Over the past 10 years, major progress has been made in the knowledge of urinary lithogenesis, including the potential pathogenetic role of Randall's plaques and renal tubular crystal retention. Urine supersaturation is the driving force of this process and can be induced by some risk factors, including low urine volume, high urinary excretion of
calcium oxalate and
uric acid and low urinary excretion of
citrate. Primary
hypercalciuria can be due to intestinal overabsorption renal leak and bone reabsorption of
calcium. Prophilaxis is mainly conducted with
thiazides and low
calcium diet which is indicated only in the intestinal form.
Primary hyperoxaluria is treated with
pyridoxine and may require in the severe forms simultaneous renal and
liver transplantation. Enteric
hyperoxaluria is secondary to
fatty acids malabsorption and requires diet, oral
calcium and cholestiramine. Hyperuricosuria is caused by diet endogenous overproduction, mainly due to enzymatic defects or high renal excretion of
uric acid. Urine alkalinization with K or K and
Mg citrate can prevent stone formation even in idiopathic
uric acid nephrolithiasis, in which a defect of urine acidification is supposed to be the main abnormality, and in hypocitraturic patients.
Cystinuria is a rare inherited defect with an intense clinical impact. It can be classified in three forms and
urinary stone formation is the role. Increased solubility and conversion of
cystine in a more soluble form are the main goals of the prophylaxis which includes K
citrate and
thiol agents administration.
Tiopronin is preferred to
D-penicillamine due to its lower side effects.