The clinical consequences of obesity on the kidneys, with or without metabolic abnormalities, involve both renal function and structures. The mechanisms linking obesity and renal damage are well understood, including several effector mechanisms with interconnected pathways. Higher prevalence of urinary albumin excretion, sub-nephrotic syndrome, nephrolithiasis, increased risk of developing CKD, and progression to ESKD have been identified as being associated with obesity and having a relevant clinical impact. Moreover, renal replacement therapy and kidney transplantation are also influenced by obesity. Losing weight is key in limiting the impact that obesity produces on the kidneys by reducing albuminuria/proteinuria, declining rate of eGFR deterioration, delaying the development of CKD and ESKD, and improving the outcome of a renal transplant. Weight reduction may also contribute to appropriate control of cardiometabolic risk factors such as hypertension, metabolic syndrome, diabetes, and dyslipidemia which may be protective not only in renal damage but also cardiovascular disease. Lifestyle changes, some drugs, and bariatric surgery have demonstrated the benefits.

Prediabetes is a significant metabolic status since there is high potential for future progression of diabetes mellitus (DM). People with prediabetes are at increased risk of cardiovascular disease (CVD) and mortality. Endothelial and microvascular dysfunction is considered a key step towards the development and progression of CVD. Importantly, endothelial and microvascular dysfunction can be detected and monitored using non-invasive procedures in peripheral organs and tissues, including the retina, kidney, skin and skeletal muscle. Structural and functional alterations of the microvasculature have been consistently documented in the above microvascular beds in patients with diabetes mellitus. In contrast, such alterations remain understudied in prediabetes, but are currently receiving attention as markers of subclinical and future CVD. The aim of this review is to summarize available evidence regarding the presence of subclinical microvascular and endothelial dysfunction in prediabetes and their impact on cardiovascular risk.

Background: Understanding the causes of hypertension is important in order to prevent the disease. Gut microbiota (GM) seems to play an important role, but the detailed physiology remains elusive, with alpha diversity being the most studied indicator. Objectives: This review aimed to systematically synthesize data on gut microbiota (alpha diversity) and hypertension. Methods: Databases, including MEDLINE/PubMed, Scopus, and EMBASE, and citations were systematically queried. We retrieved articles reporting the association between gut microbiota and hypertension. A valid critical appraisal tool was also used to investigate the quality of the included studies. Results: Eighteen eligible studies met our inclusion criteria. In this report, we focused on the following indices of alpha diversity: Shannon, Chao1, Simpson, and Abundance-based Coverage Estimator (ACE) indices. Several studies observed a significantly lower Shannon index in hypertensive patients compared to the healthy control group. Nevertheless, no statistically significant difference was found for the Chao1, Simpson, and ACE indices between hypertensive patients and controls. A higher Firmicutes-to-Bacteroidetes ratio (F/B ratio) was consistently observed in hypertensive patients compared to healthy controls, indicating potential dysbiosis in the gut microbiota. Conclusions: Our systematic review indicates that hypertensive patients may exhibit an imbalance in gut microbiota, evidenced by decreased alpha diversity and an elevated F/B ratio. However, the absence of statistically significant differences in secondary diversity indices (Chao1, Simpson, and ACE) highlights the need for further research. Well-designed, large-scale studies are necessary to clarify these associations and explore the role of gut microbiota in hypertension development.