ACUTE KIDNEY INJURY

Define AKI

• Isolated oliguria: low urine output, stable creatinine
  • Often pre-renal, kidney is hypoperfused and compensates by reducing urine output
• Non-oliguric: elevated creatinine with normal urine output

KDIGO criteria

• Stage I AKI
  • Cr 1.5-1.9 times baseline.
  • Cr increase >0.3 mg/dL.
  • Urine output <0.5 ml/kg/hr for 6-12 hours.
• Stage II AKI
  • Cr 2-2.9 times baseline.
  • Urine output <0.5 ml/kg/hr for 12-24 hours.
• Stage III AKI 
  • Cr >3 times baseline.
  • Cr >4 mg/dL.
  • Initiation of dialysis.
  • Urine output <0.3 ml/kg/hr for >24 hours.
  • Anuria >12 hours.

Evaluate the cause

• Labs: electrolytes (including Ca/Mg/Phos), CK, UA
• Renal & bladder ultrasound to exclude hydronephrosis

Causes of AKI

• Pre-renal:  disorders of perfusion
  • Shock of any etiology (e.g., hypovolemic shock, cardiogenic shock).
  • Hepatorenal syndrome.
  • Congestive nephropathy (systemic congestion impairs venous outflow).
  • Abdominal compartment syndrome.
  • Hypertensive emergency.
  • Thrombotic thrombocytopenic purpura & hemolytic uremic syndrome.
• Intrinsic renal failure
  • Nephrotoxic medications
    • Antibiotics: Vancomycin, aminoglycosides, amphotericin, sulfonamides
    • Antivirals: -acyclovirs
    • ACEI/ARBs
    • NSAIDs
    • Antihypertensives if hypotensive
    • Many chemo drugs
  • Cellular lysis (rhabdomyolysis, hemolysis, tumor lysis syndrome).
  • Acute glomerulonephritis.
  • Acute tubulointerstitial nephritis (ATIN).
  • Acute tubular necrosis (ATN).
• Post-renal:  Urologic obstruction
  • Prostate obstruction.
  • Occluded or malpositioned Foley catheter.
  • Nephrolithiasis.

FeNa

• Recent evidence shows it is actually not helpful in differentiating pre-renal vs. intrinsic renal failure. Nevertheless, here it is in case you are stubborn (FeNa>2%= intrinsic renal failure, FeNa<1%= pre-renal failure)

---

If a patient is taking diuretics, the FeUrea is more accurate as they are iatrogenically spilling sodium into their urine

---

Approach to the oliguric patient (<0.5cc/kg/hr)

1. Exclude obstruction with bedside ultrasound
2. Hemodynamic eval- VS trends, BP  meds, cardiac history, bolume status, HYPERtension (can cause intrinsic dx)
3. Volume challenge?- If hypovolemic
4. Vasopressor challenge?- if MAP <65
5. Inotrope challenge?- If very poor cardiac output
6. Furosemide stress test- 1-1.5mg/kg furosemide, >200mL urine output within 2h indicates good response (if poor response, suggest renal failure and potential need for dialysis)

---

Treatment

Hemodynamics are key

• MAP: Want MAP>65mm for most patients, but MAP>80mm in chronic hypertensives
• Maintain euvolemia: generally avoid fluids, if they are non-oliguric then they aren't hypoperfusing. Give fluids only if undeniable evidence they are hypovolemic
• Avoid volume overload: leads to intra-capsular edema in the kidney that worsens perfusion (like compartment syndrome) + venous backflow congestion
  • Diurese if needed
• Phosphate Binder: Initiate if phosphate >6mg/dL with calcium acetate (667mgx2 TID) or sevalamer (800mg PO TID)
• Dialysis indications: acidosis refractory to IV bicarb, electrolyte abnormalities (hyperkalemia), fluid overload refractory to diuretics, uremic symptoms (delirium, asterixis, pericardial effusion)

Best fluids?

• Hypovolemia and uremic acidosis: isotonic bicarbonate (D5W w/ 150mEq/L sodium bicarb)
  • Shoot for pH>7.2, bicarb level ~17
• Hypovolemia and normal serum bicarbonate: Lactated Ringers

Dialysis disequilibrium syndrome

• Rapid reduction in BUN levels--> osmotic shifts--> cerebral edema
• Management: Dialysate with higher sodium concentrations, hypertonic saline to reverse cerebral edema