Renal stone prevalence around 10 % in developed high income countries.
Increasing prevalence (++ increased detection with imaging).
EAU – first time stone formers had 26 % recurrence within 5 years, highly recurrent disease seen in 10 % of stone patients. Traditionally quoted 30 – 50 % patients will recur within 5 years.
Risk factors:
Obesity, diabetes and metabolic syndrome
Obesity linked with more excretion of oxalate, uric acid, sodium and phosphorous.
Obesity also linked with lower urine pH and uric acid stone formation.
Mechanisms not entirely clear.
Dietary
Hydration is key.
High PRAL (potential renal acid load) diets – increased acids reduce urinary citrate.
High salt and high oxalate diets increase risk.
Inflammatory bowel disease
Unabsorbed fatty acids bind to calcium in gut -> less oxalate bound to calcium in gut, so more oxalate reabsorbed and excreted in urine.
Malabsorption leads to less reabsorption and therefore urinary excretion of citrate and magnesium.
Chronic dehydration related to short gut, diarrhoea or high output ileostomies.
Decolonisation of GI tract of the oxalate fermenting bacteria Oxalobacter fromigenes
Weight loss surgery
Hyperoxaluria clearly demonstrated after weight loss surgery although cause not clearly defined – as above.
Highest risk with Roux en Y – causes hyperoxaluria, reduced urine volume and hypocitraturia.
Urinary diversions (and neuropathic bladder)
Systemic metabolic acidosis – causes hypercalciuria and hypocitraturia.
Chronic UTIs and urease producing organisms.
Urinary stasis.
Foreign bodies such as sutures, staple lines and mucus.
Hyperoxaluria if long segments of small bowel resected.
Table from EAU – risk of CKD with certain stone types and syndromes:
