
A recent study indicated a causal relationship between environmental factors and both Immunoglobulin Nephropathy (Igan) and membranous nephropathy (MN).
Igan is the most widespread glomerulonephritis in the world, bearing a considerable risk of kidney failure. Previous research has indicated a “four -stroke” progression scheme for Igan, although more recent studies have noted its inability to approach the geographic distribution of the disease, racial diversity and clinical heterogeneity.1
MN is an autoimmune disease triggered by self-antibodies attacking podocytes antigens, which leads to in situ production of immune complexes. However, little is known about pathogenesis or etiology. 40 to 60% of patients with nephrotic syndrome are growing towards a terminal renal disease or die from cardiovascular or thrombotic events.2.3
“Previous analyzes (Mendelian randomization (MR)) have revealed that external environmental factors can influence the progression of the disease by modifying the internal environmental factors of an individual (for example, personal behavior and metabolism)”, wrote Chunmin Li, department of Nephrology, Tongren hospital of the University of Wuhan and colleagues. “We have carried out an RM analysis in two stages to dissect the role of mediation of individual behavior, metabolism in the association of the external environment with the disease, offering new information on their prevention.”1
Investigators collected data from the Association of the Genome Association (GWAS) to study relations between the 68 collective environmental exhibitions and IGAN and MN. The risk factors were then divided into 5 main categories: socio -economic factors, air pollution, metabolic factors, physical measures and behavioral factors. Gwas studies with larger sample sample sample and greater recence have been chosen as a source of instrumental variables (IV) for exposure.1
The Igan data set was derived from a meta-analysis of 477,784 European samples (15,587 cases and 4,62,197 witnesses) and 24,182646 nucleotide polymorphisms (SNP) led by British biobank genetics and Finnish genetics. The primary MN was acquired from 5 European cohorts totaling 7,979 individuals (2150 MN primary cases and 5829 witnesses) and 5,327,688 SNP led by the Kiryluk laboratory.1
Causative connections have been estimated using 3 different methods: weighted median (WM), MR-EGGER and weighted reverse variance (IVW). Global estimates using IVW have been used as main effects, with WM and MR-EGGER as supplements. All IVs of the study had f> 10 values, ranging from 27 to 808, and the number of SNP varied from 2 to 300.1
In total, 20 pairs of causal relationships and 8 new relationships have been identified. Igan has presented new relationships with cheese consumption, consumption of fresh fruit, saturation of transferrine, cognitive performance, insomnia and intelligence. A causal association also appeared between the MN and the supply of beef, as well as a moderate physical activity to vigorous.1
Li and his colleagues also carried out an RM analysis of reverse causation, which indicated a negative causal relationship between the Igan and the report (gold) (ratio of ratings, .97; 95%IC, .947- .983; P <0.001), cheese intake (gold, .970; 95%IC, .947-993; P = 0.011), cognitive performance (gold, .928; 95% IC, .879-98; P = .008), Intelligence (or, .949; 95% IC, .927-.972; P <0.001), and the circumference of the hip (gold, .937; 95% IC, .893-984; P = .009). However, he predicted a positive causal relationship between Igan and triglycerides (gold, 1.091; 95%CI, 1.026-1.16; P = .005).1
The team noted that the results of this study can provide clinicians with methods to prevent or prevent the development and prognosis for Igan and MN. However, they also asked that more research be carried out both in the causal relationship between these external factors and nephropathy and the avoidance process.1
“This research provides a potential basis for creating etiological evaluation evaluation and precise risks for Igan and MN,” wrote Li and colleagues.1
References
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Li C, Wen Q, Zhang Y, Wu J. Causal Associations between environmental factors and the risk of IGA nephropathy and membranous nephropathy: an analysis of randomization and mendelian mediation bidirectional. Ren fails. 2025; 47 (1): 2486620. DOI: 10.1080/0886022X.2025.2486620
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Stamellou e, seikrit C, tang scw, et al. IGA nephropathy. Nat revise Primers. 2023; 9 (1): 67. Published on November 3023, 2023. DOI: 10.1038 / S41572-023-00476-9
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Claudio P. Primary membranous nephropathy: an endless story. J Nephrol. 2023; 36 (2): 563-574. DOI: 10.1007 / S40620-022-01461-3