Francisco R. Spivacow

Bone mineral density in patients with hypercalciuric nephrolithiasis.

Bone mineral density was studied in 50 adult patients with renal lithiasis and metabolic diagnosis of idiopathic hypercalciuria. Thirty were premenopausal women and 20 were men under 55 years of age, Bone density at the lumbar spine (LSBD) was 0.940 +/- 0.106 g/cm2 in the hypercalciuric patients compared to 1.112 +/- 0.037 g/cm2 in a cohort of age- and sex-matched controls (p < 0.001). LSBD was independent of age and was negatively correlated with the duration of stone disease (r = -0.52, p < 0.001). Thus we conclude that patients with idiopathic hypercalciuria have a decrease in their LSBD that is probably related to a negative calcium balance sustained over time.

Tolerability of oral pamidronate in elderly patients with osteoporosis and other metabolic bone diseases

Abstract Oral pamidronate (APD) is being used increasingly in the treatment of a variety of bone diseases. In a retrospective chart review of patients at three research centers (a 558.3 patient-year sample), the side effects of treatment with oral, low-dose APD administered in enteric-coated, soft gelatin capsules were analyzed in a group composed primarily of elderly women with osteoporosis. Although 21.8% of the patients experienced various gastrointestinal side effects, 89.1% complied with the treatment schedule. Among patients who discontinued therapy, two had duodenal ulcerations and one had hemorrhagic gastritis. There was a statistically significant negative correlation ( r

Which Vitamin D in Chronic Kidney Disease: Nutritional or Active Vitamin D? Or Both?

As vitamin D insufficiency is very common world-wide, vitamin D supplementation has generated much debate and subsequent research not only in the general population but also in patients with chronic kidney disease (CKD). Several observational and mechanistic studies have suggested that vitamin D’s actions may be more broad and significant than originally appreciated, far exceeding bone and mineral metabolism. This is probably due to the fact that most tissues in the body express vitamin D receptors. As patients with kidney disease cannot convert 25-hydroxyvitamin D [25(OH)D] to its more active form, 1,25-dihydroxy vitamin D [1,25(OH)2D] because of reduced activity of the enzyme 1α-hydroxylase in the kidneys to produce classic bone and mineral effects, nephrologists have traditionally replaced patients with kidney disease with active vitamin D, 1,25-dihydroxvitamin D, or related analogs. Multiple observational studies in patients with CKD have shown that they not only have low levels of 1,25(OH)2D, but also low 25(OH)D levels. The fact that there is also extrarenal conversion of 25(OH) vitamin D to 1,25(OH)2 vitamin D in CKD in multiple tissues leading to autocrine effects, has led to the speculation that CKD patients should also need to be supplemented with nutritional vitamin D. This chapter outlines the available evidence on the controversy about which vitamin D is better for patients with kidney disease: Active vitamin D, nutritional or both.

Ambulatory Metabolic Evaluation of 1515 Stone Forming Patients in Argentina

Stone forming patients were placed on a controlled diet with 1200 mg Ca, 800 mg P, 200 mg Mg and 100 mmol Na per day during 7 days. Two 24 h urine samples were collected on the sixth and seventh days. On the eighth day, following a 12 h fast, a blood sample was taken, 300 mL of distilled H2O were drunk and a 2 h urine sample was obtained. In all blood and urine samples, calcium, sodium, magnesium, phosphate, creatinine and urate were quantified. In 24 h samples oxalate and citrate were also determined. Hypercalciuria was defined by daily calcium excretion above 300 mg in men and 220 mg in women. Patients with a fasting calcium to creatinine ratio or calcium per 100 mL GFR value above 0.11 were considered to have renal hypercalciuria. Hyperuricosuria was diagnosed as a 24 h urinary uric acid above 750 mg in women and 800 mg in men, hyperuricemia as a serum uric acid higher than 7 mg% and hypomagnesuria as a daily magnesium excretion below 70 mg. A 24 h citrate excretion less than 350 mg was considered hypocitraturia and an oxalate excretion over 50 mg, hyperoxaluria.