Acute Kidney Injury

Chronic Kidney Disease

Acute on Chronic Kidney Disease

ROR

Campbell-Walsh Urology, 11th ed.

 Acute Kidney Injury
• Definisi :
– Penurunan akut ( jam – hari ) fungsi ginjal yg
ditandai dg azotemia ( kenaikan serum kreatinin )
baik dg atau tanpa oliguria
• Tanda cardinal dari Acute Kidney Injury adalah
adanya penurunan dari glomerular filtration
rate (GFR)
• Klasifikasi : pre-renal, intrinsik dan post-renal
• GFR dihitung / diperkirakan dg :
1. Clearence Creatinine ( overestimasi 10 – 20 % )
2. Cockcroft-Gault ( margin error 30 % )
• Clearence creatinin ( not GFR ) utk pria :
( 140 – umur ) x BB
72 x serum kreatinin
• Utk wanita : hasil x 0.85

3. MDRD ( Modification of Diet in Renal Disease )

• GFR : 186 x serum kreatinin -1.154 x umur -0.203
x 0.742 ( wanita ) x 1.210 ( afrika amerika )
Prerenal Azotemia ( 21 % )
• Disebabkan oleh hipoperfusi renal transient yg
mengakibatkan penurunan akut GFR
• Respon baik dg penggantian cairan ditandai dg
kembalinya fungsi ginjal ( sesuai keadaan awal /
previous baseline ) dlm 24 – 72 jam
• Penyebab :
– Volume depletion
– Decrease in Cardiac Output
– Redistribution of Extracellular Fluid
• Tx : Optimalisasi volume cairan + tx underlying
disease
Penyebab pre-Renal :
Post Renal Azotemia ( 10 % )

• Disebabkan adanya obstruksi pd traktus urinarius ( pd

ke-2 ginjal )
• Ditandai dg :
– Hematuria
– Flank / abdominal pain
– Gejala uremia
– Riwayat operasi / Radiasi / Tumor
• Evaluasi adanya extravasasi urin ( fungsi ginjal baik tp
terjadi kenaikan ureum-kreatinin e.c reabsorbsi )
• Diagnosis dg USG utk mencari adanya hidronefrosis
• Tx : release obstruksi
Intrinsik Renal Disease
Glomerulonefritis Akut ( GNA ) : 4 %
Acute Intertitial Nephritis ( AIN ) : 2 %
Acute Tubuler Nephritis ( ATN ) : 45 %

• GNA (Glomerulonefritis Akut ) :

 Tanda Patognomonis GNA
proteinuria + hematuria + silinder eritrosit ( dismorfik )
 GNA + penurunan fungsi ginjal  RPGN ( Rapidly
Progressive Glomerulonephritis )
 Tipe RPGN ( dx dg biopsi renal + serologi test )
- Tipe I : anti glomerular basement membrane
- Tipe II : immune complex
- Tipe III : pauci-immune
• AIN (Acute Intertitial Nephritis):
 Suspek : AKI dg urin sedimen abnormal + riwayat minum
obat, klinis :
- demam, rash, eosinofilia
- Steril piuria + silinder lekosit + eosinofiluria
 Penyebab :
- obat-obatan ( onset 3 – 5 hari )
- Sarcoidosis / streptococus / legionella / inf. virus
 Gambaran histologi : edema intersisial + infiltrasi
limfosit T dan monosit
 Tx : stop obat penyebab + kortikosteroid / sitotoksik
• ATN (Acute Tubuler Nephritis) :
 Penyebab
- Hipoperfusi – iskemia renal
- Zat Nefrotoksik ( endogen / eksogen )
Kombinasi ke-2 penyebab  sumbatan di tubulus proksimal
oleh mioglobin / hemoglobin
 Perjalanan Penyakit
1. Fase Oligouria ( < 24 jam : 150 – 300 cc/hr )
2. Fase Poliuria
- kreatinin terus naik dlm 24 – 48 jam berikut s/d flat
kmd turun + waspada : 25 % kematian pd fase ini
2. Fase Recovery
- serum kreatinin kembali mendekati nilai awal
Patofisiologi ATN
Oxidative stress during reperfusion after
ischemia is associated with cellular
damage
ALGORITMA AKI
Manajemen AKI
 Chronic Kidney Disease
• Definisi :
Kerusakan ginjal (sustained kidney damage) dg ditandai GFR <
60 mL/mnt/1.73 m2 dalam waktu ≥ 3 bulan
 A new classification system now includes
the cause of kidney disease (if known), the estimated GFR
(eGFR), and the level of albuminuria
Patofisiologi CKD : mekanisme progesivitas

• Defisit nefron ( sebab partial nefrektomi, BBLR, parenkimal injury )

– Predisposisi untyk terjadinya progresif renal disease dan
hipertensi
• Apoptosis
– e.c iskemia, toksin atau mediator endogen  renal damage 
renal mass reduction  Peningkatan Tekanan Hidrostatik
Glomerulus  Renal injury
– Mediator endogen : adanya “lethal factors” + tidak adanya
“survivor factors “
• Hiperfiltrasi ( respon thd berkurangnya massa nefron ) + Hipertensi +
Neurogenic factors  glomerulosclerosis + interstitial fibrosis :
angiotensi II + NO  aktivasi simpatis  hipertensi on CKD
Penyebab CKD
Manajemen CKD :
early detection – delay progression
Comprehensive Renoprotection Strategy
Kriteria Renal Replacement Therapy
Manajemen Pre Operative
• Assesment Resiko Pre Operative :
1. Patient-specific
2. Procedure-specific
3. Anesthesia-specific
• Parameter yg perlu diperhatikan :
– TD ≥ 180/110 mmHg  high risk for ischemic events
– FEV 1 < 1 L  high risk of complication ( low > 2 L )
– GDS < 200 mg/dL ( > 300 mg/dL  high risk of infection )
– Carefully with Hipoglycemia
– Avoided if Malnourished state ( albumin < 3.5 g/dL,
prealbumin < 30 mg/dL, skore assesment subyektif global
nutrisional < 5 )
 Acute on Chronic Kidney Disease
Patients with chronic kidney disease (CKD), as evidenced by a
low eGFR or presence of proteinuria, are at higher risk for
developing AKI, a condition known as acute on chronic kidney
disease (ACKD). CKD is a strong risk factor for cardiovascular
events, and patients with CKD are at particular mortality risk if
they develop ACKD.
 Tanda klinis
• Acidemia
• Hyperkalemia
• Volume/fluid overload
• Hypocalcemia/hyperphosphatemia (as a
consequence of secondary hyperparathyroidism)
• Hyponatremia
• Uremia (elevated BUN, platelet dysfunction,
changes in mental status, pericarditis)
Acute on Chronic Renal Failure Management
Terima Kasih