QW50-August 2025

Question: Select each option to validate with explanations

Clinical Case Scenario

A 65-year-old patient is 3 weeks post-double lung transplantation. He presents with a rapid rise in serum creatinine (from baseline 0.9 mg/dL to 2.8 mg/dL over 5 days). Urine output remains adequate. His immunosuppression regimen includes tacrolimus (trough level 18 ng/mL), mycophenolate mofetil, and prednisone. In view of decline in post transplant pulmonary function test values, the patient underwent a CT angiogram of thorax. He has also developed a new onset dry cough with lethargy and irritability.

On examination he is conscious, alert. Vital parameters as:

HR: 84/min

BP:128/76 mmHg

RR: 16/min

Temp: 37 C

Chest X-ray shows no acute pathology.

Lactate: 1.4 mmoL/L

Urinalysis shows:

Protein +

Sugar Absent

Ketone Absent

Nitrite Absent

Pus cells 1-2

RBCs Nil

Casts Nil

Crystals Nil

Epithelial cells Absent

Question: What is the MOST likely cause of his acute kidney injury?

A. Sepsis-induced AKI

B. Tacrolimus nephrotoxicity

C. Radiocontrast nephropathy

D. Volume depletion

Wrong Answer: A. Sepsis-induced AKI: Contradicted by: Afebrile status, stable vitals, normal chest X-ray, lack of leukocytosis. Sepsis is common post-transplant but unlikely without supporting evidence.

Right Answer: B. Tacrolimus nephrotoxicity: Strongest link: Elevated tacrolimus trough (18 ng/mL) exceeds typical target ranges (usually 8-12 ng/mL early post-transplant)#, directly linking to nephrotoxicity. Classical Presentation: Asymptomatic rise in creatinine, mild proteinuria, absence of other clear triggers. Timing: Common in the early post-transplant period during intense immunosuppression.

Clinical Pearls

1. Calcineruin Inhibitors (CNIs) are a major culprit: Tacrolimus/Cyclosporine nephrotoxicity is a leading cause of AKI in solid organ transplant recipients.
2. Therapeutic drug monitoring is crucial: High trough levels strongly suggest toxicity.
3. Clinical context matters: Absence of fever, hypotension, or overt volume depletion helps rule out alternatives.
4. Urinalysis pattern: Mild proteinuria without active sediment (casts, cells) is typical for CNI toxicity, unlike ATN (granular casts) or GN (dysmorphic RBCs, casts).
5. Timeline: Contrast nephropathy has a characteristic timeframe; AKI weeks post-op points strongly to drugs or late infections.

Wrong Answer: C. Radiocontrast nephropathy: Timing: Typically peaks 24-72 hours post-contrast; presentation at day 4 is less classic. Risk: Less likely with stable renal function at time of contrast and adequate hydration. Severity: Rarely causes such a marked rise without other risk factors.

Wrong Answer: D. Volume depletion: Contradicted by: Adequate urine output, stable vital signs (especially normotension), and lack of clinical signs (e.g., dry mucous membranes, low JVP).

Reference:

1. Karkal CR, Shetty DD, Amzajerdi SH, Pasumarthi T, Nagaraju SP, Prabhu RA, Mallayasamy S. Therapeutic drug monitoring of tacrolimus in kidney transplant patients: Insights from an Indian tertiary care clinical setting. J Appl Pharm Sci. 2025;15(05):156–162.

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