Primary Causes & Pathophysiology
Most cases arise by ascending infection (germs travelling upward) from periurethral flora (germs around urine opening). Uropathogenic Escherichia coli (bladder-kidney infecting gut bacteria) adhere with P fimbriae (hair-like anchors) and ascend. Vesicoureteral reflux (backward urine flow) and stasis (poor drainage) aid ascent to pelvis and medulla (inner kidney). Bacterial toxins and neutrophil response (pus-cell defence) cause tubular injury (damage to urine-forming tubes). Papillary ischaemia (poor blood flow to kidney tips) and microabscesses (tiny pus pockets) may follow.
P-fimbriated strains colonise periurethral area then ascend via ureters to pelvis causing tubular inflammation
Capsular and urease-producing strains ascend especially with stones and catheters causing tissue injury
Biofilm formation (slime layers on catheters) and impaired washout allow ascent in catheterised or obstructed systems
Stasis (stagnant urine) raises pelvic pressure and impairs clearance allowing bacterial growth in pelvis
Backward urine flow carries bladder bacteria to kidneys while incomplete emptying sustains colonisation
Bloodborne bacteria lodge in cortex (outer kidney) forming microabscesses without ascending infection