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Chronic renal failure (CRF) animal model

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Chronic renal failure

Introduction to CRF Animal Models

Chronic renal failure (CRF) represents the end stage of chronic kidney disease, characterized by the irreversible decline in renal function resulting from the progressive deterioration of various chronic renal conditions. It is marked by nephron loss, glomerulosclerosis, tubulointerstitial fibrosis, and declining renal function, and may ultimately progress to end-stage renal disease. Animal models of chronic renal failure can reliably replicate key pathological processes, including chronic renal injury, inflammatory responses, and fibrosis, thereby facilitating a systematic dissection of the molecular mechanisms underlying disease onset and progression, as well as in-depth investigations into renal injury and repair. These models provide critical experimental evidence for developing preventive and therapeutic strategies for chronic kidney disease and for advancing the discovery of innovative therapeutics.

Advantages of Aniphe BioLab’s CRF Animal Model Platform Services

The Ailinfei CRF model platform offers a variety of well-established modeling protocols, with stable models and comprehensive supporting assays, providing end-to-end support for research into the mechanisms of renal failure and for evaluating the efficacy of new drugs.

	Comprehensive modeling methods 5/6 nephrectomy and other mainstream models allow for the modulation of varying degrees of renal injury, making them suitable for a wide range of experimental protocols.
	Model quality control is reliable. A standardized modeling protocol ensures stable model establishment, minimal variability in outcome measures, and excellent reproducibility of experimental data.
	One-stop service Integrated delivery of model establishment and animal husbandry, regular blood and urine sampling, and pathological and molecular assays.
	Personalized customization Adjust the modeling cycle and sampling time points as needed, supporting the establishment of composite renal disease models.
	Data compliance is eligible for submission. Renal function and pathological parameters are tested on each batch, with complete original records.
	High delivery efficiency Standard models are in stock, and multiple business lines are advanced in parallel, saving customers’ R&D time.

Modeling cycle	10–12 weeks
Laboratory animals	Mice, rats, rabbits, and miniature pigs
Positive drug	Commonly used agents such as benazepril, losartan, and enalapril serve as positive controls and exert renal protective effects by ameliorating glomerular hyperfiltration, suppressing inflammation, and delaying renal fibrosis.
Application areas	It is primarily used for research on the pathogenesis of chronic renal failure, screening of anti‑renal fibrosis and nephroprotective agents, evaluation of drug efficacy, and preclinical studies of innovative therapeutic strategies.

Construction of a CRF animal model

5/6 nephrectomy: This method involves partial nephrectomy combined with contralateral total nephrectomy, thereby reducing the number of functioning renal units and inducing compensatory hyperfiltration along with progressive renal injury. It reliably reproduces hallmark pathological features such as glomerulosclerosis, tubulointerstitial fibrosis, and declining renal function, making it the most widely used classic modeling approach in chronic renal failure research.

Losartan treatment data

5/6 nephrectomy successfully induced chronic renal dysfunction in rats, elevating BUN and serum creatinine levels, upregulating renal Desmin expression, and causing pathological damage to the glomeruli. Following treatment with losartan, renal Desmin expression decreased and glomerular pathology improved, demonstrating a renoprotective effect. In this study, no significant reductions were observed in the serum markers BUN or creatinine; the therapeutic benefits were primarily reflected in the amelioration of local renal pathological changes and the downregulation of Desmin protein expression.

5/6 nephrectomy–induced chronic renal failure can trigger adipose remodeling in the epididymis, characterized by an overall reduction in adipocyte diameter and a shift in cellular size distribution. Losartan treatment effectively reverses these adipose morphological abnormalities and improves the distribution of adipocyte sizes, thereby providing histomorphological evidence for the drug’s ability to correct the adipokine imbalance associated with renal failure. These findings refine the mechanistic pathway underlying losartan’s renoprotective effects: in addition to its direct actions on the kidney to mitigate pathological injury, the drug also modulates peripheral adipose tissue architecture, thereby attenuating secondary renal damage arising from dysregulated lipid metabolism.

In this experiment, an oral glucose tolerance test was conducted, with three groups: a sham‑operation control group (C), a 5/6 nephrectomy–induced renal failure model group (N), and a losartan‑treated intervention group (NA) (n = 8 per group; results are presented as mean ± standard error). Plasma glucose and insulin levels were monitored dynamically over a 120‑minute period.

The trends in blood glucose and insulin levels across the groups were similar, and at each time point, there were no statistically significant differences among the three groups in either blood glucose or insulin concentrations. These findings indicate that the 5/6 nephrectomy model established in this study did not substantially disrupt glucose tolerance or insulin secretion in rats, and that losartan treatment likewise did not exert a marked effect on overall carbohydrate metabolism or circulating insulin levels.

RT‑PCR was used to assess the expression of adipokines in adipocytes. Compared with the sham‑operated control group, rats subjected to a 5/6 nephrectomy exhibited decreased mRNA levels of adiponectin and leptin, along with increased resistin mRNA, indicating an imbalance in adipokine expression. Following treatment with losartan, the expression of all three adipokines was effectively normalized, suggesting that losartan can reverse the adipokine dysregulation induced by chronic renal failure, thereby exerting a renoprotective effect.