Gut Microbiota Dysbiosis in Lupus Nephritis


Hager Zanaty


Begins enrollment in 6 months


Gut Microbiota Dysbiosis in Lupus Nepheritis


Genetic: DNA extraction and PCR amplification

Study type


Funder types



Gut microbiota in LN

Details and patient eligibility


Evaluate dysbiosis of some intestinal microbiota in adult patients with lupus nephritis compared to healthy controls.

Full description

Systemic Lupus Erythematosus (SLE) is an autoimmune disease resulting in multi-organ inflammation with complex clinical manifestation including neuropsychiatric, lupus nephritis..etc. However, the actual cause of SLE is still unknown [1]. Various etiologies have been postulated which can be categorized into genetic and environmental such as age, gender, ultra-violet exposure, dietary intake, alcohol, and lifestyle behavior [2]. Lupus nephritis is one of the most severe manifestations of SLE with high mortality rate and 10% of them eventually develop end-stage renal disease within 5 years after diagnosis [3,4]. There are trillion of microbes inhabited human gut which dominated by 4 phyla; Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria. In healthy human gut, 98% of gut microbiota is dominated by Bacteroidetes and Firmicutes. Every species of gut microbiota play their own role in modulating immune system. Many factors could alter gut communities such as infant transition, dietary habit, age, gender and antibiotic consumption [5, 6]. Firmicutes responsive in fatty acids and carbohydrates absorption whereas Bacteroidetes correspond to polysaccharides absorption [7]. Recently, enormous reports highlighted on the association of autoimmune diseases with dysbiosis of gut microbiota [8-11], During the autoimmune disease condition, the symbiotic relationship is broken due to various factor such as dietary habit that change microbiota diversity. The decrease of microbial diversity was found in autoimmune diseases such as SLE and inflammatory bowel disease (IBD), presented by reduce commensal bacteria (Firmicutes and Bacteroidetes) and increase of detrimental bacteria (Proteobacteria and Actinobacteria) [12]. Alteration of gut microbiota expresses as Firmicutes/Bacteroidetes ratio (F/B) potentially act as the measurement for pathological condition in SLE patients which cause systemic inflammation. The decreased ratio of F/B microbiome in SLE patients occur either by the reduction in Firmicutes or increase abundance of Bacteroidetes [13]. In human study, altered short chain fatty acids (SCFA) fecal level in lupus patient with low F/B ratio suggest the potential link of gut absorption function with microbes [14]. Hence, it is necessary to identify the exact mechanism on how the gut microbiota promote SLE and LN pathogenesis in human studies.


60 estimated patients




18 to 50 years old


No Healthy Volunteers

Inclusion criteria

  • Adult male and female patients diagnosed with lupus nephritis. Adult age and sex matched healthy individuals will be included as a control group.

Informed consent will be obtained from each study participant.

Exclusion criteria

  • Subjects at age<18 years. Diseases affecting the gut microbiota (e.g. chronic diarrhea, Crohn's disease, or ulcerative colitis).

Patients on maintenance dialysis, with diabetes or pregnancy, using antibiotics, probiotics, prebiotics, or synbiotics in the previous 4 weeks.

Patients with critical condition (hypertension emergency,urgency, acute myocardial infarction or stroke within the last 6 months) and suspected/confirmed renal vascular disease.

Trial design

60 participants in 2 patient groups

Patient with lupus nepheritis
Genetic: DNA extraction and PCR amplification
Healthy persons of the same age
Genetic: DNA extraction and PCR amplification

Trial contacts and locations



Central trial contact

Hager Zanaty; Rasha Madkour, Lecturer

Data sourced from

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