oxalates and Bone-Diseases--Metabolic

Hypercalciuria is the most common metabolic abnormality that causes urolithiasis. The pathogenetic mechanisms responsible for hypercalciuria include enhanced gastrointestinal absorption of calcium, increased bone resorption and/or decreased renal reabsorption of calcium; the main dietary factors promoting hypercalciuria are high dietary sodium intake and protein-rich diet. The authors discuss pathophysiology of hypercalciuria and genetic factors behind 'idiopathic hypercalciuria'. The simplified diagnostic approach to hypercalciuria is outlined herein, and available therapeutic interventions of proven efficacy in idiopathic hypercalciuria are presented as well. Dietary intervention for hypercalciuria should include reduced sodium, protein and oxalate intake. Thiazide diuretics, in conjunction with a low-sodium diet, tend to reduce urinary calcium excretion and ameliorate idiopathic hypercalciuria. Potassium citrate acts as an inhibitor of calcium stone formation in the urinary tract. A low-calcium diet should generally be avoided, as it may increase urinary oxalate excretion and actually promote stone formation. In addition, a low-calcium diet may lead to negative calcium balance in subjects with hypercalciuria, and therefore increases the risk of osteopenia.

Topics: Bone Diseases, Metabolic; Bone Resorption; Calcium; Dietary Proteins; Humans; Hypercalciuria; Intestinal Absorption; Kidney; Oxalates; Sodium Chloride Symporter Inhibitors; Sodium, Dietary

To investigate bone mineral densitometry findings in patients with normocalciuric urinary system stone disease, we compared 150 patients with normocalciuric calcium stone disease (group 1) and 60 subjects of a control group (group 2). The patients were compared according to bone mineral content (BMC), bone area (BA), bone mineral density (BMD), T-score and Z-score values of femur neck, total femur and lumbar spine (L2-L4) by dual energy absorptiometry. We found that 76.6% of the patients in group 1 and 20.0% in group 2 had low BMD; 11.3% of patients in group 1 had osteoporosis and 65.4% had osteopenia. In the control group, there was no osteoporosis, but 20.0% of the subjects had osteopenia. In group 1, there was hyperoxaluria in 26.0% of patients, hypocitraturia in 15.3% of patients, hyperuricosuria in 6.0% of patients, both hypocitraturia and hyperoxaluria in 8.6% of patients in a 24-h urine analysis. Urine analysis was normal in 44.0% of patients. Our results showed a severe loss of bone mass in patients with urinary system normocalciuric calcium stone disease. Thus, the necessary precautions concerning bone mass protection should be taken and the patients should be informed about this issue.

Topics: Absorptiometry, Photon; Adult; Bone Density; Bone Diseases, Metabolic; Calcium; Citrates; Female; Femur; Humans; Lumbar Vertebrae; Male; Middle Aged; Osteoporosis; Oxalates; Recurrence; Urolithiasis

A 15-year-old patient with severe bone disease (with bilateral fractures of hips and shoulders) due to primary hyperoxaluria type 1 (PH1) was treated with combined liver-kidney transplantation after a 4-year hemodialysis period. Normalization of excessive oxalate synthesis brought in by the liver graft combined with the slow excretion of skeletal oxalate stores by the renal graft led to progressive improvement of clinical, radiological, and histological evidence of oxalate osteopathy. This allowed bilateral hip replacement 3 years after transplantation, which led to complete physical rehabilitation of the crippled patient. Combined liver-kidney transplantation constitutes the treatment of choice for end-stage renal failure due to PH1, even in the face of severe oxalate bone disease.

Topics: Adolescent; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Creatinine; Female; Femur Head; Hip Fractures; Hip Prosthesis; Humans; Hyperoxaluria, Primary; Kidney Failure, Chronic; Kidney Transplantation; Liver Transplantation; Oxalates; Shoulder Fractures

Topics: Amino Acid Metabolism, Inborn Errors; Bone Diseases, Metabolic; Child; Female; Glycine; Humans; Oxalates

Topics: Amino Acid Metabolism, Inborn Errors; Bone Diseases, Metabolic; Child; Female; Glyoxylates; Humans; Kidney Failure, Chronic; Kidney Transplantation; Oxalates; Radiography; Transplantation, Homologous