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Bacterial and host determinants of renal scarring
H Lomberg1, P de Man, C Svanborg Edén
1Department of Clinical Immunology, University of Göteborg, Sweden.
Abstract:
This review summarizes recent work examining the interaction between host and parasite in recurrent urinary tract infection (UTI) and renal scarring. Virulence in uropathogenic E. coli has been defined by the severity of acute disease. Isolates from patients with acute pyelonephritic strains differ from those causing asymptomatic bacteriuria by multiple traits which contribute to virulence, and which are coexpressed in a non-random manner. The single marker most characteristic for the pyelonephritogenic clones is bacterial adherence to uroepithelial cells binding specifically to the disaccaride Gal alpha 1-4 Gal beta within the globoseries of glycolipids. The notion that the most severe consequence of acute pyelonephritis, i.e. renal scarring, was caused by the most virulent clones, was contradicted by comparison of pyelonephritic strains isolated from children with and without scarring. The virulent clones were significantly less frequent in patients with renal scarring (22%) than in patients with recurrent pyelonephritis not developing renal scars (62%). In view of the unexpected inverse association of bacterial virulence with renal scarring lack of Gal alpha 1-4 Gal beta binding capacity of E. coli strains was found to predict the risk for renal scarring among boys with first-time acute pyelonephritis. Vesicoureteric reflux (VUR) is widely accepted as a host determinant of susceptibility to pyelonephritis and renal scarring. In our study the frequency of renal scarring was 57% among girls with VUR as compared to 8% of those without. The reflux alone did however, not explain the selection of bacteria of low virulence. Individuals prone to UTI and renal scarring were found to be a genetically selected subgroup of the general population. A correlation between P1 blood group phenotype and susceptibility to UTI and between blood group non-secretor state and renal scarring was found. The mechanisms behind these relationships need to be defined. The bacterial and host parameters combined indicate that host parameters are essential for the tendency to develop renal scarring after acute pyelonephritis.
Insights
Host factors, not just bacterial virulence, are key in recurrent urinary tract infections (UTIs) and kidney scarring. Genetic predisposition and vesicoureteric reflux influence susceptibility to UTIs and renal scarring.
Area of Science:
- Microbiology
- Immunology
- Genetics
Background:
- Recurrent urinary tract infections (UTIs) and subsequent renal scarring are significant health concerns.
- Uropathogenic Escherichia coli (E. coli) virulence is traditionally linked to disease severity.
- Host-parasite interactions in recurrent UTIs and renal scarring require further elucidation.
Purpose of the Study:
- To review recent research on host-parasite interactions in recurrent UTIs and renal scarring.
- To investigate the role of bacterial virulence factors and host determinants in the development of renal scarring.
- To explore genetic predispositions and their correlation with UTI susceptibility and renal scarring.
Main Methods:
- Review of existing literature on uropathogenic E. coli virulence and host factors.
- Analysis of bacterial adherence properties, specifically Gal alpha 1-4 Gal beta binding.
- Examination of host factors including vesicoureteric reflux (VUR) and blood group phenotypes (P1, non-secretor).
Main Results:
- Bacterial virulence, characterized by Gal alpha 1-4 Gal beta binding, was inversely associated with renal scarring in children.
- Lack of Gal alpha 1-4 Gal beta binding predicted renal scarring risk in boys with first-time pyelonephritis.
- Vesicoureteric reflux significantly increased renal scarring risk in girls, but did not fully explain the selection of less virulent bacteria.
- Genetic factors, including P1 blood group and non-secretor status, correlated with UTI susceptibility and renal scarring.
Conclusions:
- Host parameters are crucial in determining the tendency for renal scarring after acute pyelonephritis.
- Bacterial virulence alone does not fully explain renal scarring; host genetic factors play a significant role.
- Further research is needed to define the mechanisms linking genetic factors to UTI susceptibility and renal scarring.