In Vitro Models for Kidney Disease Research
Preclinical Kidney Disease R&D Solutions
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In Vitro Models for Kidney Disease Research

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Kidney disease remains a complex challenge in drug development, demanding research models that accurately mimic human pathophysiology. At Ace Therapeutics, we bridge this gap by offering advanced in vitro models tailored for renal research, enabling robust preclinical evaluation of therapeutic candidates. Our platforms are designed to recapitulate critical aspects of kidney function and disease progression, empowering researchers to make informed decisions early in the drug discovery pipeline.

Why Choose In Vitro Models for Renal Research?

In vitro systems provide a controlled, scalable, and ethically aligned approach to study kidney disease mechanisms. Key advantages include

  • Human relevance Primary human cell-based models reduce interspecies variability.
  • Disease-specific modeling Customizable platforms for acute kidney injury (AKI), chronic kidney disease (CKD), and rare genetic disorders.
  • High-throughput compatibility Enable screening of compound libraries with efficiency.
  • Mechanistic insights Study cellular pathways, toxicity, and fibrosis in a targeted environment.

Ace Therapeutics' Renal In Vitro Model Portfolio

We offer a suite of in vitro models that replicate key aspects of renal physiology and pathology. These models are instrumental in evaluating drug efficacy, toxicity, and mechanistic pathways.

Model Type Application Key Features
Primary proximal tubule cells Nephrotoxicity screening, drug transport studies Functional transporters, polarization
Podocyte cultures Glomerular disease, proteinuria mechanisms Disease induction (e.g., LPS, hyperglycemia)
3D microphysiological systems Tubulointerstitial fibrosis, CKD progression Multicellular architecture, ECM remodeling
Patient-derived renal cells Rare genetic disorders (e.g., ADPKD, Alport syndrome) Genotypic-phenotypic correlations

Advanced Technical Capabilities

Our interdisciplinary team supports multifaceted kidney disease research through

Cell-Based Disease Modeling

  • Functional primary renal cells (podocytes, mesangial, tubular epithelia) for filtration and transport studies.
  • Genetic nephropathy models and iPSC-derived vascularized nephron organoids.
  • Diabetic (AGE/high glucose) and IgA nephropathy (gd-IgA1) induction systems.

Senescence & Aging Profiling

  • SA-β-galactosidase quantification under hypoxia/oxidative stress.
  • Senolytic screening via p16/p21 pathway modulation (qPCR/Western blot).
  • Telomere length analysis (Flow-FISH) and SASP factor multiplex profiling (IL-6, MMP-3, PAI-1).

Fibrosis Mechanism Analysis

  • TGF-β/Smad3 pathway activation in renal fibroblasts (α-SMA, collagen I/III).
  • ECM deposition quantification (hydroxyproline/Sirius Red assays) and EMT tracking (E-cadherin/vimentin).
  • miRNA/siRNA antifibrotic target discovery platforms.

Inflammatory Pathway Interrogation

  • NLRP3 inflammasome activation (ATP/nigericin priming).
  • Monocyte/macrophage chemotaxis assays and cytokine storm simulation (TNF-α/IL-1β/IFN-γ).
  • NF-κB/MAPK pathway inhibition profiling using phospho-protein arrays.

Nephrotoxicity Screening

  • Dual cytotoxicity/apoptosis panels (LDH, caspase-3/7, Annexin V).
  • Transporter-mediated toxicity assessments (OAT1/OCT2 inhibition).
  • Mitochondrial stress profiling (Seahorse XF) and crystallopathy risk evaluation.

Disease Microenvironment Engineering

  • Hypoxic chambers (1% O2) for ischemic injury modeling.
  • Shear stress systems for glomerular endothelial mechanobiology.
  • ECM hydrogel scaffolds and hyperglycemic/uremic toxin combinations (CML, indoxyl sulfate).

High-Content Phenotypic Analysis

  • Live-cell imaging of tight junction dynamics (ZO-1/occludin).
  • Multi-parametric cytotoxicity profiling (ROS, Ca2+ flux).
  • AI-driven podocyte foot process morphometry.

Modular Co-Culture Platforms

  • Glomerular tri-cultures (podocyte-mesangial-endothelial crosstalk).
  • Tubulointerstitial models (epithelial-fibroblast-macrophage interplay).
  • 3D microfluidic kidney-on-chip with vascular perfusion.

Enhancing Research Outcomes Through Strategic Model Selection

Selecting the optimal in vitro system requires alignment with your research objectives. Consider these factors

  • Disease mechanism Glomerular vs. tubular vs. vascular pathology.
  • Cell source Primary cells, immortalized lines, or iPSC-derived progenitors.
  • Functional readouts Barrier integrity, cytokine secretion, or metabolic activity.

Our scientists collaborate closely with clients to design fit-for-purpose studies, balancing biological complexity with experimental feasibility.

Frequently Asked Questions (FAQs)

How do your models address interspecies differences in renal research?

We prioritize human-derived cells and validate key functional markers (e.g., megalin/cubilin expression in proximal tubules) to enhance translational relevance.

Can you model drug-induced kidney injury?

Yes. Our proximal tubule platforms are widely used for nephrotoxicity profiling, with endpoints including ATP depletion, ROS production, and tubular injury markers.

How do you measure nephrotoxicity in vitro?

We assess nephrotoxicity through biomarkers such as KIM-1 and NGAL, as well as functional assays evaluating cell viability and transporter activity.

Do you offer coculture systems for immune-kidney interactions?

We provide macrophage-renal epithelial cocultures to study inflammation-driven fibrosis and cytokine-mediated damage.

What quality controls ensure model consistency?

All cell batches undergo viability testing, morphology checks, and functional validation (e.g., albumin uptake assays).

HOW WE WORK

Make Order

Make Order

Experimental Scheme

Experimental Scheme

Implementation

Implementation

Conclusion

Conclusion