Type 2 diabetes mellitus represents 30–50% of the cases of end stage renal disease worldwide. Thus, a correct evaluation of renal function in patients with diabetes is crucial to prevent or ameliorate diabetes-associated kidney disease. The reliability of formulas to estimate renal function is still unclear, in particular, those new equations based on cystatin-C or the combination of creatinine and cystatin-C. We aimed to assess the error of the available formulas to estimate glomerular filtration rate in diabetic patients. We evaluated the error of creatinine and/or cystatin-C based formulas in reflecting real renal function over a wide range of glomerular filtration rate (from advanced chronic kidney disease to hyperfiltration). The error of estimated glomerular filtration rate by any equation was common and wide averaging 30% of real renal function, and larger in patients with measured glomerular filtration rate below 60 mL/min. This led to chronic kidney disease stages misclassification in about 30% of the individuals and failed to detect 25% of the cases with hyperfiltration. Cystatin-C based formulas did not outperform creatinine based equations, and the reliability of more modern algorithms proved to be as poor as older equations. Formulas failed in reflecting renal function in type 2 diabetes mellitus. Caution is needed with the use of these formulas in patients with diabetes, a population at high risk for kidney disease. Whenever possible, the use of a gold standard method to measure renal function is recommended.

We are entering a new era in the management of adiposity-based chronic disease (ABCD) with type 2 diabetes (T2D) and related chronic kidney disease (CKD). ABCD, T2D and CKD can affect almost every major organ system and have a particularly strong impact on the incidence of cardiovascular disease (CVD) and heart failure. ABCD and the associated insulin resistance are at the root of many cardiovascular, renal and metabolic (CKM) disorders, thus an integrated therapeutic framework using weight loss (WL) as a disease-modifying intervention could simplify the therapeutic approach at different stages across the lifespan. The breakthrough of highly effective WL drugs makes achieving a WL of >10% possible, which is required for a potential T2D disease remission as well as for prevention of microvascular disease, CKD, CVD events and overall mortality. The aim of this review is to discuss the link between adiposity and CKM conditions as well as placing weight management at the centre of the holistic CKM syndrome approach with a focus on CKD. We propose the clinical translation of the available evidence into a transformative Dysfunctional Adipose Tissue Approach (DATA) for people living with ABCD, T2D and CKD. This model is based on the interplay of four essential elements (i.e. adipocentric approach and target organ protection, dysfunctional adiposity, glucose homeostasis, and lifestyle intervention and de-prescription) together with a multidisciplinary person-centred care. DATA could facilitate decision-making for all clinicians involved in the management of these individuals, and if we do this in a multidisciplinary way, we are prepared to meet the adipocentric challenge.

Obesity represents a serious and growing disease worldwide. The pathophysiological changes secondary to chronic inflammation lead to the development of diseases that increase the morbidity and mortality of individuals. Chronic kidney disease (CKD) is a condition with deleterious effects that acts bidirectionally with obesity. From approximately 20% to 30% of individuals share phenotypes of CKD and obesity, increasing their cardiovascular risk and the risk of other complications. Obesity and CKD form a vicious cycle in which inflammation is the central axis of multiorgan damage. Despite increasing the risk of cardiac and renal mortality, CKD progresses in relation to body mass index and albuminuria. Nowadays, the implementation of the new medications aimed at mitigating the peak of inflammation is becoming a cornerstone of treatments for obesity, diabetes, cardiovascular diseases, and renal disease.

This study aimed to investigate obesity-related glomerulopathy (ORG) at cellular, structural, and transcriptomic levels. Thirty Wistar rats were randomized into two groups: 15 rats were fed with a standard diet (SD-rats), and 15 rats were fed with a high-fat diet (HFD-rats). After 10 weeks, the weight, kidney function, histological features, and transcriptomic changes were assessed. HFD-rats gained significantly more weight (55.8% vs. 29.2%; p < 0.001) and albuminuria (10,384.04 ng/mL vs. 5845.45 ng/mL; p < 0.001) compared to SD-rats. HFD-rats exhibited early stages of ORG, with predominant mesangial matrix increase and podocyte hypertrophy (PH). These lesions correlated with differentially expressed (DE) genes and miRNAs. Functional analysis showed that miR-205, which was DE in both the kidneys and urine of HFD-rats, negatively regulated the PTEN gene, promoting lipid endocytosis in podocytes. The downregulation of PTEN was proved through a higher PTEN/nephrin ratio in the SD-rats and the presence of lipid vacuoles in HFD-podocytes. This study has found a specific targetome of miRNAs and gene expression in early stages of ORG. Also, it emphasizes the potential value of miR-205 as a urinary biomarker for detecting podocyte injury in ORG, offering a tool for early diagnosis, and opening new avenues for future therapeutic research of obesity-related glomerulopathy.

Obesity increases the risk of cardiovascular disease, diabetes and chronic kidney disease. Obesity-related glomerulopathy (ORG) is a potentially reversible cause of kidney disease that often progresses silently until it reaches irreversible stages. However, we are still lacking a sensitive and specific biomarker to identify patients with obesity who are at risk of developing CKD. The role of microRNAs (miRNAs) has emerged as a promising area for diagnostic and therapeutic applications in kidney disease. Recent research has highlighted the specific roles of various miRNAs in renal function, showing that their dysregulation can contribute to the development of kidney diseases. This review will discuss the emerging role of miRNAs in the context of ORG, focusing on their potential as biomarkers and therapeutic targets for this increasingly prevalent disease.

Obesity represents a serious and growing disease worldwide. The pathophysiological changes secondary to chronic inflammation led to the development of diseases that increase the morbidity and mortality of individuals. Chronic kidney disease (CKD) is a condition with deleterious effects that acts bidirectionally with obesity. Approximately 20% to 30% of individuals share phenotypes of CKD and obesity, increasing their cardiovascular risk and the risk of other complications. Obesity and CKD form a vicious cycle in which inflammation is the central axis of multiorgan damage. Despite increasing the risk of cardiac and renal mortality, CKD progresses in relation to body mass index and albuminuria. Nowadays, the implementation of the new medications aimed at mitigating the peak of inflammation are becoming as cornerstone treatments for obesity, diabetes, cardiovascular diseases, and renal disease.