Diabetic nephropathy (DN) is one of the most significant microvascular complications of diabetes mellitus. Its incidence can reach 30%-40% after 20 years of diabetes duration, among which 5%-10% of patients will progress to end-stage renal disease, where renal function is essentially lost, and only hemodialysis or kidney transplantation can sustain or save lives. Given the current lack of effective clinical measures for treating diabetic nephropathy, exploring new strategies for its prevention and treatment is of great significance. Diabetic nephropathy is caused by persistent hyperglycemia, and its key pathological features include chronic inflammatory cell infiltration in kidney tissue, podocyte apoptosis in the glomeruli, pyroptosis of renal tubular epithelial cells, and renal fibrosis. Therefore, the key to treating diabetic nephropathy lies in inhibiting chronic renal inflammation and alleviating the resulting tissue and cell damage; reducing glomerular podocyte apoptosis and renal tubular epithelial cell pyroptosis, lowering proteinuria levels, and delaying the pathological progression of diabetic nephropathy; suppressing renal fibrosis; and regenerating new renal tissue cells to partially restore renal tissue structure and function. Current clinical treatments for diabetic nephropathy primarily involve strict glycemic control and the use of angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists. Numerous clinical studies have shown that these therapeutic measures can only partially delay the onset and slow the progression of diabetic nephropathy, but cannot reverse renal damage. Accumulating evidence indicates that mesenchymal stem cells (MSCs) can migrate and home to injured kidney tissues, directionally differentiate into renal parenchymal cells to repair and regenerate damaged tissue cells; secrete nutritional factors to improve local blood supply and the microenvironment of renal tissue; and release anti-inflammatory and immunomodulatory factors, exerting potent anti-inflammatory and immunomodulatory effects, thereby reducing inflammatory injury and apoptosis of renal tissue cells and alleviating renal fibrosis. Therefore, mesenchymal stem cells have emerged as a new hope for the treatment of diabetic nephropathy.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
15
Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, WUHAN, HUBEI
Wuhan, China
RECRUITINGAdverse Events
The number of Adverse Events associated with UC-MSCs intervention per treatment arm
Time frame: From Baseline (0 W) to 48 weeks after treatment
Kidney function
Change in GFR from baseline
Time frame: From Baseline (0 W) to 24 weeks after treatment
Kidney function
Change in cystatin C from baseline
Time frame: From Baseline (0 W) to 48 weeks after treatment
Kidney function
Change in serum creatinine from baseline
Time frame: From Baseline (0 W) to 48 weeks after treatment
Kidney function
Change in eGFR from baseline.
Time frame: From Baseline (0 W) to 48 weeks after treatment
Kidney function
Change in 24-hour urinary protein from baseline
Time frame: From Baseline (0 W) to 48 weeks after treatment
Kidney function
Change in urine albumin/creatinine ratio from baseline
Time frame: From Baseline (0 W) to 48 weeks after treatment
Change in HbA1c
Change in Glycosylated Hemoglobin (HbA1c) from baseline
Time frame: From Baseline (0 W) to 48 weeks after treatment
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