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Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS

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Published on: November 8, 2015

Temsirolimus-induced glomerulopathy.

Hassane Izzedine¹, Erfaneh Boostandoot, Jean Philippe Spano

¹Department of Nephrology, Pitié-Salpêtrière Hospital, Paris, France. hassan.izzedine@psl.ap-hop-paris.fr

|February 13, 2009

Summary

This summary is machine-generated.

Temsirolimus, a cancer drug, can cause significant proteinuria in patients with advanced renal cell carcinoma. Stopping the drug led to a notable decrease in protein loss, highlighting a potential kidney complication.

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Area of Science:

Nephrology
Oncology
Pharmacology

Background:

Advanced renal cell carcinoma (RCC) treatment often involves targeted therapies.
Temsirolimus is an mTOR inhibitor used in advanced RCC management.
Drug-induced kidney injury is a growing concern in cancer therapy.

Observation:

A 58-year-old male patient with advanced RCC developed severe proteinuria (8.5 g/24h) five days post-temsirolimus infusion.
The patient presented with proteinuria but no hematuria or renal insufficiency.
Kidney biopsy showed ischemic glomeruli and focal segmental glomerulosclerosis (FSGS).

Findings:

Temsirolimus administration was temporally associated with the onset of high-grade proteinuria.
Renal biopsy confirmed ischemic glomerular injury and FSGS, indicative of drug-induced nephrotoxicity.
Proteinuria significantly improved after temsirolimus discontinuation, decreasing to 2.80 g/day.

Implications:

Clinicians should monitor for proteinuria in patients receiving temsirolimus for advanced RCC.
Early recognition and withdrawal of temsirolimus may mitigate severe kidney damage.
This case underscores the importance of recognizing temsirolimus-induced nephropathy, specifically FSGS, in cancer patients.