Authors
Lan Anh Thi Ke, Anh Ngoc Nguyen, Nguyet Minh Pham, Linh Phuong Dang, Hai Yen Thi Tran, Quan Duy Vo
Published in
Kidney diseases (Basel, Switzerland). Volume 12. Issue 1. Pages 693-710. Epub Jun 18, 2026.
Abstract
Kidney disease is a major global health burden with limited regenerative treatment options. Induced pluripotent stem cells (iPSCs) offer patient-specific pluripotency and the potential to generate renal cells and organoids, making them a promising approach for kidney repair.
A systematic literature search was conducted in PubMed, ScienceDirect, Web of Science, and Cochrane Library for peer-reviewed studies investigating the therapeutic application of iPSCs in kidney disease up to February 2026. Risk of bias was assessed using the SYRCLE tool. Random effects meta-analyses were performed, and subgroup and meta-regression analyses were conducted to explore potential sources of heterogeneity.
In this search, 23 preclinical studies encompassing 372 animals met the inclusion criteria, and no eligible human trials were identified. iPSC-based therapy was associated with reduced mortality (OR = 0.17; 95% CI: 0.05-0.52; p = 0.002) and improvements in blood urea nitrogen, serum creatinine, and histological injury scores. Subgroup and meta-regression analyses suggested that therapeutic response was influenced by biological factors, including cell type, disease model, delivery route, and treatment conditions. Notably, stronger effects were observed in acute kidney injury models and with direct iPSC-based interventions. However, substantial heterogeneity was observed across most renal outcomes (I 2 > 90%), indicating considerable variability among studies.
iPSC-based therapy demonstrates beneficial effects in experimental kidney disease, particularly in acute models. However, the high degree of heterogeneity, potential risk of bias, and limited safety data constrain the reliability and generalizability of these findings. Further optimization of therapeutic strategies and rigorous long-term safety evaluations are required to support clinical translation.
PMID:
42553915
Bibliographic data and abstract were imported from PubMed on 05 Aug 2026.
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