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Updated: May 9, 2026

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers
12:22

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers

Published on: January 22, 2013

Multi-target tyrosine kinase inhibitor-associated renal thrombotic microangiopathy: a pooled analysis of 31 cases

Miao Liu1, Xingchen Zhou2

  • 1Department of Pharmacy, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.

Frontiers in Pharmacology
|May 8, 2026
PubMed
Abstract

Insights

Multi-target tyrosine kinase inhibitors (TKIs) can cause renal thrombotic microangiopathy (TMA). Sunitinib is a high-risk TKI, and combination therapy accelerates TMA onset. Early detection and TKI withdrawal are crucial for patient outcomes.

Area of Science:

  • Oncology
  • Nephrology
  • Pharmacology

Background:

  • Multi-target tyrosine kinase inhibitors (TKIs) are crucial for solid tumors.
  • Renal thrombotic microangiopathy (TMA) is a severe adverse event associated with TKIs.
  • The precise relationship between TKIs and renal TMA requires further definition.

Purpose of the Study:

  • To delineate the clinical features of TKI-associated renal TMA.
  • To characterize the onset patterns of TKI-associated renal TMA.
  • To evaluate the outcomes of patients with TKI-associated renal TMA.

Main Methods:

  • Systematic literature search of PubMed, Embase, Cochrane Library, and Web of Science.
  • Inclusion of case reports and series of renal TMA linked to 7 multi-target TKIs.
  • Descriptive analysis of extracted clinical data.

Main Results:

  • Thirty-one cases of TKI-associated renal TMA were identified, with sunitinib being the most implicated agent.
  • The dominant clinical presentation included hypertension, acute kidney injury (AKI), and nephrotic proteinuria, with less common microangiopathic hemolytic anemia (MAHA).
  • While 90% of patients improved after TKI discontinuation, a significant proportion developed chronic kidney disease (CKD) or end-stage renal disease (ESRD).

Conclusions:

  • TKI-associated renal TMA typically manifests as hypertension, proteinuria, and AKI.
  • Sunitinib poses the highest risk, and combination TKI therapy can accelerate TMA onset.
  • Continuous patient monitoring and prompt TKI discontinuation are essential, despite the common occurrence of residual CKD.
Keywords:
adverse drug reactionhypertensionproteinuriarenal injurythrombotic microangiopathytyrosine kinase inhibitor

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