KDIGO Definition of AKI ( 2012 )

Defined by any of the following:

 Increase in SCr by ≥0.3 mg/dL within 48 hours

 Increase in Scr by ≥1.5 times baseline, which is known or

presumed to have occurred within the prior seven days

 Urine volume <0.5 mL/kg/h for six hours

KDIGO Classification of AKI ( 2012 )
Stage Serum creatinine Urine output

1 1.5-1.9× baseline <0.5 ml/kg/hr for 6-12 hrs

OR
>0.3 mg/dL 
<0.5 ml/kg/hr > 12 hrs
2 2-2.9× baseline

3 3 times baseline <0.3 ml/kg/hr > 24 hrs

OR OR
increase in Cr to ≥4.0 mg/dL Anuria > 12 hrs
OR
Initiation of RRT

KDIGO Clinical Practice Guideline for AKI. Kidney Int 2012

 Prerenal AKI
 Intravascular volume depletion:
-bleeding, GI loss, Renal loss, Skin loss (burn), Third space loss, poor
oral intake (NPO, AMS, anorexia)

 Decreased effective circulating volume:

-congestive heart failure, cirrhosis, nephrotic syndrome, sepsis

 Decreased flow through renal artery:

-RAS or occlusion (compartment syndrome), hepatorenal syndrome,
hypercalcemia
-pharmacologic impairment (RAAS blocker, NSAIDs, CNI)
 Prerenal Azotemia Tx
 In early stages can be rapidly corrected by aggressive
normalization of effective arterial volume.

 Correction of volume deficits

 Optimization of cardiac function
 Discontinuation of antagonizing medications
 NSAIDs/COX-2 inhibitors
 Diuretics
 RAAS blockers
 Renal / Intrinsic AKI
 Tubule: ATN (sepsis, ischemic, toxins)
 Interstitium: AIN (Drug, infection, neoplasm)
 Glomerulus: AGN (primary, post-infectious,
rheumatologic, vasculitis, HUS/TTP)
 Vasculature:
 Atheroembolic dz, renal artery thromboembolism, renal artery
dissection, renal vein thrombosis
 Intratubular Obstruction
 myoglobin, hemoglobin, myeloma light chains,
uric acid, tumor lysis, drugs (bactrim, indinavir,
acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
 Acute Tubular Necrosis (ATN)
 Direct toxic Injury (20%)
 Sepsis (48%)
 Exogenous
 Ischemia (32%)  Radiocontrast
 prolonged prerenal azotemia  Aminoglycosides
 Vancomycin
 Hypotension  Amphotericin B
 hypovolemic shock  Cisplatin
 cardiopulmonary arrest  Acyclovir
 Calcineurin inhibitors
 cardiopulmonary bypass  HIV meds (tenofovir)
 Endogenous (pigment
nephropathy)
 Rhabdomyolysis
 Hemolysis
Postrenal AKI: Classification
 Level of obstruction
 Upper tract (ureters)
 Lower tract (bladder outlet or urethra)

 Degree of obstruction
 Partial vs. Complete

 Type
 Anatomic lesion (unilateral vs. bilateral)

 Functional

 Duration (Acute vs Chronic)

 Cause (Congenital vs Acquired)
Etiologies: Upper tract
obstruction
 Intrinsic:  Extrinsic:
 Nephrolithiasis  Retroperitoneal or pelvic
 Blood clot malignancy
 Papillary necrosis  Endometriosis/Prolapsed
 Cancer uterus
 Abdominal aortic
aneurysm or Iliac artery
aneurysm
 Retroperitoneal fibrosis
Etiologies: Lower tract
obstruction
 BPH or prostate cancer
 Bladder cancer
 Urethral strictures
 Bladder stones
 Blood clots
 Functional obstruction as a result of
neurogenic bladder
 Postrenal AKI tx
 Prompt recognition and relief of obstruction can prevent the
development of permanent structural damage.
 Lower tract obstruction (bladder catheter)
 Upper tract obstruction
 ureteral stents

 percutaneous nephrostomies

 Monitor for post-obstructive diuresis

 Recovery of renal function dependent upon duration of
obstruction.
 U/A, Urine protein/Cr, Urine Eosinophilla
 FeNa, FeUrea
 CPK, uric acid
 Urine microscopy:
 Muddy brown casts in ATN
 WBC casts in AIN
 RBC casts in AGN

 Post-void residual (>100-150 ml c/w voiding dysfunction)

 bladder catheterization
 renal ultrasound
Management of AKI: general principle

 No therapy to date have shown efficacy in treating

AKI.
 Identify the etiology and treat the underlying cause
 Optimization of hemodynamics to increase renal
perfusion
 Lack of benefit – low dose dopamine, loop diuretics
only if markedly fluid overload
 Identify and aggressively treat infection (early
removal of foley catheters, and minimize indwelling
lines)
Management of AKI:
treat complications
 Correct fluid imbalances: strict I/O’s, daily wts. determine
fluid balance goals daily, fluid selection or diuresis, readjust for
UOP recovery, post diuresis or dialysis
 Electrolyte imbalances (low K/phos diet, binder)
 Metabolic acidosis (Bicarb deficit, mode and rate of
replacement)
 Nutrition: adjust TPN/protein intake
 Medication dosing: adjustment for eGFR to avoid under or over
dosing, timing for dialytic therapy, reassess dosing for renal
recovery or dialysis modality)
 Procedural considerations (prefer non-contrast CT,
appropriate to delay contrast exposure, prophylaxis)