AKI Workup in Hematopoietic Stem Cell Transplant Conditioning
Immediately discontinue all nephrotoxic medications including calcineurin inhibitors (if feasible), aminoglycosides, amphotericin B, acyclovir, and NSAIDs, as each nephrotoxin increases AKI odds by 53% and these agents are major contributors to AKI in HSCT recipients. 1, 2
Initial Assessment and Staging
Stage AKI using KDIGO criteria based on serum creatinine and urine output to guide management intensity and prognosis 1:
- Stage 1: Creatinine 1.5-1.9× baseline or ≥0.3 mg/dL increase, or urine output <0.5 mL/kg/h for 6-12 hours 1
- Stage 2: Creatinine 2.0-2.9× baseline, or urine output <0.5 mL/kg/h for ≥12 hours 1
- Stage 3: Creatinine ≥3× baseline or ≥4.0 mg/dL, or urine output <0.3 mL/kg/h for ≥24 hours, or anuria for 12 hours 1
Measure serum creatinine daily during the conditioning period and for at least 7 days after AKI diagnosis, as AKI occurs at a mean of 19.4 days post-HSCT and early AKI (within 2 weeks) significantly increases mortality 1, 3.
Etiology-Specific Workup
Mandatory Initial Investigations
Obtain urinalysis with microscopy to detect hematuria, proteinuria, or abnormal sediment that would suggest glomerular disease, thrombotic microangiopathy (TMA), or BK virus nephritis 1, 4.
Check complete blood count with peripheral smear, LDH, haptoglobin, and indirect bilirubin to evaluate for TMA, which is a major cause of AKI in allogeneic HSCT and requires complement-directed therapy 2, 4.
Measure liver enzymes, bilirubin, and coagulation studies to assess for hepatic sinusoidal obstruction syndrome (SOS/VOD), which causes AKI through hepatorenal physiology 2, 3.
Obtain blood and urine cultures to identify sepsis, the most common cause of AKI in HSCT recipients 2, 3.
Additional Targeted Testing
Consider serum cystatin C measurement as it shows significant positive correlation with serum creatinine and negative correlation with creatinine clearance, and is independently associated with AKI development in HSCT recipients 5.
Perform renal ultrasound only if postrenal obstruction is suspected (rare in HSCT) or to exclude structural abnormalities 1.
Check BK virus and adenovirus PCR in urine and blood if urinalysis shows hematuria or if unexplained AKI persists, as these viruses cause specific renal manifestations in HSCT 4.
Hemodynamic and Volume Assessment
Reassess volume status and hemodynamic parameters including blood pressure, heart rate, jugular venous pressure, and presence of edema 1, 6.
Hold all diuretics immediately upon AKI diagnosis to prevent further renal hypoperfusion 1, 6.
Target mean arterial pressure ≥65 mmHg with isotonic crystalloid resuscitation if hypovolemia is present, avoiding starch-containing fluids which are associated with harm 6.
Use vasopressors (norepinephrine preferred over dopamine) if fluid resuscitation fails to restore adequate blood pressure 6.
Monitoring for Complications
Evaluate daily for fluid overload, metabolic acidosis, and hyperkalemia as these complications indicate potential need for renal replacement therapy 1, 6.
Monitor for graft-versus-host disease (GVHD) in allogeneic HSCT recipients, as acute GVHD is a major independent risk factor for AKI development 2, 3.
Assess for engraftment syndrome/cytokine storm which can manifest with fever, rash, pulmonary infiltrates, and AKI 4.
Nephrology Consultation
Obtain nephrology consultation when the etiology of AKI is unclear, when AKI persists beyond 48 hours despite initial management, or when subspecialist care is needed for conditions like TMA or GVHD-related kidney injury 1, 6.
Critical Pitfalls to Avoid
Do not use estimated GFR equations (MDRD, CKD-EPI) to assess kidney function in AKI, as these are inaccurate in the acute setting; instead use timed urine creatinine clearance for persistent AKI in steady state 1.
Avoid the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which dramatically increases AKI risk 1, 6.
Do not delay recognition that AKI within 48 hours of onset typically heralds rapid reversal, whereas persistent AKI beyond 48 hours frequently becomes acute kidney disease (AKD) and carries worse prognosis 1.
Recognize that allogeneic HSCT recipients have considerably higher AKI incidence (up to 85%) compared to autologous HSCT (28%) due to cyclosporine use and GVHD development 2, 3.
Understand that AKI requiring dialysis in HSCT carries >80% mortality, making prevention and early intervention paramount 7, 3.