Chronic Kidney Disease Model

Introduction

Chronic kidney disease (CKD) is a common health problem characterized by low awareness, high prevalence, and high mortality, with a global prevalence of 13%. It has been demonstrated that there is a strong association among the reduction in glomerular filtration rate (GFR), the risk of developing cardiac functional and structural diseases, and cardiovascular (CV) events.

Disease models

Animal models provide reliable means for studying the pathological mechanisms of kidney diseases, identifying therapeutic approaches, and developing prevention strategies. The SMOC has long been dedicated to autoimmune disease research and has established a variety of CKD disease models based on different induction methods, providing powerful tools for the efficacy evaluation and safety assessment of related drugs.
The SMOC has long been dedicated to autoimmune disease research and has developed a variety of mouse models of atopic dermatitis using agents such as oxazolone (OXA) and 2,4-dinitrofluorobenzene (DNFB), providing powerful tools for the efficacy evaluation and safety assessment of related drugs.

5/6 nephrectomy induced CKD model in C57BL/6 mice

After 5/6 nephrectomy in mice, the remaining renal units take over the whole‑body blood filtration function. The dramatic hemodynamic changes directly lead to glomerular hyperfiltration, which subsequently causes glomerulosclerosis and destruction of the remnant nephrons, resulting in chronic renal failure with tubulointerstitial fibrosis characterized mainly by glomerular hypertrophy and sclerosis.

To ensure the survival rate of the mice, a two‑step surgical procedure is often used for nephrectomy:

  1. After one week of acclimatization, the mouse is anesthetized and two‑thirds of the left kidney is resected.

  2. Seven days after the first surgery, the entire right kidney is removed.

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Fig.1 Body weight of 5/6 nephrectomy induced CKD model in C57BL/6.

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Fig.2 5/6 nephrectomy induced CKD model in C57BL/6. (A) serum UREA; (B) serum CRE.

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Fig.3 5/6 nephrectomy induced CKD model in C57BL/6. (A) pathological score; (B) typical pathology image of H&E stain; (C) fibrosis score; (D) typical pathology image of Masson stain.image.png

Fig.4 5/6 nephrectomy induced CKD model in C57BL/6. (A) relative expression of α-SMA mRNA in kidney; (B) relative expression of Col1a1 mRNA in kidney; (C) relative expression of TGF-β mRNA in kidney.

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Fig.5 5/6 nephrectomy induced CKD model in C57BL/6. (A) RBC; (B) HGB; (C) HCT%.

Adenine induced CKD model in C57BL/6 mice

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Fig.1 Clinical symptoms of CKD mouse model. (A) body weight (B) survival percentage. ***P<0.001 vs Adenine.

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Fig.2 Serum biochemical analysis and gross anatomy analysis of CKD mouse model. (A) serum BUN; (B) serum CRE; (C) left kidney index: left kidney weight / body weight; (D) right kidney index: right kidney weight / body weight . *P<0.05, **P<0.01, ***P<0.001 vs Adenine.

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Fig.3 Kidney H&E pathology of CKD mouse model. (A) typical pathology image; (B) histological score; (C) MCC950 80mpk can relieve glomerulosclerosis induced by adenine. *P<0.05, **P<0.01, ***P<0.001 vs Adenine.

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