Diabetic Nephropathy
Conditions
Keywords
Human umbilical cord mesenchymal stem cell
Brief summary
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.
Interventions
DRUGUC-MSCs
UC-MSCs :5\*10E5、1\*10E6、2\*10E6 UC-MSCs/kg body weight/100mL saline containing 1% human albumin
DRUGPlacebo
saline containing 1% human albumin/100mL
Sponsors
Tongji Hospital
Wuhan Hamilton Biotechnology Co., Ltd
Study design
Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
30 Years to 70 Years
Healthy volunteers
No
Inclusion criteria
* Type 2 diabetes with a disease duration of ≥ 5 years (no age limit for subjects diagnosed with diabetic nephropathy by renal biopsy). * Age 30-70 years, no gender restriction. * Diagnosis of diabetic nephropathy (see Appendix 1). * Estimated glomerular filtration rate (eGFR) between 15 and 60 mL/min/1.73 m². * During the 3-month period prior to enrollment, received antihypertensive therapy centered on renin-angiotensin system inhibitors (RASIs) to control blood pressure, achieving the following targets: systolic blood pressure ≤150 mmHg and diastolic blood pressure ≤ 100 mmHg. * At the screening/baseline visit, must have received a stable dose of an SGLT2 inhibitor (empagliflozin, dapagliflozin, canagliflozin, or ertugliflozin) for ≥ 3 months, or a stable dose of nateglinide for ≥ 3 months, or a stable combination of an SGLT2 inhibitor and nateglinide for ≥ 3 months, and continue the same stable dose throughout the trial. * No positive
Exclusion criteria
. * Voluntary participation in the clinical trial, good compliance, ability to understand and sign the informed consent form for this study, and capability to complete the entire trial treatment and follow-up schedule according to the study protocol. (Final eligibility will be determined by the investigator based on comprehensive clinical symptom assessment.)
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Adverse Events | From Baseline (0 W) to 48 weeks after treatment | The number of Adverse Events associated with UC-MSCs intervention per treatment arm |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Kidney function | From Baseline (0 W) to 24 weeks after treatment | Change in GFR from baseline |
| Change in HbA1c | From Baseline (0 W) to 48 weeks after treatment | Change in Glycosylated Hemoglobin (HbA1c) from baseline |
Countries
China
Contacts
CONTACTRUI ZENG
PRINCIPAL_INVESTIGATORGANG XU
Tongji Hospital
Outcome results
None listed