Acute Kidney Injury (AKI)¶

Terra Swanson

Background:¶

Definition based on 2012 KDIGO Guidelines:
- Rise in serum creatinine (sCr) > 0.3 mg/dL within 48 hours, or increase > 1.5 x baseline in 7 days
- Urine volume \<0.5 cc/Kg/H for at least 6 H

Pre-renal/hemodynamic AKI:
- Volume depletion: GI losses, hemorrhage, burns, critical illness increased insensible losses
- Decreased effective circulating volume: cardiorenal, hepatorenal, hemodynamic effects of ACEi/ARB
- Afferent arteriole constriction [NSAIDs, Iodinated contrast]
- Renal vein thrombus
Intra-renal: Glomerular, tubular, or interstitial diseases
- ATN = Most common form of intrinsic AKI. Can be Ischemic or toxic
  - Toxins can be broken down further into endogenous (e.g. rhabdo) and exogenous (e.g. drugs)
- Acute Interstitial Nephritis (AIN): Usually drug induced (NSAIDs, PPIs, beta lactam abx)
- Glomerulonephritis
- Other causes:
  - Crystalline nephropathy: IV acyclovir, tumor lysis, ethylene glycol
  - Small vessel disease: MAHA, TTP, HUS
  - Large vessel disease: Aortic dissection, renal artery stenosis
Post-renal: Can occur at any level of the GU system
- Ureteral: stones, external compression (malignancy, LAD, abscess)
- Bladder: neurogenic bladder, malignancy, obstructing blood clot
- Urethra: BPH, prostate cancer, prostatitis
Pre-renal azotemia and acute tubular necrosis comprise the majority of inpatient acute kidney injuries

History and volume exam
Labs: CMP, urinalysis, protein/Cr ratio
500cc-1L IV fluid challenge: If sCr improves to baseline in \<48H then the insult was likely pre-renal. If not, then look for other etiologies
Evaluate for obstruction: I/O cath, Foley, Post Void Residual >250 cc
Who needs a renal ultrasound?
- No obvious cause of AKI
- Abrupt oliguria or anuria (think renal vein thrombus or obstruction)
- High suspicion for bladder outlet obstruction (PVRs might give you same data)
- Add doppler to evaluate for renal artery stenosis (or if working up resistant hypertension)
Urine Electrolytes
- FENa \<1% or FEUrea \<33% (if on diuretics) suggest pre-renal physiology
- Caveat, only validated in oliguric patients and more difficult to interpret after fluids, diuretics, etc
- Not needed in the initial work-up of all patients with AKI. If high suspicion for pre-renal etiology, trial fluid challenge and assess response first
Urine sodium can be used to assess Na avidity: UNa > 40 suggests ATN and UNa \< 20 suggests pre-renal

All causes
- Minimize fluctuations in blood pressure
- Consider holding anti-hypertensive medications, especially ACEi/ARB (remember to determine plan to resume at/after discharge)
- Avoid unnecessary nephrotoxins
- Dose-adjust medications for changing renal function
Pre-Renal
- True volume depletion- Intravenous volume expansion
- Cardiorenal syndrome- Decongestion/diuresis
- Hepatorenal syndrome- See Hepatology section for more information
Post-renal
- Relieve Obstruction: I/O cath, foley, Urostomy (Urology), percutaneous nephrostomy (IR)
- Monitor for post-obstructive diuresis
Intra-renal
- ATN- supportive care, monitor for post-ATN diuresis. If delayed recovery, may need outpatient dialysis
- Glomerulonephritis- Consult AKI service for assistance with biopsy and selecting immunosuppressive agents if needed
- AIN- Review meds, consult nephrology for possible biopsy and recommendations for steroids
Monitor for renal recovery
- Suspect concomitant ATN if sCr declines with volume expansion, diuresis, or relief of obstruction but remains a few points above baseline
When to consult Nephrology
- Urgent indication for dialysis (see “Renal Replacement Therapy”)
- Abrupt anuria
- Cr worsening or urine output inadequate w/o clear cause
- Need for kidney biopsy

Rhabdomyolysis: UA positive for blood but no RBCs on microscopy
- Toxic damage due to myoglobin
- Serologic markers of muscle injury: elevated CK, AST>AST with normal ALK Phos
- Fluids adjusted to urine output goal of 200-300 mL/hr until CK declines
  - Consider isotonic bicarb for initial 1-2L of IVF urine alkalinization to reduce precipitation
- Avoid calcium repletion for hypocalcemia unless symptomatic
Post-obstructive diuresis
- Necessary process to clear accumulated uremic toxins
- Replace ~50% of urine output to prevent pre-renal azotemia
- Monitor calcium, phosphorus, and magnesium in severe post-obstructive diuresis

Trey Richardson

When someone develops an AKI do your due diligence and evaluate for the usual causes of AKI, regardless of when they were given contrast
Mechanism of injury: direct toxic effect leading to tubular necrosis and arteriolar vasoconstriction leading to medullary ischemia

sCr increase by 0.5mg/dl or 25% increase in sCr from baseline 48 H after radiologic procedure where intravenous contrast was administered

Normal kidney function: incidence of CI-AKI is 1-3%
Pre-existing CKD: Incidence of CI-AKI may be as high as 20% in patients with CKD 4-5
Other risk factors include: diabetes, heart failure, and advanced age
No real sCr or eGFR threshold below which iodinated contrast is contraindicated, especially in patients for whom imaging will alter management (e.g. acute stroke, PE, STEMI)

Volume expansion with isotonic crystalloid (PRESERVE Trial) in patients with AKI or eGFR \<30 ml/min/1.73m^2 who are clinically hypo or euvolemic
- 1cc/kg/hr for 6-12 hours before/during and 6-12 hours after the procedure in patients at high risk for CI-AKI. This rate can be decreased based on the risk for hypervolemia
If the patient is volume overloaded, they probably should not receive volume expansion prior to a contrasted study
Never delay a necessary procedure out of concern for worsening renal function. If in doubt, talk to nephrology

Iodinated contrast does not need to be dialyzed immediately
Avoid giving if you are trying to preserve residual kidney function in ESRD on PD

Contraindicated in any AKI or if GFR \<30 in CKD given risk of nephrogenic systemic fibrosis.