Gab. Kuliah Nefro

8/12/2019 Gab. Kuliah Nefro

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Prof. Dr. dr.Syarifuddin Rauf, SpAK

Bagian Ilmu Kesehatan Anak FK - UNHAS

RS Dr. Wahidin Sudirohusodo Makassar


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GLOMERULONEFRITIS AKUTGNA)


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Proliferasi dan inflamasi glomeruli

Sekunder oleh mekanisme imunologik

Antigen: bakteri, virus, parasit & zat lain.


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GLOMERULONEFRITIS AKUTPASCA STREPTOKOKKUS

GNAPS)


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1. Angka kejadian

Lebih sering umur 6-7 thn, jarang < 3 thn

Lakilaki > perempuan (2:1)

10- 12 % kasus infeksi strept. hemolitikus

grup A

Kaplan: 50% kasus asimtomatik pd epidemi

GNAPS didahului ISPA atau piodermi


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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


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a. Periode latent: 13 minggu

b. Edema

c. Hematuri

d. Hipertensi

e. Oligouria

f. Gejala-gejala lain: lelah, malaise, letargi

& anoreksia

g. Kelainan laboratorium

MANIFESTASI KLINIK


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URIN:

Hematuri, warna kemerah-merahan atau

seperti air daging

Proteinuri : kualitatif dan kuantitatif

> 6 bulan proteinuri persisten

biopsi ginjal


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DARAH:

Titer ASTO meningkat

Menurunnya kadar C3

LED meninggi

Hipoproteinemi ringan

Pemeriksaan bakteriologik


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Bila memenuhi 4 gejala berikut

Hematuri makroskopik atau mikroskopik

Edema

Hipertensi

ASTO meningkat

C3 menurun

Diagnosis GNAPS


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SINDROM NEFROTIK SN)


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1. Edema Masif

2. Proteinuri Masif

3. Hipoproteinemi (< 2,5 g/dl)

4. Hiperkolesterolemi

(>250 mg/dl)


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ANGKA KEJADIAN

Anak > dewasa

Anak: 13 tahun

> 5 tahun

Wila Wirya (1992): 6 kasus/100.000 penduduk

< 14 thn/thn

Jumlah kasus di Indonesia (210 juta pend.) :

5040 SN


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ETIOLOGI

Tidak diketahui: SN idiopatik

Genetik : SN kongenital

HLA-B12, HLA B8

Pencetus : Infeksi virus/bakteri

Alergi


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PATOMEKANISME

Soluble antigen- antibody complex

Teori elektrokemik


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KOMPLIKASI YANG TERJADI PADA

GNAPS DAN SN:

1.HIPERTENSI ENSEFALOPATI

2. EDEMA PARU

3. SYOK HIPOALUMINEMI

4. GAGAL GINJAL


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URINARY TRACT INFECTIONUTI)


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Infection from renal parenchyme

orificium urethrae externa

Significant bacteriuria

With or without symptoms

DEFINITION


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2

Pathogenic bacteria

Colony count : > 100.000/ml urine

> 1x lab. examinations

Significant bacteriuria


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3

Relapsing UTI :

Recurrent UTI

Same microorganism

Reinfection UTI :

Recurrent UTI

Different microrganism


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ETIOLOGY

Bacteria :

E. Coli

Klebsiella

Proteus

Pseudomonas

Other microorganisms :

Protozoa

Virus


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CLASSIFICATION

Clinically : 1. Symptomatic UTI

2. Asymptomatic UTI

Complication :A. Simple UTI

B. Complication UTI

Localization : 1. Upper UTI

2. Lower UTI


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PATHOGENESIS

1. Hematogenic

2. Percontinuitatum

3. Lymphogenic


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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.

DIAGNOSIS


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PATHOGENESIS

Neonates Baby & Child

(>1 month)

Hematogen

(Septicemia)

Percontinuitatum

(Ascending)

Bacteria enter to

Urinary tract

Symptomatic UTI Asymptomatic UTI

Colonization on GIT

Certain focus

: Periurethra/Perineum

: Subpreputium

?


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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


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BLOOD:

Leucocytosis

Increased BSR (> 30 mm/hour)

Increased CRP (> 30 ug/ml)


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1. Eradicate acute infection

2. Detection, prevention, & treatment

recurrent infection

3. Detection & surgical correction

abnormality of anatomical structure

MANAGEMENT


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Sudden loss or decreased of kidneys

function

Imbalance of water & electrolyte blood

Increased of waste products (Ureum &

Creatinin)


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A. Prerenal: Decrased blood flow

Diarrhea dehydration

Hemorrhage

Burns

Septic shock

ETIOLOGY:


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B. Renal:

Acute Tubular Necrosis

Acute Nephritic Syndrome

Nephrotic syndrome

Acute Pyelonephritis


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C. Postrenal: Urinary tract obstruction

Tumors

Kidneystones

Nephrocalcinosis


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1. Prerenal:

Perinatal hemorrhage (birth trauma, placenta

abruption)

Neonatal hemorrhage (severe intraventricular

hemorrhage, adrenal hemorrhage)

Perinatal asphyxia

Hyaline membrane disease

Etiology of ARF in Newborn:


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2. Renal :

Acute Tubular Necrosis (perinatal asphyxia)

Maternal-fetal transfer:

Antibodies

Infections: syphilis, Cytomegalovirus

3. Postrenal :Congenital malformations of urinary

collecting system


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CLINICAL MANIFESTATIONS:

1. Decreased urine volume (Oligouria Anuria)2. Generalized swelling

3. Changes in mental status:

UnconsciousDelirium/confusion

Coma

4. Seizures5. Nausea, vomiting

6. Anemia

7. Kusmaul respiration


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DIAGNOSISClinical Manifestations

Lab. Examination:

Serum Ureum increased

Serum Creatinin increased

Creatinin Clearance

Serrum Potasium


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TREATMENT1. 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


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3. Emergency condition:

Hyperkalemia:

Ca Glukonas

Potassium exchange resin

(Kayexalate) Oral/rectal

Metabolic acidosis: Bicarbonate Natricus


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Renal function progresses to decrease

slowly

Imbalance of water & electrolyte

Increased of waste products (Blood

ureum & creatinin)


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< 5 years old:

Hypoplasia / Dysplasia kidney

Congenital structure of urinary tract

Vesicoureteral reflux

Congenital Nephrotic Syndrome

ETIOLOGY:


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515 years old :

Hereditary diseases: Alports syndrome,

sistinuri

Primary glomerulonephritis: Nephritic

Syndrome

Secondary glomerulonephritis : SLE,SHS


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TREATMENT1. Conservative Treatment:

The aims of this treatment:

Preparing the child & family for the

treatment of CRF

Slowly progression to End Stage RF


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2. Replacement therapy:

The aims is to replace the function of the

unfunction kidney by:

Dialysis:

Peritoneal dialysis (PD)

Hemodialysis

Transplantation


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Complication of SLE

Damage to glomerulus

Progressive loss of kidney function


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1. Unknown

2. Genetic factor :

HLA Antigen (HLA-DR2, HLA-DR3)

High incidence in monozygotic twin

High incidence in family

ETIOLOGY:


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3. Nongenetic factor:

Longterm treatment of certain drugs

(>6 months) hydralazine

Sex hormone: estrogen SLE (>)

Viral infection

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)


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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

Autoimune disorder

Damage to: Joints

Heart

Lungs

Blood vessels

Kidneys

Skin

PATHOGENESIS


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PATHOGENESIS

Autoimune process

Antinuclear Antibody (ANA)

+ Ds-DNA (Antigen)

Soluble Ag-Ab Complex

MBG

Deposition of: ANA + Ds-DNA + C3

Renal symptoms

GENERAL SYMPTOMS


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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


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CLINICAL MANIFESTATIONS:RENAL SYMTOMPS

1. PROTEINURIA:

(+)(++) (30-100 mg/dl)

Haematuria (+)/(-)

2. ACUTE NEPHRITIC SYNDROME

3. NEPHROTIC SYNDROME

DIAGNOSIS


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DIAGNOSIS

Clinical Manifestations

Lab. Examination:

Blood: Anti Nuclear Antibody (+)

LE cell (+)

Ds-DNA (+)

C3 & C4

CLASIFICATION HISTOPATHOLOGIC


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CLASIFICATION HISTOPATHOLOGIC

I. Normal histopathologic feature

II. Mesangial Glomerulonephritis

III. Focal Segmental Proliferative Glomerulonephritis

IV. Diffuse Proliferative Glomerulonephritis

V. Membranous Glomerulonephritis

TREATMENT


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TREATMENT

Class I & II : Symptomatic treatment

No specific treatment

Class III,IV&V: Symptomatic treatment

Specific treatment

Corticosteroid

Immunosuppressive


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KIDNEY :


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KIDNEY :

1. AGENESIS: BILATERAL RENAL AGENESIS

= Potters Syndrome

Oligohydramnion

Pulmonary hypoplasia

Low-set ears

2. RENAL HYPOPLASIA : The kidney is small

Normal nephron


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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)

I P C K


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I P C K

Autosomal Recessive Polycystic Kidney

Enlargement of distal tubulus & colligents

ductus

Glomerulus & proximal tubulus normal

Liver enlargement

URETER


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URETER

Duplication of ureter

Ureterocele

Ectopic ureter

VESICO URETERAL REFLUX


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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


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BLADDER (VESICA URINARIA)

Agnesia

Bladder neck obstruction

Agnesia / atresia urethra

Congenital posterior urethral valves

URETHRA


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SHS : Systemic disease

Vasculitis on :

Skin purpura

Joint arthritis

Digestive tract abdominal pain

Kidney glomerulonephritis

INCIDENCE


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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

INCIDENCE



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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)



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2. Gastrointestinal Symptoms:

Abdominal pain : 35-85% of cases

Gastrointestinal bleeding: melena,

hematemesis, bloody stool

Invagination, intestinal perforation


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3. Joint Symptoms:

Arthritis

Arthralgia

Ankles & knees: most commonly

affected

The three signs: Classic triad of SHS

RENAL INVOLVEMENT (SHS NEPHRITIS)


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Haematuria associated with proteinuria

Acute Nephritic Syndrome

Nephrotic Syndrome

Renal Failure

RENAL INVOLVEMENT (SHS NEPHRITIS)

PATHOPHYSIOLOGY


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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


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1. Self Limiting Disease

2. Supportive & symptomatic Treatment:

Fluid intake

Antihypertensive Hypertensive patient

Diuretic Oligouria

Antibiotic Infection

Analgesics Arthralgia

MANAGEMENT


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3. Specific treatment:

Corticosteroid (Prednison 1-2 mg/kgBW)

Severe Abdominal pain

GI bleeding

Renal treatment

R/ Acute Nephritic syndrome

Nephrotic Syndrome

Renal Failure


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Gab. Kuliah Nefro

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