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Diabetic kidney disease (DKD) animal model

Diabetic kidney disease (DKD) animal model

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Diabetic nephropathy
Urinary system disease model

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Diabetic nephropathy

Introduction to DKD Animal Models

Diabetic kidney disease (DKD) is one of the most common microvascular complications of diabetes and a leading cause of end-stage renal disease (ESRD). Its key pathological features include persistent proteinuria, glomerular hypertrophy, mesangial matrix expansion, thickening of the glomerular basement membrane, and renal interstitial fibrosis. Animal models are typically established by streptozotocin (STZ) administration, genetic diabetes models (such as db/db mice and ZDF rats), or a combination of a high-fat diet and STZ treatment, thereby mimicking the progressive structural and functional damage to the kidneys under hyperglycemic conditions. These models effectively recapitulate the pathogenesis and progression of clinical diabetic kidney disease.

Service Advantages of Aniphe BioLab’s DKD Animal Model Platform

Aniphe BioLab has established a well‑established animal model platform for diabetic kidney disease (DKD), offering end‑to‑end services from disease model generation to efficacy evaluation, thereby providing robust preclinical support for research on diabetic complications and renal diseases.

Comprehensive model coverage

A wide variety of model types

It supports multiple classic DKD models, including STZ‑induced, HFD + STZ–induced, db/db mice, and ZDF rats.
Standardization of the modeling process

Model establishment is stable and reliable.

A standardized modeling workflow ensures stable phenotypes of hyperglycemia, proteinuria, and renal pathological changes.
Multidimensional Evaluation System

The evaluation system has been improved.

Multidimensional assessments, including blood glucose, urinary albumin, serum creatinine (Scr), blood urea nitrogen (BUN), renal histopathology, and molecular biomarkers, can be performed.
Adapted for multi-cycle studies

Research covering the entire disease course

It supports pharmacological efficacy evaluation across different stages, including early renal injury, declining renal function, and renal fibrosis.
Standardization of Data Delivery

One-stop project services

We offer a comprehensive suite of solutions, including model development, sample testing, pathological analysis, and data statistical analysis.
Modeling cycle

5 days

1  Laboratory animals

C57BL/6 male mice

1  Positive drug

Pharmacotherapy: duloxetine (increases the urethral closure pressure), phenylephrine (an α‑agonist).
Biological/surgical comparisons: autologous muscle-derived stem cells, mesenchymal stem cell transplantation, periurethral fillers (such as collagen), and pelvic floor electrical stimulation.

1  Application areas

Neuro‑muscular mechanisms underlying stress urinary incontinence (SUI) induced by childbirth and aging; regenerative evaluation of sphincter repair using stem cells and hydrogels; pharmacological screening to identify agents—administered orally or locally—that enhance urethral closure pressure; preclinical optimization of physical therapies (magnetic/electrical stimulation) and pelvic floor reconstructive surgery.

 

Experimental results

Construction of a DKD animal model

SPF-grade C57BL/6 mice were fed a high-fat diet for 4–6 weeks, resulting in a significant increase in body weight. The mice received five consecutive intraperitoneal injections of streptozotocin (STZ) after a 12-hour fast; blood glucose was measured one week later (random blood glucose ≥ 16.7 mmol/L and fasting blood glucose ≥ 11.1 mmol/L) to confirm successful model establishment. The animals were then maintained on the high-fat diet for an additional 3–4 months, during which urinary creatinine and urinary albumin levels were assessed to evaluate the success of model induction.

Masson’s trichrome staining results

Masson’s trichrome staining revealed that, compared with the normal control group (Control), the diabetic nephropathy model group (Model) exhibited a marked increase in blue‑stained collagen fibers in renal tissue, with significantly enhanced fibrosis in the renal tubules and interstitium. Renal tubular architecture was disorganized, and tubular morphology was compromised, indicating that the kidneys of the diabetic nephropathy model animals had developed pronounced interstitial fibrosis, confirming successful model establishment.

 

 

PSA staining results

PAS staining revealed that, compared with the control group, the diabetic nephropathy model group exhibited a marked increase in purple‑red glycogen and positive deposits of polysaccharides in renal tissue. Additionally, glomerular basement membrane thickening, extensive accumulation of glycoproteins in the tubular basement membrane, and more pronounced structural damage to the renal tubules were observed. These findings indicate that the model group displayed typical pathological changes characteristic of diabetic nephropathy, including abnormal deposition of basement membrane extracellular matrix, confirming the successful establishment of the model.

 

 

Biochemical test results

Compared with the control group, the diabetic nephropathy model group exhibited significantly elevated serum levels of blood urea nitrogen (BUN), creatinine (CRE), and urinary albumin (ALB), with intergroup differences reaching a highly significant level (* * *P<0.001). These findings indicate that renal function was impaired in the model animals, characterized by azotemia and substantial proteinuria, consistent with the typical features of renal dysfunction in diabetic nephropathy, thereby confirming the successful establishment of the diabetic nephropathy animal model.