# Microfluidic innovations in chronic kidney disease and renal fibrosis: from mechanistic insights to clinical applications

**Authors:** Anqi Liu, Kun Xiao, Hongli Lin

PMC · DOI: 10.3389/fmed.2026.1723501 · Frontiers in Medicine · 2026-02-10

## TL;DR

Microfluidic technology offers new ways to study and treat chronic kidney disease and renal fibrosis by enabling better models, diagnostics, and therapies.

## Contribution

This review highlights how microfluidics advances mechanistic understanding, diagnostics, and therapies for CKD and fibrosis.

## Key findings

- Organ-on-a-chip systems replicate key CKD pathophysiology with higher resolution than traditional models.
- Microfluidic biosensors enable non-invasive, high-sensitivity detection of CKD biomarkers.
- Integration with AI and multi-omics improves data interpretation and personalized therapy design.

## Abstract

Chronic kidney disease (CKD) and renal fibrosis remain major global health burdens, with limited options for early diagnosis and effective therapy. Conventional approaches, such as kidney biopsy and imaging, are invasive or insensitive to early-stage changes. Microfluidic technology has emerged as a transformative platform that enables precise modeling of renal microenvironments, sensitive biomarker detection, and physiologically relevant drug testing. This review evaluates recent advances in microfluidics for CKD and fibrosis, with emphasis on mechanistic insights, diagnostic innovations, and therapeutic strategies.

Mechanistic studies using organ-on-a-chip systems, including glomerulus- and tubule-on-a-chip, have replicated critical pathophysiological processes such as proteinuria-induced podocyte injury, epithelial–mesenchymal transition, FAO dysregulation in tubular cells, and immune cell-mediated inflammation. These models provide superior resolution compared with 2D culture or animal models and have identified novel fibrotic pathways—how they work: by perfusing media through microchannels to simulate shear stress; advantages: dynamic real-time monitoring; disadvantages: high cost and limited throughput; limitations: often lack full multi-cellular integration; translational value: patient-specific modeling for precision nephrology. Diagnostic innovations include microfluidic biosensors for non-invasive, high-sensitivity detection of CKD biomarkers such as albumin and neutrophil gelatinase-associated lipocalin (NGAL), as well as multiplex platforms that analyze multiple analytes in urine or blood simultaneously. Wearable epidermal patches have further extended applications to continuous monitoring of electrolytes and metabolites, enhancing patient-centered management. Therapeutically, microfluidic systems support high-throughput drug screening under physiologically relevant perfusion, enabling more predictive antifibrotic testing. Microfluidic-assisted nanodelivery platforms improve drug targeting and bioavailability, while organoid-on-chip systems enhance stem cell differentiation and regenerative potential. Integration with artificial intelligence and multi-omics further refines data interpretation, biomarker discovery, and personalized therapy design.

Microfluidic technologies bridge the gap between bench and bedside by enabling mechanistic discovery, sensitive biomarker detection, and translational therapeutic testing in CKD and fibrosis. Despite significant advances, challenges remain in scalability, reproducibility, and regulatory approval. Addressing these hurdles through interdisciplinary collaboration will be essential. With continued innovation, microfluidic systems hold strong promise for advancing precision nephrology and improving patient outcomes.

## Linked entities

- **Proteins:** LOC100189571 (uncharacterized LOC100189571), LCN2 (lipocalin 2)
- **Diseases:** chronic kidney disease (MONDO:0005300), renal fibrosis (MONDO:0000494)

## Full-text entities

- **Genes:** Ren (renin) [NCBI Gene 24715] {aka RATRENAA, RENAA, Ren1}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 59086] {aka Tgfb}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, NPHS1 (NPHS1 adhesion molecule, nephrin) [NCBI Gene 4868] {aka CNF, NPHN, nephrin}, LCN2 (lipocalin 2) [NCBI Gene 3934] {aka 24p3, MSFI, NGAL, p25}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, MMP7 (matrix metallopeptidase 7) [NCBI Gene 4316] {aka MMP-7, MPSL1, PUMP-1}, Lcn2 (lipocalin 2) [NCBI Gene 170496] {aka Sip24}, SLC22A6 (solute carrier family 22 member 6) [NCBI Gene 9356] {aka HOAT1, OAT1, PAHT, ROAT1}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}, CPT1A (carnitine palmitoyltransferase 1A) [NCBI Gene 1374] {aka CPT I, CPT1, CPT1-L, CPTI-L, L-CPT1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, DKK3 (dickkopf Wnt signaling pathway inhibitor 3) [NCBI Gene 27122] {aka CRRL, REIC, RIG}
- **Diseases:** proteinuria (MESH:D011507), metabolic dysfunction (MESH:D008659), renal (MESH:D006030), diabetic kidney disease (MESH:D003928), malaria (MESH:D008288), hypoxia (MESH:D000860), nephroids (MESH:D002292), hypoxic (MESH:D002534), KoC (MESH:D007674), immune-mediated injury (MESH:C567355), tubular injury (MESH:D000230), cancer (MESH:D009369), diabetes (MESH:D003920), infection (MESH:D007239), atrophy (MESH:D001284), hydronephrosis (MESH:D006869), CKD (MESH:D051436), liver fibrosis (MESH:D008103), cytotoxic (MESH:D064420), kidney stone (MESH:D007669), epithelial damage (MESH:D009375), Renal fibrosis (MESH:D005355), nephrolithiasis (MESH:D053040), endothelial inflammation (MESH:D007249), glomerulonephritis (MESH:D005921), HL (MESH:C538324), Disease (MESH:D004194), mitochondrial dysfunction (MESH:D028361), PMC (MESH:D020967), nephrotoxic compounds (MESH:D005597), deaths (MESH:D003643), hyperglycemic (MESH:D006944), hypertension (MESH:D006973)
- **Chemicals:** acetylcarnitine (MESH:D000108), calcium (MESH:D002118), glucose (MESH:D005947), creatinine (MESH:D003404), glutathione (MESH:D005978), citrate (MESH:D019343), aspirin (MESH:D001241), lipid (MESH:D008055), argininic acid (MESH:C000225), uric acid (MESH:D014527), oxalate (MESH:D010070), lactic acid (MESH:D019344), nicotine (MESH:D009538), fatty acid (MESH:D005227), FAO (-), cisplatin (MESH:D002945), oxygen (MESH:D010100), salt (MESH:D012492)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rodentia (rodent, order) [taxon 9989], Heyndrickxia coagulans (species) [taxon 1398]
- **Cell lines:** KoC — Homo sapiens (Human), Induced pluripotent stem cell (CVCL_E011), MDCK — Canis lupus familiaris (Dog), Spontaneously immortalized cell line (CVCL_0422)

## Full text

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## Figures

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## References

70 references — full list in the complete paper: https://tomesphere.com/paper/PMC12930372/full.md

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Source: https://tomesphere.com/paper/PMC12930372