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PubMed1985

Crystallization conditions in urine of patients with idiopathic recurrent calcium nephrolithiasis and with hyperparathyroidism.

The highest degree of urinary supersaturation with respect to calcium oxalate monohydrate (COM) and brushite at which secondary nucleation and growth of small amounts of COM and hydroxyapatite (HAP) are inhibited was determined by new and simple methods. There were 39 subjects who produced 24 h-urine collections (11 idiopathic stone formers (ISF), 12 patients suffering from primary hyperparathyroidism (HPT) and 16 healthy controls (HC). These subjects had a moderate calcium and low oxalate intake. The results obtained were compared with the state of urinary saturation and with urine chemistry. The measurements of crystallization conditions with respect to COM were repeated in 26 subjects (11 ISF, 5 HPT, 10 HC) after a dietary oxalate load. In 24 h-urines of HC diluted to 2.4 1/24 h the degree of supersaturation necessary to induce crystallization of COM and HAP was 2-5 times higher than the state of urinary saturation measured under the same test conditions. ISF showed a decreased pyrophosphate concentration and a decreased inhibitory activity to HAP crystallization in their 24 h-urine. The urinary inhibitory activity towards crystallization of HAP showed a positive correlation to urinary pyrophosphate concentration. In the 24 h-urine of HPT hypercalciuria and increased saturation with respect to brushite which reached values to induce HAP crystallization were found. After a dietary oxalate load urinary supersaturation with respect to COM reached values to induce COM crystallization in ISF and HPT but not in HC.

Adult↗
PubMed1997

Cell cultures and nephrolithiasis.

While the physical chemistry of stone formation has been intensively studied during the last decade, it has become clear that the pathophysiology of renal stone disease cannot be explained by crystallization processes only. In recent years, evidence has emerged that the cells lining the renal tubules can have an active role in creating the conditions under which stones may develop. Since it is difficult to study these mechanisms in vivo, cultured renal tubular cells have become increasingly popular for the study of physiological and cell biological processes that are possibly linked to stone disease. In this paper, we discuss the possible contribution of cellular processes such as transepithelial oxalate transport and crystal--cell interaction to the formation of renal stones. Experimental studies that have been performed with cultured renal cells to elucidate the mechanisms involved in these processes will be summarized.

Animals↗
PubMed1986

[Questionable significance of the chemical analysis of a single 24-hour urine sample in recurrent calcium oxalate nephrolithiasis].

Chemical findings were obtained from 24 h urine samples of 43 male calcium-oxalate stone-formers on an unrestricted diet. Results were compared with data from 51 age-matched healthy blood donors. No differences were found in the excreted quantities of calcium, oxalic acid, uric acid and inorganic phosphate, nor in the calcium to creatinine ratio or the activity product of calcium and oxalic acid. The only differences were a higher output of magnesium and a higher magnesium to calcium ratio for controls. The extent of these differences, however, does not justify further subdivision of the group of stone-formers. The diagnostic and therapeutic significance of the chemical analysis of one 24 h urine sample is doubtful for this group of patients.

Adult↗
PubMed1986

[Peroral calcium administration test with free diet in idiopathic calcium nephrolithiasis--possibilities and limits].

Seventeen patients who recurrently formed idiopathic calcium kidney stones (SF) and 25 age- and sex-matched healthy blood donors (H) were challenged by an oral calcium load (1 g) after an overnight fast. Their usual diet was not changed before the test. Urine samples were taken before, 2 1/2, and 4 h after the calcium load. A blood sample was drawn 3 3/4 h after calcium loading. Before and 2 1/2 h after calcium dosage urinary measurements of calcium, magnesium, phosphate, oxalate, uric acid, and creatinine did not reveal any differences between SF and H. According to the calciuria after 4 h SF were separated in normocalciurics (NCSF) and hypercalciurics (HCSF). Nine-tenths of the NCSF had higher serum ionic calcium levels than H after calcium load (P less than 0.001), whereas HCSF were not different from H. Serum phosphate in SF was lower than in H (P less than 0.001). Carboxy-terminal parathormone, measured in 3 NCSF and 2 HCSF, was normal. Depending on the calciuria or calcemia 4 h after an oral calcium load, 16 of 17 SF showed a metabolic abnormality (hypercalcemia or hypercalciuria). It is concluded that intestinal calcium absorption in SF might be increased to variable rates.

Administration, Oral↗