Prof. Dr. dr.

Syarifuddin Rauf, SpAK

Bagian Ilmu Kesehatan Anak FK - UNHAS

RS Dr. Wahidin Sudirohusodo Makassar

GLOMERULONEFRITIS
AKUT (GNA)

Proliferasi dan inflamasi glomeruli

Sekunder oleh mekanisme imunologik

Antigen: bakteri, virus, parasit & zat lain.

GLOMERULONEFRITIS AKUT
PASCA STREPTOKOKKUS
(GNAPS)

1. Angka kejadian
Lebih sering umur 6-7 thn, jarang < 3 thn
Laki laki > perempuan (2:1)
10- 12 % kasus infeksi strept. hemolitikus
grup A
Kaplan: 50% kasus asimtomatik pd epidemi
GNAPS didahului ISPA atau piodermi

2. Etiologi
Streptokokus hemolitikus grup A (tipe M)
NEFRITOGENIK
Faringitis (serotipe tersering 12, lalu 1,3,4,6,25)
Piodermi (serotipe tersering 49, lalu 2,53,55,
56,57,58,60

MANIFESTASI KLINIK
a. Periode latent: 1 3 minggu
b. Edema
c. Hematuri
d. Hipertensi
e. Oligouria
f. Gejala-gejala lain: lelah, malaise, letargi
& anoreksia
g. Kelainan laboratorium

URIN:
Hematuri, warna kemerah-merahan atau
seperti air daging
Proteinuri : kualitatif dan kuantitatif
> 6 bulan

proteinuri persisten

biopsi ginjal

DARAH:
Titer ASTO meningkat
Menurunnya kadar C3
LED meninggi
Hipoproteinemi ringan
Pemeriksaan bakteriologik

Diagnosis GNAPS
Bila memenuhi 4 gejala berikut
Hematuri makroskopik atau mikroskopik
Edema
Hipertensi
ASTO meningkat
C3 menurun

SINDROM NEFROTIK (SN)

1. Edema Masif
2. Proteinuri Masif
3. Hipoproteinemi (< 2,5 g/dl)
4. Hiperkolesterolemi
(>250 mg/dl)

ANGKA KEJADIAN
Anak > dewasa
Anak: 1 3 tahun
> 5 tahun
Wila Wirya (1992): 6 kasus/100.000 penduduk
< 14 thn/thn

Jumlah kasus di Indonesia (210 juta pend.) :

5040 SN

ETIOLOGI
Tidak diketahui: SN idiopatik
Genetik

: SN kongenital
HLA-B12, HLA B8

Pencetus : Infeksi virus/bakteri

Alergi

PATOMEKANISME
Soluble antigen- antibody complex
Teori elektrokemik

KOMPLIKASI YANG TERJADI PADA

GNAPS DAN SN:
1.HIPERTENSI ENSEFALOPATI
2. EDEMA PARU
3. SYOK HIPOALUMINEMI
4. GAGAL GINJAL

URINARY TRACT INFECTION

(UTI)

DEFINITION

Infection from renal parenchyme

orificium urethrae externa
Significant bacteriuria
With or without symptoms

Significant bacteriuria

Pathogenic bacteria
Colony count : > 100.000/ml urine
> 1x lab. examinations

Relapsing UTI :
Recurrent UTI
Same microorganism
Reinfection UTI :
Recurrent UTI
Different microrganism

ETIOLOGY
Bacteria :
E. Coli
Klebsiella
Proteus
Pseudomonas
Other microorganisms :
Protozoa
Virus

CLASSIFICATION

Clinically : 1. Symptomatic UTI

2. Asymptomatic UTI
Complication :
A. Simple UTI
B. Complication UTI
Localization : 1. Upper UTI
2. Lower UTI

PATHOGENESIS

1. Hematogenic
2. Percontinuitatum
3. Lymphogenic

DIAGNOSIS

Clinically :
1. Upper UTI (Pyelonephritis) :
Fever, back/flank pain & with or
without lower UTI symptoms
2. Lower UTI (Cystitis) :
Suprapubic punction, dysuria,
frequent voiding etc.

PATHOGENESIS
Neonates

Baby & Child

(>1 month)

Colonization on GIT
Certain focus

Hematogen
(Septicemia)

Percontinuitatum
(Ascending)

: Periurethra/Perineum
: Subpreputium

?
Bacteria enter to
Urinary tract

Symptomatic UTI

Asymptomatic UTI

LAB. EXAMINATIONS

URINE :
1. Urinalysis :

Leukocyte > 5-10/HPF

Erythrocyte : +/-

2. Urine culture :
a. Mid : stream urine :
C.C. : > 100.000/ml urine
b. Catheterization :
C.C. : > 10.000/ml urine
c. Suprapubic punction :
C.C. : > 1000/ml urine

BLOOD :
Leucocytosis
Increased BSR (> 30 mm/hour)
Increased CRP (> 30 ug/ml)

MANAGEMENT

1. Eradicate acute infection

2. Detection, prevention, & treatment
recurrent infection
3. Detection & surgical correction
abnormality of anatomical structure

Sudden loss or decreased of kidneys

function
Imbalance of water & electrolyte blood
Increased of waste products (Ureum &
Creatinin)

ETIOLOGY:
A. Prerenal: Decrased blood flow
Diarrhea dehydration
Hemorrhage
Burns
Septic shock

B. Renal:
Acute Tubular Necrosis
Acute Nephritic Syndrome
Nephrotic syndrome
Acute Pyelonephritis

C. Postrenal: Urinary tract obstruction

Tumors
Kidneystones
Nephrocalcinosis

Etiology of ARF in Newborn:

1. Prerenal:
Perinatal hemorrhage (birth trauma, placenta
abruption)
Neonatal hemorrhage (severe intraventricular
hemorrhage, adrenal hemorrhage)
Perinatal asphyxia
Hyaline membrane disease

2. Renal :
Acute Tubular Necrosis (perinatal asphyxia)
Maternal-fetal transfer:
Antibodies
Infections: syphilis, Cytomegalovirus

3. Postrenal : Congenital malformations of urinary

collecting system

CLINICAL MANIFESTATIONS:
1. Decreased urine volume (Oligouria Anuria)
2. Generalized swelling
3. Changes in mental status:
Unconscious
Delirium/confusion
Coma
4. Seizures
5. Nausea, vomiting
6. Anemia
7. Kusmaul respiration

DIAGNOSIS
Clinical Manifestations
Lab. Examination:
Serum Ureum increased
Serum Creatinin increased
Creatinin Clearance
Serrum Potasium

TREATMENT
1.

The goal of the treatment is to identify & treat

reversible causes like prerenal causes
(diarrhea dehydration) & post renal causes
(e.g. obstructive uropathy by surgeon
procedure)

2.

Medical drugs:
Antibiotics: To prevent infection
Diuretics: to treat oligouria or anuria
Diazepam: To handle convulsion

3. Emergency condition:
Hyperkalemia:
Ca Glukonas
Potassium exchange resin
(Kayexalate) Oral/rectal
Metabolic acidosis: Bicarbonate Natricus

Renal function progresses to decrease

slowly
Imbalance of water & electrolyte
Increased of waste products (Blood
ureum & creatinin)

ETIOLOGY:
< 5 years old:
Hypoplasia / Dysplasia kidney
Congenital structure of urinary tract
Vesicoureteral reflux
Congenital Nephrotic Syndrome

5 15 years old :
Hereditary diseases: Alports syndrome,
sistinuri
Primary glomerulonephritis: Nephritic
Syndrome
Secondary glomerulonephritis : SLE,SHS

TREATMENT
1.

Conservative Treatment:
The aims of this treatment:
Preparing the child & family for the
treatment of CRF
Slowly progression to End Stage RF

2. Replacement therapy:
The aims is to replace the function of the
unfunction kidney by:
Dialysis:
Peritoneal dialysis (PD)
Hemodialysis
Transplantation

Complication of SLE
Damage to glomerulus
Progressive loss of kidney function

ETIOLOGY :
1. Unknown
2. Genetic factor :
HLA Antigen (HLA-DR2, HLA-DR3)
High incidence in monozygotic twin
High incidence in family

3. Nongenetic factor:
Longterm treatment of certain drugs
(>6 months) hydralazine
Sex hormone: estrogen SLE (>)
Viral infection

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

Autoimune disorder
Damage to:

Joints
Heart
Lungs
Blood vessels
Kidneys
Skin

PATHOGENESIS
Autoimune process

Antinuclear Antibody (ANA)

+ Ds-DNA (Antigen)

Soluble Ag-Ab Complex

MBG

Deposition of: ANA + Ds-DNA + C3

Renal symptoms

GENERAL SYMPTOMS
Fever
Malar rash:

A rash shaped like butterfly

Usually found on the bridge
of the nose & cheeks

Inflammation of the joints (arthritis)

Anorexia
Weight loss
Anemia

CLINICAL MANIFESTATIONS:
RENAL SYMTOMPS

1. PROTEINURIA:
(+)(++) (30-100 mg/dl)
Haematuria (+)/(-)
2. ACUTE NEPHRITIC SYNDROME
3. NEPHROTIC SYNDROME

DIAGNOSIS
Clinical Manifestations
Lab. Examination:
Blood:

Anti Nuclear Antibody (+)

LE cell (+)
Ds-DNA (+)
C3 & C 4

CLASIFICATION HISTOPATHOLOGIC

I.

Normal histopathologic feature

II.

Mesangial Glomerulonephritis

III. Focal Segmental Proliferative Glomerulonephritis

IV. Diffuse Proliferative Glomerulonephritis
V.

Membranous Glomerulonephritis

TREATMENT
Class I & II :

Symptomatic treatment
No specific treatment

Class III,IV&V:

Symptomatic treatment
Specific treatment
Corticosteroid
Immunosuppressive

KIDNEY :
1. AGENESIS : BILATERAL RENAL AGENESIS
= Potters Syndrome
Oligohydramnion
Pulmonary hypoplasia
Low-set ears
2. RENAL HYPOPLASIA :

The kidney is small

Normal nephron

3. Horseshoe kidney :
Fusion of the renal parenchyma
Joined at the lower pole
4. Polycystic kidney :
a. Infantile Polycystic Kidney (IPCK)
b. Adults Polycystic Kidney (APCK)

IPCK
Autosomal Recessive Polycystic Kidney
Enlargement of distal tubulus & colligents
ductus
Glomerulus & proximal tubulus normal
Liver enlargement

URETER

Duplication of ureter
Ureterocele
Ectopic ureter

VESICO URETERAL REFLUX

Reflux of urine from the bladder into ureter
Damage the upper urinary tract by bacterial
Infection
Causes :

Congenital anomalous development

of the ureterovesical junction
Bladder outlet obstruction

BLADDER (VESICA URINARIA)

Agnesia
Bladder neck obstruction

URETHRA
Agnesia / atresia urethra
Congenital posterior urethral valves

SHS :

Systemic disease
Vasculitis on :
Skin purpura
Joint arthritis
Digestive tract abdominal pain
Kidney glomerulonephritis

INCIDENCE
Age incidence :
All ages
75% of cases : 2-11 years
Sex incidence : : = 2 : 1
50% of cases : preceded by upper respiratory
infection group A streptococci

CLINICAL MANIFESTATIONS
1. PURPURA :
Erythematous macular palpable purpura
Ecchymotic
Associated with subcutaneous edema
(extremities, scalp, periorbital region,
hands, feet, scrotal area)
Lower legs, ankles, dorsal foot ( symmetric)

2. Gastrointestinal Symptoms:
Abdominal pain : 35-85% of cases
Gastrointestinal bleeding: melena,
hematemesis, bloody stool
Invagination, intestinal perforation

3. Joint Symptoms:
Arthritis
Arthralgia
Ankles & knees: most commonly
affected
The three signs: Classic triad of SHS

RENAL INVOLVEMENT (SHS NEPHRITIS)

Haematuria associated with proteinuria

Acute Nephritic Syndrome
Nephrotic Syndrome
Renal Failure

PATHOPHYSIOLOGY
INCITING FACTOR (URIStreptococcus)

IgA complexes (IgA1 & IgA2)

Deposite in glom. basement membrane (gbm)

Activate complement

Immune complexes in gbm (IgA,IgG+C3)

Renal symptoms

MANAGEMENT
1. Self Limiting Disease
2. Supportive & symptomatic Treatment:
Fluid intake
Antihypertensive Hypertensive patient
Diuretic Oligouria
Antibiotic Infection
Analgesics Arthralgia

3. Specific treatment:
Corticosteroid (Prednison 1-2 mg/kgBW)
Severe Abdominal pain
GI bleeding
Renal treatment
R/ Acute Nephritic syndrome
Nephrotic Syndrome
Renal Failure