The link between childhood urinary tract infection (UTI), vesicoureteric reflux (VUR) and segmental renal scarring had long been recognised when a piglet model provided a possible unifying theory of causality. VUR was central to this, allowing infected urine to reach the kidney, and then enter the tubules of particular shaped renal pyramids (70% of human kidneys have this feature). This could cause permanent segmental scarring very quickly; the 'big bang' reflux nephropathy model. Because only young children appear vulnerable to initiate scarring, it has been assumed that kidneys mature out of this risk.
More recently, others have argued that most 'focal defects' are congenital, and that the association with VUR is not causal, but just one of shared dysplasia. Their argument hinges on most defects being present at first imaging, and a lack of evidence of benefit from interventions. They therefore argue for minimising investigations after childhood UTI; the NICE guidelines are grounded in this philosophy.
Recent evidence from transplanted adult human kidneys challenges these views; reflux nephropathy occurs dramatically fast in 70% of kidneys with VUR after exposure to one brief UTI. This provides a powerful argument that most native kidney scars are also acquired in this way, and that childhood UTI management strategies to date respond too slowly to prevent scarring in most vulnerable infants. However, prevention should be possible, but would require more awareness and quicker treatment in primary care, and increased diagnostic, therapeutic and investigative rigor. NICE's recommendations will not help this goal.
- Reflux nephropathy
- Renal imaging tests
- Renal scarring
- Urinary tract infection
- Vesicoureteric reflux (VUR)
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