Deposition of circulatin immune
complexes activate the complement
cascade lead to
complement-mediated damage,
leukocyte infiltration,
activation of procoagulant factors, and
release of various cytokines
 Tata laksana
Class l and ll do not need therapy
Class lll-Vl, hidrosiklorokuin 6-6,5
mg/KgBB ideal dan kotikosteroid
(siklofosfamid oral/IV bulanan selama 6
bulan)
Class Vl renal transplantation
DIABETIK NEPHROPHATY
 One of secondary etiology of Nephrotic
Syndromes
Heavy proteinuria
Minimal hematuria
Hypolbuminemia
Hypercholesterolemia
Edema
Hypertension
 Single most common cause of CKD in US
(45% receive renal replacement therapy)
40% of patients with DM1 or DM2 develop
nephropathy (prevalence DM2/DM19/1)
Faktor risiko
Hiperglikemia
Hipertensi
Dislipidemia
Merokok
Fam history
Gen polimorfism menyerang aktivitas RAA axis
 Dalam 1-2 tahun setelah onset DM muncul
perubahan morfologi ginjal
Kontrol glukosa darah dan tekanan darah
inhibisi RAA sistem mencegah progresifitas