Metabolic syndrome, obesity and kidney stones

To give a comprehensive and focused overview on the current knowledge of the causal relations of metabolic syndrome and/or central obesity with kidney stone formation.

Previous reports were reviewed using PubMed, with a strict focus on the keywords (single or combinations thereof): urolithiasis, nephrolithiasis, kidney stones, obesity, metabolic syndrome, bariatric surgery, calcium oxalate stones, hyperoxaluria, insulin resistance, uric acid stones, acid-base metabolism.

Obesity (a body mass index, BMI, of >30 kg/m(2)) affects 10-27% of men and up to 38% of women in European countries. Worldwide, >300 million people are estimated to be obese. Epidemiologically, a greater BMI, greater weight, larger waist circumference and major weight gain are independently associated with an increased risk of renal stone formation, both for calcium oxalate and uric acid stone disease.

There are two distinct metabolic conditions accounting for kidney stone formation in patients with metabolic syndrome/central obesity. (i) Abdominal obesity predisposes to insulin resistance, which at the renal level causes reduced urinary ammonium excretion and thus a low urinary pH; the consequence is a greater risk of uric acid stone formation. (ii) Bariatric surgery, the only intervention that facilitates significant weight loss in morbidly obese people, carries a greater risk of calcium oxalate nephrolithiasis. The underlying pathophysiological mechanisms are profound enteric hyperoxaluria due to intestinal binding of calcium by malabsorbed fatty acids, and severe hypocitraturia due to soft or watery stools, which lead to chronic bicarbonate losses and intracellular metabolic acidosis.