Lect 5 W1 Kidney

Acute glomerulonephritis
Primary:
Secondary:

Nephritis: inflamasi dan proliferasi Cara bedain sama ISK itu hypertension
glomerulus Most prevalent post streptococcus (group A B
Immunological mechanism hemolytic strep/GABHS)
Sudden onset 7-14 days after pharyngitis
Hematuria (first symptom), hypertension, 14-21 days after impetigo
edema, renal insufficiency Hipertensi anak beda2 tergantung table
Present at any age

Pathogenesis
o Exuberant response towards Strep infection
o Excess amount of antibody
o Ag-Ab complex

Clinical features AGN

Lab: Urinalysis, renal function test, anemia normochromic normocytic, Evidence of streptococcal (culture, titer
ASTO), immunological test

DDX AGN
o Acute exacerbation of chronic GN
o Henoch-scholen

Management of GN
o Supportive & symptomatic care
o Hospitalized if: hypertension, oliguria, significant edema
o Bed rest, fluid restriction
o Anti-hypertension

Prognosis
o 2-3 weeks
o HT up to 4 weeks
o C3 levels after 4-8 weeks jadi normal

Streptococcal pharyngitis
o Use modified Centor criteria o Point 1 or less: <10%, no antibiotic
o Absence of cough, swollen and tender o Point 2: 11-17%, antibiotic based on culture
cervical lymph nodes, temp >38.0 C, or RADT
Tonsillar exudate or swelling, age 3-14(+1), o Point 3:
15-44 yr (0), >44yr (-1) o Point 4:

Nephritis syndrome
SN: proteinuria, hypoalbuminemia + edema
Occurs at all aged but more prevalent in 1.5-6 years
More common in boys

Pathophysiology
o Unknown immunological process – change glomerular permeability to albumin

Signs and symptoms

o Proteinuria: albumin >50 mg/kg/day (+3)

Lab
o Urinalysis

General management
o Edema berat baru di opnam o Steroid: prednisone/prednisolone 2
o Edema: salt restriction, diuretics mg/kg/day(pediatrician)
o Proteinuria: No benefit of protein restriction Harus Complete immunization (includes PCV)
in children, routine monitoring sebelum dikasih steroid

Summary
Lect 1 W2 Kidney
Acute Kidney Injury
Penurunan fungsi ginjal secara tiba2
Bisa dalam jam atau hari
Retention of metabolic waste products

Classification
Baca sendiri

Anatomy
Pre renal, renal, post renal
Aorta abdominalis - Artery renalis – membentuk lengkung glomerulus

Etioligy
Pre renal – 60-70%
Renal/intrinsic – 25-40%
Post renal –

Pre renal disease

Two major causes of reduced renal perfusion:
o Volume depletion
o Relative hypotension
Result from:
o True hypoperfusion due to bleeding, gastrointestinal, urinary or cutaneous losses
o Effective volume depletion in heart failure, shock or cirrhosis
Missed

Intrinsic
Tubular cell injury
Acute interstitial nephritis
Acute

Lect 2 W2 Kidney

Acute tubular necrosis

Kidney injury caused by damage to the kidney tubule cells

Risk factors
Preexisting CKD
DM
Preexisting hypovolemia or poor renal perfusion
Older age

Lect 1 W4 Kidney
Diabetic Nephropathy
Muncul 5 tahun setelah onset diabetes
Normal <30

Type 1:
4% by 10 years
25% by 25 years

Type 2:

Take home point

Persistent albuminuria
Progressive decline of GFR
Elevated arterial blood pressure

Chronic Kidney Disease

With or without decreased GFR, pathologic abnormalities
GFR <60 ml/min

Measurement of kidney function

Glomerular Filtration Rate

Classification
NKF K/DOQI Classification system
KDIGO

Take home points

Mortality caused by cardiovascular disease

Preventing progression
- Edukasi: penyakit yang seumur hidup
- Diet control: restriksi protein 0,8 gram/kg/hari(proteinuria)
- Glycemic control: target dibawah 7 m1c(???)
- Hypertension control: target BP <130/80
- ACEI and ARB: apalagi kalo udah ada proteinuria, buat BP. Kurangin tekanan darah
pada glomerular

Pathogenesis
- Renal preglomerular
- Glomerular
- Glomerular sclerosis

Treatment
Dari ppt
- Statin untuk dyslipidemia

Make sure proteinuria karena persistent bukan physiologis

Protein yang boleh loss, 0-30
Albumin gaboleh loss

Management issues
Dari ppt
- Stage 1 + 2: Education, detection, measure to slow progression
- Stage 3: Cardivascular
- Stage 4: renal replacement therapy
- Stage 5: gabisa ngapa2in lagi

Lect 2 W4 Kidney
Concept of glomerular hypertension
- Kidney damage – increase GFR is not good

Hypertension in CKD
Ring of hell

Mechanism of hypertension

Therapy
- Block the RAAS
- Diuretic
- CCBs
- Adrenergic inhibitors: Central alpha agonist
- Vasodilators

Kalau ada sumbatan terdengar bruit

Renovascular hypertension
Fibromuscular dysplasia, early onset <30 thn
Atherosclerosis plak udah tua >55 thn
BP tinggi dengan acute lung edema
Tiga stages
Can reach renal artery stenosis

Glomerulosclerosis – penumpukan kapur dari apoptosis pada lokasi podocyte

Kalau udah terjadi degenerasi hyaline

Genes
- APOL1: remodeling akan menjadi lebih besar, lebih lebay

Clinical manifestation
- Proteinuria
- Left ventricle hypertrophy
- High blood pressure

Statin diberikan yang atorfa statin

ABCD meds for hypertension

A-A GABOLEH, ACE and ARB
A-C BOLEH, ACE-Calcium antagonist. ACE-Thiazide
Bila gagal kasih A-C-D

Essential hypertension target ginjal

Lect 5 W4 Kidney
Nutrition
Masalah yang berhubungan dengan nutrisi pada penderita CKD
Gangguan ekskresi
- Regulasi TBW
- Metabolit protein
- Metabolit lain: Phospor

Gangguan endokrin
- Hormon Eritropoietin
- Aktivasi VitD – Calcium – PTH
- Renin – RAAS terganggu

Gangguan nutrisi: malnutrisi

- Asupan kurang: appetite loss, palatability, mual, muntah. Ureum tinggi membuat
tidak nafsu makan sementara ureum tinggi itu inflamasi yang membuat
breakdown cepet
- Liat ppt

Phosphor buat vessels jadi kaku

Asama urat pada urin datang dari pemecahan DNA (Deoxyribo Nucelic Acid)
DNA ADA PADA INTI SEL
Asam urat dari jeroan
Tananam bagian luarnya cellulose dan kita gapunya enzyme buat breakdown itu, daging
lipoprotein membrane kita punya enzyme buat breakdown itu

Pasien CKD anemia karena mereka dilarang makan protein

Vitamin D dari matahari dan susu percuma kalo liver and ginjalnya rusak.
Kasihnya Vitamin D3 aktif