An observational study in Chronic Kidney Disease stage3, Chronic Kidney Disease stage4 and Chronic Kidney Disease Stage 1, sponsored by Cardenal Herrera University. Recruiting at 1 site in Spain. Open to participants aged 18 Years to 90 Years. Per ClinicalTrials.gov, last updated 2025-12-30.
Sponsored by Cardenal Herrera University · Observational
Chronic kidney disease (CKD) is the progressive damage to kidney function, associated with an increased risk of cardiovascular diseases, such as stroke or myocardial infarct, particularly in the most severe stages of CKD, in which the patient requires dialysis. Several risk factors are reported for CKD, such as diabetes mellitus, obesity and hypertension. One of the most increasingly recognized risk factors is the fat tissue malfunction, known as adiposopathy. The accumulation of fat tissue around the organs in conditions of obesity or diabetes accelerates the production of pro-inflammatory factors that may worsen the kidney and heart damage. New antidiabetic medications, such as glucagon-like peptide-1 receptor agonists (GLP-1RA), have proven beneficial effects on the kidney and heart due to several mechanisms, including anti-inflammatory actions and a potential action on the fat tissue.
The aim of this study is to assess the link between adiposopathy and CKD, by investigating the changes in adiposopathy measures throughout treatment with GLP-1RA to a sample of patients with CKD.
Chronic kidney disease (CKD) is defined as an irreversible abnormality of kidney structure and/or function lasting for more than three months. CKD is a major global health burden, affecting over 10% of the worldwide population and representing a leading cause of morbidity and mortality. Its progression to end-stage kidney disease (ESKD) drastically increases cardiovascular risk and is associated with a five-year survival rate of only approximately 50%. The principal risk factors for CKD-hypertension, obesity and type 2 diabetes (T2DM) in particular-are intrinsically linked through the dysfunction of fat/adipose tissue (AT), also known as adiposopathy.
Adiposopathy is a key driver of cardiorenal risk in CKD. Evidence from bioimpedance, imaging techniques (CT, MRI), and molecular biology studies confirm that alterations in adipose tissue-including its quantity, distribution (e.g., perirenal, epicardial), radiodensity, and the secretion of pro-inflammatory adipokines-are powerful triggers of cardiorenal damage and mortality in these patients. This understanding frames obesity, T2DM, cardiovascular diseases (CVDs), and CKD as different manifestations of a shared spectrum, now termed adiposity-based chronic disease (ABCD), necessitating an "adipocentric" therapeutic approach.
One hallmark feature of adiposopathy is the reprogramming and increase in size of certain region-specific adipose tissue. Perivisceral adipose tissue plays a pivotal role in adiposity-based chronic diseases as it releases adipokines and cytokines that not only contribute to the systemic pro-inflammatory and oxidative stress processes but may also influence the function of the organs surrounded by this tissue.
GLP-1RA stimulates the receptor for glucagon-like peptide-1 (GLP-1), an incretin-like hormone released in the large intestine that reduces serum glucose concentrations by stimulating the glucose-dependent release of insulin, inhibiting the hypersecretion of glucagon (except in hypoglycemia periods) and promoting satiety. GLP-1RA reduced the incidence of cardiovascular death in patients with T2DM compared with placebo and decreased the incidence of major kidney events, also reducing the progression of kidney dysfunction and the risk of death. In animals, the observed morphological changes generated by GLP-1RA could be underlined by potential actions on adipose tissue remodeling, as these drugs upregulated the expression of AT-browning related genes in perivisceral white adipose tissue from murine models, although the transcriptomic effects from GLP-1RA on the adiposopathy process are still unknown.
3,144 studies on the registry are indexed under Renal Insufficiency, Chronic; 704 are open to participants now.
This study's planned enrollment of 250 is above the median of 200 across 867 observational studies indexed under Renal Insufficiency, Chronic.
Browse Renal Insufficiency, Chronic studies →Cardenal Herrera University is the lead sponsor of 104 studies on the registry; 23 are open to participants now.
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Patients will be assigned to the different groups according to current treatment criteria:
SGLT2i: patients with CKD and T2DM with an eGFR ≥20ml/min/1.73m2; patients with CKD and eGFR ≥20ml/min/1.73m2, accompanied by an urinary albumin-to-creatinine ratio (ACR) ≥200mg/g; patients with CKD and heart failure, irrespective of level of albuminuria; or subjects with CKD and eGFR 20-45ml/min/1.73m2, with ACR \<200mg/g.
GLP-1RA/tirzepatide: In patients with T2D and CKD who have not achieved individualized glycemic targets despite use of metformin and SGLT2i treatment, or who are unable to use those medications.
Other treatments: patients not meeting the criteria to be treated with SGLT2i or GLP-1RA/tirzepatide
Exclusion Criteria:
Patients receiving GLP-1RA, mainly semaglutide: weekly administration, subcutaneous form, from 0.25mg (starting dose) to 1mg (maintenance dose) with monthly increase (0.25-0.5-1mg)
Drug: GLP-1 receptor agonist · Drug: SGLT2 inhibitor
There will also be another comparative group of patients under SGLT2i
Drug: GLP-1 receptor agonist · Drug: SGLT2 inhibitor
Patients not under SGLT2i or GLP-1RA/Tirzepatide influence, but receiving other treatments that are part of CKD and diabetes standard care
Patients receiving tirzepatide: weekly administration, subcutaneous form, starting dose 2.5mg, maintenance 5mg
Drug: Tirzepatide · Drug: Other drugs
Semaglutide: weekly subcutaneous administration, starting dose 0.25mg, maintenance dose 1mg
Also known as: semaglutide, liraglutide, dulaglutide, exenatide
dapagliflozin: oral administration from 5 to 10mg/day
Also known as: dapagliflozin, empagliflozin, canagliflozin
subcutaneous injection: starting dose 2.5 mg, maintenance 5mg (weekly administration)
Patients not under SGLT2i or GLP-1RA influence, but receiving other treatments which are part of CKD standard care: mineralocorticoid receptor agonists, metformin, ACE inhibitors, ARBs...
Also known as: ARBs, ACE inhibitors, Metformin, DPP4i, non steroidal mineralocorticoid receptor agonists
Ultrasonography change in perirenal adipose tissue thickness
Change in perirenal adipose tissue thickness as measured with ultrasonography
Time frame: 16 months
Change in estimated glomerular filtration rate
Change in eGFR as per the CKD-EPI formula
Time frame: 16 months
Ultrasonographic Change in epicardial adipose tissue thickness
Change in epicardial adipose tissue thickness as measured with ultrasonography
Time frame: 16 months
Change in serum leptin levels
Serum leptin levels measured with proteomic analysis
Time frame: 16 months
Change in visceral fat area
Changes in visceral fat area (cm2) as measured with body composition measures (bioimpedance)
Time frame: 16 months
Ultrasonographic Change in subcutaneous adipose tissue
Change in subcutaneous adipose tissue thickness as measured with ultrasonography
Time frame: 16 months
Ultrasonographic Change in preperitoneal adipose tissue thickness
Change in preperitoneal adipose tissue thickness as measured with ultrasonography
Time frame: 16 months
Ultrasonographic Change in intrahepatic adipose tissue
Change in intrahepatic adipose tissue echogenicity
Time frame: 16 months
Change in subcutaneous fat area
Change in subcutaneous fat area (cm2) as measured with bioimpedance
Time frame: 16 months
Changes in muscle mass (kg)
Changes in muscle mass as measured with bioimpedance
Time frame: 16 months
Change in serum adiponectin levels
Serum adiponectin levels measured with proteomic analysis
Time frame: 16 months
Change in urinary levels of Kidney Injury Molecule-1
Change in urinary levels of KIM-1 measured with ELISA, as an early marker of kidney damage
Time frame: 16 months
Change in systemic inflammation markers
Change in serum C-reactive protein levels
Time frame: 16 months
Change in systemic inflammation markers
Change in serum interleukin-6 levels
Time frame: 16 months
Change in systemic inflammation markers
Change in serum tumor necrosis factor-alpha levels
Time frame: 16 months
Plan to share: No — Due to ethical restrictions and in accordance with General Protection Data Regulation, no identifiable patient information will be shared.
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Cardenal Herrera University