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The urinary microbiome in association with diabetes and diabetic kidney disease: A systematic review
Tiscar Graells1, Yi-Ting Lin1,2, Shafqat Ahmad3,4,5
1Department of Neurobiology, Care Sciences and Society, Division of Family Medicine and Primary Care, Karolinska Institute, Huddinge, Stockholm, Sweden.
Background:
The urinary microbiome, or urobiome, is a novel area of research that has been gaining attention recently, as urine was thought to be sterile for years. There is limited information about the composition of the urobiome in health and disease. The urobiome may be affected by several factors and diseases such as diabetes, a disease that often leads to kidney damage. Thus, we need to understand the role of the urobiome to assess and monitor kidney disease related to diabetes over time.
Methods:
We conducted a systematic review to summarize knowledge about the urobiome in association with diabetes mellitus and diabetic kidney disease. The search was conducted in several electronic databases until November 2024.
Results:
Eighteen studies were selected including cross-sectional case-control studies, cross-sectional surveys and one prospective longitudinal study. In total, the urobiome of 1,571 people was sequenced, of which 662 people had diabetes, and of these 36 had confirmed diabetic kidney disease; 609 were healthy individuals, 179 had prediabetes or were at risk of type 2 diabetes mellitus and 121 did not have diabetes but had other comorbidities. Eight studies analysed data from females, one was focused on male data, and the other nine had mixed female-male data. Most of the studies had a small sample size, used voided midstream urine, and used 16S rRNA sequencing.
Conclusion:
This systematic review summarizes trends seen throughout published data available to have a first baseline knowledge of the urinary microbiome, and its microbiota, in association with diabetes including the decreased richness and α-diversity in urinary microbiota in individuals with diabetes compared to healthy controls and the decreased α-diversity with the evolution of kidney disease independently of the cause.
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