Validated in vivo models for kidney disease research and beyond
Choosing the right model is essential to accurately reflect disease mechanisms and generate relevant observations. Our in vivo studies include comprehensive biochemical, molecular, and physiological assessments to evaluate the efficacy of your molecules with high precision. This integrated approach ensures robust, clinically relevant readouts of disease progression.
We also offer advanced capabilities in non-invasive renal function monitoring, including transdermal Glomerular Filtration Rate (GFR) measurement, providing sensitive, real-time evaluation of kidney function throughout the treatment protocol.
At NEPHRIX Biosolutions, we provide a comprehensive portfolio of models tailored to diverse research needs.
Acute Kidney Injury (AKI)
AKI is a sudden and often reversible decline in renal function that can occur within a few hours or days. It happens when the kidneys are unable to filter waste products from the blood, leading to a dangerous buildup of toxins and chemical imbalances. AKI can range from mild impairment to complete renal failure.
Key Models
Chronic Kidney Disease (CKD)
CKD is characterized by progressive renal failure. In advanced stages, CKD can lead to dangerous imbalance of fluid, electrolytes, and waste in the body. CKD is a leading cause of death worldwide, affecting 14% of the population.
Key Models
Diabetic Kidney Disease (DKD)
Diabetic nephropathy, or diabetic kidney disease, is the result of the gradual loss of kidney function in individuals with type I or type II diabetes mellitus. It is the leading cause of CKD and end-stage renal disease worldwide.
Key Models
- Streptozotocin (STZ)-Induced Diabetic Nephropathy mouse and rat model
- Genetically modified db/db mice
- db/db + Angiotensin + Nephrectomy mouse model
Hypertensive Nephropathy
CKD caused by hypertension, known as hypertensive nephropathy, is the second leading cause of CKD after diabetes. Hypertension triggers a series of pathological changes in the kidneys, resulting in various forms of kidney injury, including glomerular damage, renal fibrosis and renal dysfunction. These complications not only impair renal function but also increase the risk of stroke, heart attack, and death.
Key Models
- Angiotensin II-Induced Hypertensive Nephropathy rat model
- Spontaneously Hypertensive Rat (SHR) model
- DOCA+Salt-Induced Hypertensive Nephropathy rat model
Glomerulonephritis
Glomerulonephritis refers to a group of kidney disorders characterized by inflammation of the glomeruli, the filtration units responsible for clearing waste and maintaining fluid balance. This inflammation can arise from immune dysregulation, infections, or systemic diseases, leading to impaired filtration, hematuria, and varying degrees of proteinuria.
Key Models
- IgA Nephropathy rat model
- Focal Segmental Glomerulosclerosis (FSGS) rat model
Nephrotoxicity
Nephrotoxicity refers to kidney damage caused by exposure to harmful substances, including drugs or environmental toxins. Such injury can impair the kidney’s ability to filter waste, regulate electrolytes, and maintain fluid balance, ultimately leading to acute or chronic renal dysfunction. Because nephrotoxic effects often limit the development and safe use of therapeutic compounds, in vivo models are essential to identify early kidney injury, evaluate compound safety, and guide clinical decision-making.
Key Models
- Cisplatine-induced model
- LPS-induced model
Standard Biomarker & Readout Panel
Our in vivo studies are designed with a comprehensive, multi-dimensional readout framework. The table below shows the standard panel available across disease categories – all customisable to your study objectives.
| Category | Biomarker / Readout | Sample Type | Clinical Relevance |
|---|---|---|---|
| Renal Function | Serum creatinine, BUN, cystatin C | Blood | Glomerular filtration, overall kidney function |
| GFR | Transdermal real-time GFR (FITC-sinistrin) | Non-invasive | Longitudinal renal function monitoring |
| Tubular Injury | KIM-1, NGAL | Urine / Plasma | Proximal tubule damage, early AKI detection |
| Proteinuria | Albuminuria, albumin/creatinine ratio (ACR) | Urine | Glomerular barrier integrity |
| Fibrosis | α-SMA, fibronectin, collagen I/III, TGF-β1 | Kidney tissue (IHC/WB) | Myofibroblast activation, ECM remodelling |
| Inflammation | TNF-α, IL-1β, IL-6, NF-κB, MCP-1, F4/80 | Tissue / Plasma | Innate immune activation, macrophage infiltration |
| Histology | H&E, PAS, Masson's trichrome, Sirius Red | FFPE tissue sections | Structural kidney damage, fibrosis quantification |
| Metabolic | Blood glucose, HbA1c, plasma insulin, body weight | Blood / body | Metabolic disease control, DKD context |
Frequently Asked Questions – In vivo services
NEPHRIX Biosolutions covers the full spectrum of kidney disease: Acute Kidney Injury (IRI, cisplatin, sepsis-induced AKI), Chronic Kidney Disease (adenine diet, UUO, 5/6 nephrectomy, AKI-to-CKD transition model), Diabetic Kidney Disease (STZ, db/db), Hypertensive Nephropathy (Angiotensin II, SHR, DOCA-salt), Glomerulonephritis (IgA nephropathy, FSGS), and Nephrotoxicity (cisplatin, LPS). Each model is selected based on your compound’s target and mechanism of action during the initial scientific consultation.
Study timelines depend on model complexity. Acute models such as cisplatin-induced AKI or bilateral IRI can be completed within 4 to 6 weeks from study initiation. Chronic models such as adenine-induced CKD or STZ-induced diabetic nephropathy typically require 8 to 16 weeks. The AKI-to-CKD transition model runs over 6 to 12 weeks. We provide a detailed project timeline and milestone plan during the study design phase, ahead of any commitment.
NEPHRIX Biosolutions operates both in vitro and in vivo platforms under one roof. Biomarker endpoints such as KIM-1, NGAL, α-SMA, fibronectin, and creatinine are harmonised across both platforms, enabling direct translational comparison. Compounds screened in our in vitro assays (fibrosis, inflammation, nephrotoxicity) can progress to validated in vivo models without switching CRO providers, saving time, ensuring scientific continuity, and reducing costs.
All studies at NEPHRIX Biosolutions are designed in accordance with the 3Rs framework (Replacement, Reduction, Refinement). We prioritise non-invasive monitoring tools such as transdermal GFR to reduce terminal blood sampling, leverage in vitro Go/No-Go screening to minimise unnecessary animal use, and work with accredited animal facilities compliant with European Directive 2010/63/EU. Animal group sizes are statistically justified to use the minimum number needed for robust data..
All studies at NEPHRIX Biosolutions are designed in accordance with the 3Rs framework (Replacement, Reduction, Refinement). We prioritise non-invasive monitoring tools such as transdermal GFR to reduce terminal blood sampling, leverage in vitro Go/No-Go screening to minimise unnecessary animal use, and work with accredited animal facilities compliant with European Directive 2010/63/EU. Animal group sizes are statistically justified to use the minimum number needed for robust data.
Why choose NEPHRIX Biosolutions?
Scientific Expertise
Ethical & 3R Considerations
Flexible Study Design
Gold standard and Specific Readouts
Why choose NEPHRIX Biosolutions?
Scientific Expertise
Ethical & 3R Considerations
Flexible Study Design
Gold standard and Specific Readouts