[Studies on the crystallization tendency of calcium oxalate in urine--a study of experimental and computer-assisted determination of the risk of urinary calculi formation].

In this study a method o the semiquantitative determination of the crystallization tendency for calcium oxalate in urine is described. It is based on the addition of a well-defined amount of ammonium oxalate (31.3 nmol) to a urine sample (30 ml).

[Diagnosis of intestinal oxalate hyperabsorption in patients with idiopathic recurrent calcium oxalate urinary calculi].

By oral administration of 14C-labelled oxalic acid (2.2 microns Ci; 2 mg), the mean enteral oxalate absorption in 24-h urines (collecting intervals 3, 3, 6, 12 h) of 19 healthy control subjects was determined to be 8.3%.

[Calcium and citrate excretion by patients with calculi and healthy probands during induced acidosis].

Acidosis induced increase in renal calcium excretion and decrease in renal citrate excretion was produced by means of ammonium chloride load in 15 patients with recurrent oxalate lithiasis and in 15 control subjects. The expected increase in the calcium citrate relationship in urine is more marked and more lasting in stone patients. Stone formers obviously respond to an acidotic metabolic situation by a more clear relative decrease in citrate excretion, in addition to more intensive calcium excretion, which is known.

[Calcium excretion in patients with calcium oxalate calculi in acid administration].

Acidosis induced increase in renal calcium excretion was produced by means of ammonium chloride load in 12 control persons and in 76 patients with recurrent oxalate lithiasis. This increase is more marked in stone patients - even in those with normocalciuria - than in control persons. The calcium excretion is especially increased in patients with renal hypercalciuria.