Acute Kidney Injury

Syakib Bakri
 Kasus 1
 12 orang selamat dari perahu yang tenggelam di
lautan. Setelah 3 hari terkatung-katung, semuanya
langsung di bawa ke RS Wahidin. Di IGD rata-rata
tekanan darah 90-100mmHg.
 Terdapat tanda-tanda dehidrasi. Dari pemeriksaan
laboratorium didapatkan Ureum 80-130 mg/dl.
Creatinin 1,9 – 3,6 mg/dl.
 Diagnosa ?
 Terapi ?
 Kasus 2
 Dr. PS, 50 tahun dikirim dari ambon dengan
oligouria dan peningkatan ureum creatinin.
 Sebelumnya ada kolik dan hematuria,
pernah kencing batu.
 Tekanan darah 170/100
 Anemis tidak ada, lain-lain normal
 Ureum 120mg/dl, creatinin 6 mg/dl
 Diagnosa?
 Penatalaksanaan Lanjutan?
 Kasus 3

 Laki-laki 27 tahun dikirim dari RS Bhayangkara

dengan sesak napas. Selama disana, pasien dirawat
dengan GEA & Oliguria.
 Fisis: Sesak, Tidak anemis, Rhonkhi difus kedua
paru,
 Thorax Foto: terdapat tanda edema paru
 Lab: Kreatinin 4,1mg/dl, Ureum 207 mg/dl,
Volume urin 300cc/24jam
 Diagnosa? Terapi?
 Kasus 4

 Dr. MA 60 tahun tiba-tiba oliguria

 Sebelumnya tidak ada riwayat batu ginjal
 Riwayat DM ada, HT ada. Sebelumnya
pernah diberi obat TB.
 Fisis: TD 140/80 mmHg, Anemis tidak ada,
lain-lain normal
 Diagnosa ? Pemeriksaan dan
penatalaksanaan lanjutan ?
 Acute Kidney Injury

• An abrupt and sustained decrease (days to weeks) in renal function

resulting in retention of nitrogenous (urea and creatinine) and non-
nitrogenous waste products.
Depending on severity and duration of the renal dysfunction, this
accumulation is accompanied by metabolic dysturbance, such as
metabolic acidosis and hyperkalaemia, changes in body fluid balance,
and effects on many other organ systems.
 Classified as

 Non oliguric : urine output > 400 ml / day

 Oliguric : urine output < 400 ml / day ; Anuric :

urine output < 100 ml / day
 Acute Kidney Injury

 Definitions
 Azotemia - the accumulation of nitrogenous
wastes
 Uremia - symptomatic kidney failure
 Oliguria - urine output < 400 mL/24 hours
 Anuria - urine output < 100 mL/24 hours
 AKI Criteria
AKI Stage Urine Output KDIGO AKIN RIFLE
1 <0.5 mL/kg/h for Scr to 1.5-1.9 × Scr to 1.5-2 × Risk: Scr to ≥1.5 ×
6-12 h baseline over 7 d baseline or ≥0.3 increase within 7
or≥0.3 mg/dL mg/dL absolute d, sustained for
absolute increase Scr increase ≥24 h
over 48 h within 48 h
2 <0.5 mL/kg/h for Scr to 2.0-2.9 × Scr to >2-3 × Injury: Scr to ≥2 ×
≥12 h baseline baseline increase
3 <0.3 mL/kg/h for Scr to ≥3.0 × Scr to >3.0 × Failure: Scr to
≥24 h or anuria baseline, or Scr baseline, or Scr ≥3.0 × increase or
for ≥12 h increase to ≥4.0 increase to ≥4.0 Scr increase to
mg/dL or mg/dL (with ≥4.0 mg/dL (with
initiation of RRT increase of 0.5 increase of 0.5
mg/dL) or mg/dL) or
initiation of RRT initiation of RRT
Loss: Complete
loss of kidney
function for >4 wk
ESKD: ESKD for >3
mo
 EPIDEMIOLOGY

• 1% of hospitalized patients
• 20% of patients treated in ICU
• 4-15% of patients after cardiovascular surgery
 Manifestations of AKI

 Azotemia progressing to uremia

 Hyperkalemia
 Metabolic acidosis
 Volume overload
 Hyperphosphatemia
 Accumulation and toxicity of medications
excreted by the kidney
 Classification of AKI (ARF)
Acute Kidney Injury

55% 40% 5%

Pre-renal Intrinsic Post-renal

Glomerular Interstitial Tubular Vascular

<5% 10% 85% <5%
 ACUTE KIDNEY INJURY

PRERENAL

Absolute decrease in effective blood volume

Haemorrhage
Volume depletion

Relative decrease in blood volume (ineffective arterial volume)

Congestive heart failure, Shock, Sepsis
Decompensated liver cirrhosis
Arterial occlusion or stenosis of renal artery

Haemodynamic form
NSAIDs,
ACE-inhibitors or angiotensin-II
receptor antagonists in renal-artery
stenosis or congestive heart failure, hepatorenal syndrome
Hypovolemia Baroreceptor activation Reduced affective
circulation volume

↑ Respons neurohormonal

↑ Axis renin-angiotensin ↑ Vasopressin ↑ Sympathetic nervous system

aldosterone

↑ Vasoconstriction
↑ contraction of mesangial cells
↑ Reabsorpsi natrium and water

Reduced renal blood flow and glomerular filtration rate

Acute Kidney Injury pre-renal
 Prerenal AKI:
Clinical Presentation

 History
 volume loss (e.g., diarrhea, acute blood loss)
 heart disease
 liver disease
 evidence of infection
 diuretic use
 thirst
 orthostatic symptoms
 Prerenal AKI:
Clinical Presentation

 Physical Examination
 Blood pressure and pulse
 Orthostatic changes in blood pressure
 Skin turgor
 Dryness of mucous membranes and axillae
 Neck veins
 Cardiopulmonary exam
 Peripheral edema
 Prerenal AKI:
Clinical Presentation
 BUN:Creatinine ratio
 > 20:1
 Urine indices
 Oliguria
– usually < 500 mL/24 hours; but may be non-oliguric
 Elevated urine concentration
– UOsm > 700 mmol/L
– specific gravity > 1.020
 Evidence of high renal sodium avidity
– UNa < 20 mmol/L
– FENa < 0.01
 Inactive urine sediment
 Treatment of
Prerenal AKI

 Correction of volume deficits

 Discontinuation of antagonizing medications
 NSAIDs/COX-2 inhibitors
 Diuretics

 Optimization of cardiac function

 ACUTE KIDNEY INJURY

POSTRENAL

Obstruction of collecting system or

extrarenal drainage

Bladder-outlet obstruction
Bilateral ureteral obstruction or
unilateral in one functioning kidney
 Postrenal AKI

 Urinary tract obstruction

 level of obstruction
– upper tract (ureters)
– lower tract (bladder outlet or urethra)
 degree of obstruction
– partial
– complete
 Etiologies of Postrenal
AKI

 Upper tract obstruction  Lower tract obstruction

 Intrinsic – benign prostatic
– nephrolithiasis hypertrophy
– papillary necrosis – prostate cancer
– blood clot – transitional cell cancer
– transitional cell cancer – urethral stricture
 Extrinsic – bladder stones
– retroperitoneal or pelvic – blood clot
malignancy – neurogenic bladder
– retroperitoneal fibrosis
– endometriosis
– abdominal aortic
aneurysm
 Postrenal AKI:
Clinical Presentation

 History
 Symptoms of bladder outlet obstruction
– urinary frequency
– urgency
– intermittency
– hesitancy
– nocturia
– incomplete voiding
 Postrenal AKI:
Clinical Presentation

 History
 Changes in urine volume
– anuria
– polyuria
– fluctuating urine volume
 Flank pain
 Hematuria
 History of pelvic malignancy
 Postrenal AKI:
Clinical Presentation

 Physical Examination
 Suprapubic mass
 Prostatic enlargement
 Pelvic masses
 Adenopathy
 Postrenal AKI:
Clinical Evaluation

 Diagnostic studies
 BUN: Creatinine ratio > 20:1
 Unremarkable urine sediment
 Variable urine chemistries
 Postrenal AKI:
Clinical Evaluation

 Diagnostic studies
 Post-void residual bladder volume
– > 100 mL consistent with voiding dysfunction
 Radiologic studies
– Ultrasound
– CT scan
– Nuclear medicine
– Retrograde pyelography
– Antegrade nephrostograms
 Treatment of
Postrenal AKI

 Relief of obstruction
 Lower tract obstruction
– bladder catheter
 Upper tract obstruction
– ureteral stents
– percutaneous nephrostomies
 Recovery of renal function dependent upon
duration of obstruction
 Risk of post-obstructive diuresis
 ACUTE KIDNEY INJURY

INTRINSIC RENAL

Vascular Glomerulo Acute interstitial Acute tubular

Vasculitis, nephritis nephritis necrosis
Malignant HT Drugs
Allergy

Ischaemic (50%)
Nephrotoxic (35%)

Exogenous Endogenous
Antibiotics (gentamicin) Intratubular pigments (haemoglobinuria,
Radiocontrast agents myoglobinuria)
Cisplatin Intratubular proteins (myeloma)
Intratubular crystals (uric acid, oxalate)
 Acute Tubular Necrosis

 Ischemic  Nephrotoxic
– prolonged prerenal  drug-induced
azotemia – radiocontrast agents
– hypotension – aminoglycosides
– hypovolemic shock – amphotericin B
– cardiopulmonary – cisplatinum
arrest
– acetaminophen
– cardiopulmonary
 pigment nephropathy
bypass
– hemoglobin
 Sepsis
– myoglobin
 Acute Tubular Necrosis:
Clinical Presentation
 History
 Acute illness
 Exposure to nephrotoxins
 Episodes of hypotension
 Physical examination
 Hemodynamic status
 Volume status
 Features of associated illness
 Laboratory data
 BUN:Creatinine ratio < 10:1
 Evidence of toxin exposure
 Acute Tubular Necrosis:
Clinical Presentation
 Urine indices
 Urine volume
– may be oliguric or non-oliguric
 Isosthenuric urine concentration
– UOsm  300 mmol/L
– specific gravity  1.010
 Evidence of renal sodium wasting
– UNa > 40 mmol/L
– FENa > 0.02
 Urine sediment
– tubular epithelial cells
– granular casts
 Acute Tubular Necrosis:
Treatment

 Supportive therapy
 No specific pharmacologic treatments
 Acute dialysis for:
 volume overload
 metabolic acidosis
 hyperkalemia
 uremic syndrome
– pericarditis
– encephalopathy
 azotemia
 Prognosis of
Acute Tubular Necrosis

 Mortality dependent upon comorbid conditions

 overall mortality ~ 50%
 Recovery of renal function seen in ~ 90% of
patients who survive - although not necessarily
back to prior baseline renal function
 Acute Interstitial Nephritis

 Acute renal failure due to lymphocytic

infiltration of the interstitium
 Classic triad of
 fever
 rash
 eosinophilia
 Acute Interstitial Nephritis

 Drug-induced  Infection-related
 penicillins  bacterial
 cephalosporins  viral
 sulfonamides  rickettsial
 rifampin  tuberculosis
 phenytoin  Systemic diseases
 furosemide  SLE
 NSAIDs  sarcoidosis
 Malignancy  Sjögren’s syndrome
 Idiopathic  tubulointerstitial nephritis
and uveitis
 Acute Interstitial Nephritis:
Clinical Presentation

 History
 preceding illness or drug exposure
 Physical examination
 fever
 rash
 Laboratory Findings
 eosinophilia
 Acute Interstitial Nephritis:
Clinical Presentation

 Urine findings
 non-nephrotic protinuria
 hematuria
 pyuria
 WBC casts
 eosinophiluria
 Acute Interstitial Nephritis:
Treatment

 Discontinue offending drug

 Treat underlying infection
 Treat systemic illness
 Glucocorticoid therapy may be used in patients
who fail to respond to more conservative therapy
 Acute Glomerulonephritis

 Nephritic presentation
 proteinuria
– may be in nephrotic range (> 3 g/day)
 hematuria
 RBC casts
 Diagnosis usually requires renal biopsy
 Acute Glomerulonephritis

 Etiologies
 poststreptococcal glomerulonephritis
 postinfectious glomerulonephritis
 endocarditis-associated glomerulonephritis
 systemic vasculitis
 thrombotic microangiopathy
– hemolytic-uremic syndrome
– thrombotic thrombocytopenic purpura
 rapidly progressive glomerulonephritis
 Acute Vascular Syndromes

 Renal artery thromboembolism

 Renal artery dissection
 Renal vein thrombosis

 Atheroembolic disease
 Intratubular Obstruction

 Intratubular crystal deposition

 tumor lysis syndrome
– acute urate nephropathy
 ethylene glycol toxicity
– calcium oxylate deposition
 Intratubular protein deposition
 multiple myeloma
– -Bence-Jones protein deposition
 Diagnostic Evaluation of ARF

Form of ARF BUN:Cr UNa (mEq/L) FENa Urine Sediment

Prerenal >20:1 <20 < 1% Normal

Postrenal >20:1 >20 variable Normal or RBC’s
Intrinsic
ATN <10:1 >40 > 2% Muddy brown casts;
tubular epithelial cells
AIN <20:1 >20 >1% WBC’s WBC casts,
RBC’s, eosinophils
AGN variable <40 <1% RBC’s, RBC casts

Vascular variable >20 variable Normal or RBC’s

 AKI: Management

 Indications for dialysis

 volume overload
 metabolic acidosis
 hyperkalemia
 uremic syndrome
– pericarditis
– encephalopathy
 azotemia
Thank You