# Late-Onset Normotensive Thrombotic Microangiopathy and Pyoderma Gangrenosum Following Nine Years of Sunitinib Therapy: A Case Report

**Authors:** Ryosuke Saiki, Kan Katayama, Makiko Yajima, Takeshi Sasaki, Yuri Oue, Tomohiro Murata, Kaoru Dohi

PMC · DOI: 10.1016/j.xkme.2026.101298 · Kidney Medicine · 2026-02-13

## TL;DR

A woman developed rare side effects from a cancer drug nine years after starting treatment, showing the need for long-term monitoring.

## Contribution

This case report highlights the longest latency period for sunitinib-induced thrombotic microangiopathy and pyoderma gangrenosum.

## Key findings

- Thrombotic microangiopathy and pyoderma gangrenosum occurred after 9 years of sunitinib therapy.
- Symptoms improved after discontinuing sunitinib, confirming a causal relationship.
- Thrombotic microangiopathy presented without hypertension, challenging typical diagnostic assumptions.

## Abstract

Sunitinib, a tyrosine kinase inhibitor used for metastatic renal cell carcinoma, is associated with various adverse effects. We present the case of a 60-year-old woman who developed biopsy-proven thrombotic microangiopathy and concurrent pyoderma gangrenosum after 9 years of sunitinib therapy. This case is unusual due to the extremely delayed onset of both rare toxicities. Furthermore, the thrombotic microangiopathy presented without hypertension, a typical preceding sign, which made the diagnosis challenging. The patient initially presented with a painful leg ulcer, diagnosed as pyoderma gangrenosum, and was subsequently found to have significant proteinuria and edema. A kidney biopsy confirmed thrombotic microangiopathy. Upon discontinuation of sunitinib, both the proteinuria and the pyoderma gangrenosum lesions improved significantly, confirming a causal relationship. This case represents the longest reported latency period for both sunitinib-induced thrombotic microangiopathy and pyoderma gangrenosum. It underscores the critical need for sustained clinical vigilance for severe, late-onset adverse events at any point throughout long-term sunitinib treatment and demonstrates that clinicians cannot rely solely on hypertension as a predictive marker for thrombotic microangiopathy.

## Linked entities

- **Chemicals:** sunitinib (PubChem CID 5329102)
- **Diseases:** thrombotic microangiopathy (MONDO:0019737), pyoderma gangrenosum (MONDO:0018824)

## Full-text entities

- **Genes:** TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}
- **Diseases:** proteinuria (MESH:D011507), Pyoderma Gangrenosum (MESH:D017511), leg ulcer (MESH:D007871), hypertension (MESH:D006973), renal cell carcinoma (MESH:D002292), edema (MESH:D004487), Thrombotic Microangiopathy (MESH:D057049), painful (MESH:D010146), toxicities (MESH:D064420)
- **Chemicals:** Sunitinib (MESH:D000077210)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12992925/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12992925/full.md

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Source: https://tomesphere.com/paper/PMC12992925