# Visceral Obesity and Metabolic Dysfunction in IgA Nephropathy: Nutritional and Metabolic Perspectives on Disease Progression

## TL;DR

This paper reviews how visceral obesity and metabolic syndrome worsen IgA nephropathy through immune and inflammatory pathways, suggesting that targeting these factors could slow disease progression.

## Contribution

The paper identifies a bidirectional amplification loop between obesity and IgAN progression, linking visceral adipose tissue effects to immune pathways.

## Key findings

- Visceral obesity and metabolic syndrome accelerate IgAN progression through endocrine, inflammatory, and immune pathways.
- MetS patients with IgAN show higher proteinuria, faster eGFR decline, and increased risk of end-stage renal failure.
- Nutritional and metabolic interventions, such as weight reduction and GLP-1 agonists, demonstrate renoprotective effects in obesity-related kidney disease.

## Abstract

Introduction: IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. In addition to genetic and immunological factors, visceral obesity and metabolic syndrome (MetS) are the main determinants of disease progression. This review aims to critically assess the role of visceral obesity and metabolic syndrome in driving the progression of IgA nephropathy (IgAN), with an emphasis on their underlying pathophysiological mechanisms and clinical implications. Methods: A systematic review was carried out in accordance with PRISMA guidelines. PubMed was searched (2015–2025) using terms related to IgA nephropathy, obesity, metabolic syndrome, and immunometabolic pathways. Only English-language observational and clinical studies in adults, excluding pediatric and animal studies, were included in the review. Additional sources were consulted to give context to the mechanistic aspects of obesity-related IgAN progression. Results: Visceral obesity and MetS accelerate IgAN progression through endocrine, inflammatory, and immune pathways, including cytokines derived from visceral adipose tissue, adipokines, intestinal dysbiosis, and BAFF/APRIL-mediated immune activation. MetS patients had higher proteinuria, a faster decrease in eGFR, and a higher risk of end-stage renal failure (23/65 vs. 15/60 endpoints, p < 0.001). Nutritional and metabolic interventions—including weight reduction, GLP-1 receptor agonists, dual GLP-1/GIP agonists, and bariatric/metabolic surgery—demonstrate renoprotective effects in obesity-related kidney disease and may have implications for IgAN. Conclusions: Obesity should be considered a chronic disease and a modifiable risk factor for IgAN. Nutrition-focused interventions targeting visceral obesity and metabolic dysfunction can slow the progression of the disease and should be included in renal guidelines. This review expands current knowledge by demonstrating that when sequential steps of IgAN pathophysiology are mapped with respect to endocrine and immunological effects of visceral adipose tissue, they converge on the same proinflammatory and immune pathways. This convergence suggests a bidirectional amplification loop in which obesity accelerates IgAN progression and increases the burden of complications.