Microbiota and Metabolome Associated with Immunoglobulin A Nephropathy (IgAN)

Angelis, Maria De; Montemurno, Eustacchio; Piccolo, María Cintia; Vannini, Lucia; Lauriero, Gabriella; Maranzano, Valentina; Gozzi, Giorgia; Serrazanetti, Diana Isabella; Dalfino, Giuseppe; Gobbetti, Marco; Gesualdo, Loreto

doi:10.1371/journal.pone.0099006

Cited by 202 publications

(236 citation statements)

References 67 publications

Supporting

Mentioning

203

Contrasting

Order By: Relevance

“…Microbiome profile is not only altered in CKD, it also varies by underlying etiology. 133–135 Whether the dysbiotic microbiome is a cause and/or consequence of CKD, is not quite clear. 136 The potential utility of gut microbiome as a biomarker for screening individuals with susceptibility to develop CKD remains to be investigated.…”

Section: Recent Advancesmentioning

confidence: 99%

Role of the Gut Microbiome in Uremia: A Potential Therapeutic Target

Ramezani

Massy

Meijers

et al. 2016

American Journal of Kidney Diseases

312

265

View full text Add to dashboard Cite

Also known as the “second human genome,” the gut microbiome plays important roles in both the maintenance of health and the pathogenesis of disease. The symbiotic relationship between host and microbiome is disturbed due to proliferation of dysbiotic bacteria in patients with chronic kidney disease (CKD). Fermentation of protein and amino acids by gut bacteria generate excess amounts of potentially toxic compounds such as ammonia, amines, thiols, phenols, and indoles, but generation of short chain fatty acids is reduced. Impaired intestinal barrier function in CKD permits translocation of gut-derived uremic toxins into the systemic circulation, contributing to progression of CKD, cardiovascular disease, insulin resistance, and protein energy wasting. The field of microbiome research is still nascent, but evolving rapidly. Establishing symbiosis to treat uremic syndrome is a novel concept, but if proven effective will have significant impact on the management of patients with CKD.

show abstract

Section: Recent Advancesmentioning

confidence: 99%

Role of the Gut Microbiome in Uremia: A Potential Therapeutic Target

Ramezani

Massy

Meijers

et al. 2016

American Journal of Kidney Diseases

312

265

View full text Add to dashboard Cite

show abstract

“…Interesting observations in the past couple of years indicate differences in both faecal and salivary microbiota between individuals with IgAN and healthy controls 27,28 . The lowest faecal microbial diversity was found in patients with clinically progressive IgAN.…”

Section: Role Of Mucosal Microorganismsmentioning

confidence: 99%

The mucosa–kidney axis in IgA nephropathy

2015

View full text Add to dashboard Cite

Links between IgA nephropathy (IgAN) and the mucosa have been recognized since the 1970s. In particular, the observation of visible haematuria induced by respiratory infections in patients with IgAN and the association of IgAN with diseases in which the mucosa plays a part, especially coeliac disease, have been taken as evidence of a mucosa-kidney axis. Here, we review current evidence that links the mucosa, in particular the gastrointestinal mucosa, and IgA produced by the bone marrow with IgAN. Genome-wide association studies in patients with IgAN have identified risk loci in genes involved in the intestinal mucosal integrity and immune network. Furthermore, the systemic immune response to mucosal antigens in IgAN is increased. Moreover, patients with IgAN have an increased reactivity to dietary proteins associated with subclinical intestinal mucosal inflammation. Associations between IgAN and gastrointestinal diseases have also been reported in a small number of patients, but whether these diseases share a common pathogenesis or whether gastrointestinal inflammation exacerbates IgAN is uncertain. Indeed, mucosal alterations such as infections could activate the innate immune system, aggravate a pre-existing IgAN and promote disease manifestations such as macrohaematuria. Various clinical interventions and trials targeting the mucosa or presumed mucosa-associated mechanisms have so far not yielded consistent findings and the results of ongoing trials are eagerly awaited.

show abstract

“…A recent study indicates that the microbiome in IgAN is changed, such as a decrease in Clostridium, Enterococcus, Lactobacillus, Leuconostoc, and Bifidobacterium, and an increase in Streptococcus sp. and Firmicutes [24]. Till now, the relationship between periodontal infection and IgAN is not well studied.…”

Section: Introductionmentioning

confidence: 99%

Comparative Analyses of Subgingival Microbiome in Chronic Periodontitis Patients with and Without IgA Nephropathy by High Throughput 16S rRNA Sequencing

Cao

Qiao

Tian³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Periodontitis is a prevalent chronic inflammatory disease caused by enhanced inflammation induced by dysbiotic microbes forming on subgingival tooth sites, which may disturb the balance of the microbial composition in the biofilm and finally result in the progressive destruction of the periodontal ligament and alveolar bone with periodontal pocket formation and/or gingival recession. Methods: To elucidate the correlation between subgingival microbiome and IgAN incidence in CP (chronic periodontitis at severe levels) patients, subgingival plaque samples were collected from CP patients without IgAN (Control) and CP patients with IgAN (Disease). 16S rRNA sequencing and comparative analyses of plaque bacterial microbiome between Control and Disease were performed. Results: Subgingival microbial diversity in Disease was a little higher than that in Control. Besides, significant differences were found in subgingival microbiome between Disease and Control. Compared with that in Control, at phylum level, the abundances of Proteobacteria and Actinobacteria were significantly higher while the abundances of Bacteroidetes, Fusobacteria, Spirochaetae, Synergistetes, and Saccharibacteria were significantly lower in Disease; at class level, the abundances of Betaproteobacteria, Bacilli, Actinobacteria, Flavobacteriia, and Gammaproteobacteria were significantly higher while the abundances of Bacteroidia, Fusobacteriia, Negativicutes, Clostridia, and Spirochaetes were significantly lower in Disease; at genus level, the abundances of Bergeyella, Capnocytophaga, Actinomyces, Corynebacterium, Comamonas, Lautropia, and Streptococcus were significantly higher while the abundances of Treponema and Prevotella were significantly lower in Disease. Conclusions: Our data indicated a correlation between the changes in subgingival microbial structure and IgAN incidence in CP patients, which might be used to predict IgAN incidence in CP patients.

show abstract

Microbiota and Metabolome Associated with Immunoglobulin A Nephropathy (IgAN)

Cited by 202 publications

References 67 publications

Role of the Gut Microbiome in Uremia: A Potential Therapeutic Target

Role of the Gut Microbiome in Uremia: A Potential Therapeutic Target

The mucosa–kidney axis in IgA nephropathy

Comparative Analyses of Subgingival Microbiome in Chronic Periodontitis Patients with and Without IgA Nephropathy by High Throughput 16S rRNA Sequencing

Contact Info

Product

Resources

About