Pembimbing: dr. B. Sidarto, Sp.

PD
diskusi
Acute Kidney Injury
Presentan:
Vanya Pratita S. (2009.061.115)
Jessica Fedriani (2009.061.204)
Yohanie Halim (2009.061.220)
Paulus Levin (2009.061.223)
Definition
ARF is defined as an abrupt or rapid decline in
renal filtration function.

This condition is usually marked by a rise in serum
creatinine concentration or by azotemia (a rise in
blood urea nitrogen [BUN] concentration)
Limitations:
Change in creatinine may not
correlate with change in GFR
Need to know baseline
creatinine.
No correlation between U/O
and Screat levels
Should exclude U obstruction
RIFLE Criteria
GFR and Creatinine
Epidemiology
Upon admission to hospital 1%
During hospitalization 2-5%
After Cardiopulmonary bypass. 5-15%


Hepatorenal Syndrome
AKI in Cirrhosis
Cardiorenal Syndrome Type 1
Sepsis and AKI
Etiologi (Renal)
Acute Tubular Necrosis (ATN)
ischemic or nephrotoxic tubular injury
tubulointerstitial diseases
diseases of the renal microcirculation
and glomeruli,
diseases of larger renal vessels
diseases of larger renal vessels
ATN
Part of a spectrum of manifestations of renal
hypoperfusion
Recovery typically takes 12 weeks after
normalization of renal perfusion
characterized by four phases:
initiation,
extension,
maintenance, and
recovery

Nefrotoxic ARF
Exogenous:
radiocontrast, -> intrarenal vasoconstriction
calcineurin inhibitors,
antibiotics (e.g., aminoglycosides), -> direct toxicity
and/or intratubular obstruction
chemotherapy (e.g., cisplatin),
antifungals (e.g., amphotericin B), -> intrarenal
vasoconstriction and direct toxicity
ethylene glycol
Endogenous:
rhabdomyolysis,
hemolysis
Acute interstitial nephritis
Nefrotoxic ARF (eksogenous)
accumulate in
renal tubular
epithelial cells
oxidative
stress and
cell injury
Damage in
both the
proximal and
distal tubule
Nefrotoxic ARF (endogenous)
Lysis
mioglobulin/
hemoglobin
Intrarenal
oxidative stress
injury to tubular
epithelial cells
and
inducing
intratubular cast
formation
Free cell
Hb/mioglobulin
potent inhibitors
of nitric oxide
bioactivity
intrarenal
vasoconstriction
and ischemia
AKI and Metabolic Acidosis
Anion Gap Metabolic Acidosis
Normal osmolal gap: salicylate and paraldehyde
Increased osmolal gap: methanol, ethanol,
isopropyl alcohol and ethylene glycol
Ethylene-glycol: calcium oxalate crystals
Etiology (Post-renal)


(bilateral, or unilateral in the case of one kidney):
calculi, blood clots, sloughed papillae, cancer,
external compression (e.g., retroperitoneal
fibrosis)
Ureteric
neurogenic bladder, prostatic hypertrophy,
calculi, blood clots, cancer
Bladder neck
stricture or congenital valves
Urethra
Clinical Assessment
Prerenal ARF
A : thirst and orthostatic dizziness;
initiation of treatment with diuretics, NSAIDs,
ACE inhibitors, ARBs
PF : orthostatic hypotension, tachycardia, JVP ,
skin turgor & dry mucous membranes;
stigmata chronic liver disease & portal hypertension

Nephrotoxic ATN
exposure nephrotoxic medications, radiocontrast agents,
endogenous toxins
fever, arthralgia, erythematous rash allergic
flank pain occlusion, distending renal capsule
subcutaneous nodules, livedo reticularis,
bright orange retinal arteriolar plaques,
"purple toes atheroembolization
ARF~ oliguria, edema hypertension, "active" urine sediment
acute glomerulonephritis / vasculitis
hypertension, papilledema, neurologic dysfuntion, LVH
hypertensive injury
Postrenal ARF
suprapubic & flank pain
colicky flank pain radiating to the groin
acute ureteric obstruction
nocturia, frequency, hesitancy,
enlargement prostate on RE prostatic disease
Initial diagnostic tools in AKI
Urinalysis, urine microscopy
Blood biochemistry
Radiology findings
Renal biopsy
Diagnosis: Urinary Indices


Fe Urea % <35 50 65
Fe Uric Acid % <7 >15
Fe Lithium % <7 >20
Calculation of FENa
UNa x PCr
FENa (%) = x 100
PNa x UCr
RBC cast
Hyaline cast Granular cast
Granular cast
Granular cast
WBC cast
WBC cast Oval fat body
and Hyaline cast
Diagnosis
Diagnosis: Ultrasound
R/O obstruction
Assess renal size and
parenchyma
Doppler (renal flow and
resistive index)
Normal < 0.7
High: intrarenal vascular
disease or arteriosclerosis,
ATN, urinary obstruction
and acute graft rejection.
Diagnosis: CT scan/MRI
Nephrolithiasis (non-contrast)
Pyelonephritis
Renal vein thrombosis
Assessment of renal arteries
Avoid gadolinium in GFR < 30 ml/min/1.73m
2

Biomarkers of AKI
Cystatin C - cysteine protease inhibitor
synthesized by all nucleated cells. It is freely
filtered by the glomerulus, reabsorbed
completely by tubules and not secreted.
Levels of cystatin C are not affected by gender, age,
race or muscle mass.
IL-18 - proinflammatory cytokine induced in
tubules and is detected in urine following AKI.
More specific for ischemic AKI and its levels are not
deranged in CKD, UTI or nephrotoxic AKI
Biomarkers of AKI
Kidney Injury Molecule-1 (KIM-1) - transmembrane
protein markedly overexpressed in PCT in response
to ischemic or toxic AKI.
Urinary KIM-1 helped to distinguish ischemic AKI from
prerenal azotemia and CKD
More spesific for ischemic and nefrotoxic AKI
Neutrophil gelatinase-associated lipocalin (NGAL)
- 25-kD protein massively released from renal tubular
cells after injury
Higher baseline NGAL - increased risk of worsening residual
renal function w/n 1 yr
Management of AKI
Treatment is largely supportive in nature
Pharmacologic treatments under study:
Dopamine: no benefit
Atrial Natriuretic Peptide (ANP) or ANP-analogue
(Anaritide): promising
Human Insulin like growth factor 1: no benefit
Renal Replacement therapy remains the
cornerstone of management of minority of
patients with severe AKI
Hypervolemia can usually be managed by restriction
of salt and water intake and diuretics.
Dopamin ineffective in clinical trials, may trigger
arrhythmias, and should not be used as a
renoprotective agent in this setting.
Ultrafiltration or dialysis is used to treat severe
hypervolemia when conservative measures fail.
Hyponatremia and hypoosmolality restriction of
free water intake.
hypernatremia administration of water or
intravenous hypotonic saline or isotonic dextrose-
containing solutions.

Metabolic acidosis oral or intravenous sodium
bicarbonate.
Hyperphosphatemia restriction of dietary
phosphate and by oral phosphate binders
(calcium carbonate, calcium acetate, sevalamer,
and aluminum hydroxide)
nutritional management sufficient calories and
protein to minimize catabolism.
Anemia may necessitate blood transfusion if
severe.
Recombinant human erythropoietin rarely used
Gastrointestinal prophylaxis with histamine
receptor (H2) antagonists or proton pump
inhibitors

Vasoactive drugs and AKI
Norepinephrine - in hypotensive vasodilated
patients with AKI, restoration of BP within
autoregulatory values should occur promptly
with NE.
Dopamine has no advantages over
norepinephrine.
Epinephrine and phenylephrine may be
similar in efficacy to noradrenaline limited
data
Epinephrine: associated with hyperglycemia,
hyperlactatemia, acidosis, and hypokalemia.
Terlipressin - useful in hepatorenal syndrome
Indication for dialysis
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