Tacrolimus toxicity in kidney transplant recipient after wedge liver resection: A case report and review of literature

Table 1 Approach to acute kidney injury after liver surgery

Conditions	Clinical clues
Renal hypoperfusion from intraoperative blood loss	Prolonged MAP < 65 mmHg, oliguria, history of large volume loss, improvement with fluids/transfusion
Abdominal compartment syndrome	Tense abdomen, rising airway pressures, refractory oliguria, large-volume resuscitation/bleeding/packing in major liver resection (IAH ≥ 12 mmHg; ACS > 20 mmHg + organ dysfunction)
Hepatorenal syndrome	Bland urine; no shock/nephrotoxins; no response after adequate volume resuscitation, low FENa, decompensated liver disease, usually with ascites
Ischemic ATI	Persistent creatinine rise with history of poor renal perfusion, granular casts, FENa > 2% (caution with diuretics), slow recovery, poor response to fluid resuscitation
Sepsis-associated AKI	Sepsis definition (based on Sepsis-3 criteria; infection + SOFA score) with AKI
Bile cast nephropathy	Marked cholestasis (total bilirubin usually > 20 mg/dL), bilirubinuria, bland or bile-pigmented casts
Nephrotoxic drugs (non-CNI)	Recent exposure: IV contrast, aminoglycosides, amphotericin, NSAIDs, etc. (also considered antibiotics or other drugs-associated AIN)
Acute CNI nephrotoxicity	Acute, dose-dependent afferent arteriolar vasoconstriction, temporal relation to high troughs, improves with dose reduction/cessation, biopsy rarely needed if rapid reversal

MAP: Mean arterial pressure; IAH: Intra-abdominal hypertension; ACS: Abdominal compartment syndrome; FENa: Fractional excretion of sodium; ATI: Acute tubular injury; AKI: Acute kidney injury; SOFA: Sequential Organ Failure Assessment; CNI: Calcineurin inhibitor; IV: Intravenous; NSAIDs: Non-steroidal anti-inflammatory drugs; AIN: Acute interstitial nephritis.