Human Umbilical Cord Mesenchymal Stem Cell Injection for Diabetic Nephropathy
ConditionDiabetic Nephropathy
Trial statusRecruiting
Trial phasePhase 1
Trial typeInterventional
Biological sexAll
Age30-70
SponsorTongji Hospital
About this trial
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.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
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.
Disqualifiers
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.
Patients with type 1 diabetes mellitus.
Patients with a prior history of primary glomerulonephritis, lupus nephritis, ANCA-associated vasculitis with renal involvement, Henoch-Schönlein purpura nephritis, or hepatitis B-associated nephritis.
Poor glycemic control.
Trial design
Design model
Parallel
Treatments tested in this trial
UC-MSCs
DrugUC-MSCs :5\*10E5、1\*10E6、2\*10E6 UC-MSCs/kg body weight/100mL saline containing 1% human albumin
Placebo
Drugsaline containing 1% human albumin/100mL
Treatment groups
15 Participants
are divided into 2 treatment groupsGroup A: UC-MSCsExperimental treatment 1 intervention
Group B: PlaceboPlacebo comparator 1 intervention
Trial outcomes
Primary outcomes
1
Adverse Events
The number of Adverse Events associated with UC-MSCs intervention per treatment arm
Time frame
From Baseline (0 W) to 48 weeks after treatmentSecondary outcomes
1
Kidney function
Change in GFR from baseline
Time frame
From Baseline (0 W) to 24 weeks after treatment2
Kidney function
Change in cystatin C from baseline
Time frame
From Baseline (0 W) to 48 weeks after treatment3
Kidney function
Change in serum creatinine from baseline
Time frame
From Baseline (0 W) to 48 weeks after treatment4
Kidney function
Change in eGFR from baseline.
Time frame
From Baseline (0 W) to 48 weeks after treatmentSponsors and contacts
Click on the lead sponsor to view all of their trials.
Tongji Hospital
Lead sponsor
Wuhan Hamilton Biotechnology Co., Ltd
Collaborator
Source ClinicalTrials.gov