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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty patients with proved calcium urolithiasis participated in an outpatient study designed to define the most likely metabolic problem related to the cause of the stone disease. Diagnostic categories included absorptive hypercalciuria (33 patients), renal leak hypercalciuria (20 patients), hypomagnesiumuria (27 patients), hyperuricemia and hyperuricuria (16 patients), hyperoxaluria (15 patients), normal stone-former (4 patients), renal tubular acidosis (2 patients) and suspicion of hyperparathyroidism (7 patients). Of the 80 patients 40 had more than 1 defect. Patients with a high suspicion of hyperparathyroidism were excluded from the study. Based on these criteria treatment plans incorporating medications, diet or both were instituted. Of 21 patients observed for greater than 2 years 90 per cent have shown no new stone disease.
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PMID:Outpatient evaluation of patients with calcium urolithiasis. 43 49

4 patients with nephrocalcinosis were treated with disodium ethane 1-hydroxy-1, 1-diphosphonate (EHDP) for a period of 13 months. No clinical side-effects were observed and growth proceeded normally. Radiographic changes of osteitis fibrosa cystica developed in 1 child and bone biopsy in 2 children showed defective osteoid mineralisation. It is suggested that EHDP prevented further crystal deposition in 3 children but did not prevent non-calcium stone formation in the 4th child. In view of this and the development of histological and radiographic evidence of osteomalacia and/or secondary hyperparathyroidism in these patients the value of EHDP remains dubious. On the other hand its use may be justified when rapidly increasing calcification is expected, as for example in hyperoxaluria.
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PMID:Diphosphonate therapy in nephrocalcinosis. 82 72

Farnolith (a dietary fibre preparation) was given to normal patients (n = 6) with absorptive hypercalciuria type I (n = 6) and to one patient with renal hypercalciuria. Farnolith binds calcium and reduces calcium absorption in the intestines. In normal subjects, the urine and serum parameters of calcium metabolism (total and ionized calcium, 1.25-dihydroxy-vitamin D) were unchanged. In absorptive hypercalciuria type I, a significant decrease in calcium excretion was achieved; oxalate excretion decreased as well. Low PTH values normalized; vitamin-D metabolites were not affected. In renal hypercalciuria, PTH and 1.25 DHCC were increased, whereas hypercalciuria persisted. Our investigations show that Farnolith is a reasonable treatment for absorptive hypercalciuria. Calcium homeostasis is rendered normal by Farnolith without producing secondary hyperoxaluria as sodium cellulose phosphate. Patients with primary renal calcium leakage and secondary hyperparathyroidism should not be treated with Farnolith.
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PMID:[Studies of calcium metabolism in normal persons and patients with hypercalciuria in relation to therapy with the dietary fiber preparation Farnolith]. 253 20

The high incidence of renal lithiasis in hyperparathyroidism (55 p. 100) suggests that PTH plays a causal role in stone production. It also motivates a systematic search for primary hyperparathyroidism in all patients with renal stones although it is only found in about 7 p. 100 of cases. PTH acts through the stimulation of 1.25(OH)2 vitamin D production and therefore, the absorption of calcium from the intestine, which in turn increases the filtrable calcium, hence the calciuria. In renal stones, in general, hypercalciuria represents one of the major metabolic disturbances, besides the hyperoxaluria, hyperuricosuria and the reduction of the inhibitors of crystallization. However, hypercalciuria is rarely the indirect result of excess PTH. It is usually caused by increased dietary ingestion of NaCl, meat, calcium and possibly carbohydrates.
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PMID:[Renal lithiasis in idiopathic hypercalciuria and primary hyperparathyroidism]. 376 88

Bone biopsy specimens from four patients with hyperoxaluria who underwent hemodialysis were studied. Calcium oxalate crystals are laid down in marrow spaces and sometimes inside the bone matrix and uncalcified osteoid tissue. They are clearly visible by polarizing microscope and are stained grayish-brown by Pizzolato's method. Most are surrounded by basophilic, amorphous material. By electron microscope they appear as elongated, empty spaces and after hydrogen peroxide treatment appear as fragmented, slightly electron-dense, needle-like structures. In marrow spaces, oxalate crystals aggregate in round clusters surrounded by a granulomatous reaction. This, however, cannot remove the oxalate crystals. Bone histology shows advanced renal osteodystrophy, ie, severe osteomalacia and hyperparathyroidism. The granulomatous reaction induced by the oxalate crystals probably contributes to and worsens the changes from hyperparathyroidism.
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PMID:Bone oxalosis and renal osteodystrophy. 689 47

Oral sodium cellulose phosphate, an inhibitor of intestinal calcium absorption, may reduce urinary magnesium, increase urinary oxalate, and have a limited hypocalciuric action or cause negative calcium balance in the absence of increased calcium absorption or in the presence of renal calcium "leak". To overcome these potential complications, we have taken the following precautions: oral magnesium supplements were given, a moderate oxalate restriction was imposed, a modest dose of sodium cellulose phosphate was used (usually 10 g per day), and only patients with documented absorptive hypercalciuria were treated. During a cumulative treatment period of 42.8 years, 18 patients with recurrent calcium nephrolithiasis showed a sustained reduction in urinary calcium, without developing consistent or substantial reduction in urinary magnesium, hyperoxaluria, hyperparathyroidism, or reduced bone density, Urinary saturation (relative saturation ratio) of calcium oxalate and brushite typically decreased. Remission of stone disease was found in 78 per cent of patients. We conclude that sodium cellulose phosphate is a useful drug for absorptive hypercalciuria when used appropriately.
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PMID:A cautious use of sodium cellulose phosphate in the management of calcium nephrolithiasis. 729 89

In three patients with end-stage renal failure due to primary hyperoxaluria type 1, successful combined liver-kidney transplantation enabled us to assess the insoluble oxalate pool, which was compared with the histopathological changes observed in iliac crest biopsy specimens. Good correlation was observed between the histopathological grade of bone oxalosis and the estimated oxalate content of the body. In the end-stage of oxalate bone disease, hyperparathyroidism does not play a significant role in bone resorption, which appears to be the consequence of the granulomatous reaction induced by oxalate deposition. Combined liver-kidney transplantation should be performed long before this stage. Early hepatorenal grafting in uremia secondary to primary hyperoxaluria type 1 would avoid the deleterious clinical consequences of systemic oxalosis and shorten the duration of postransplant hyperoxaluria, which may compromise the course of kidney graft.
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PMID:Combined liver-kidney transplantation in primary hyperoxaluria type 1. Bone histopathology and oxalate body content. 760 40

Enteric hyperoxaluria and primary hyperparathyroidism have been associated with the development of nephrolithiasis. We report a case involving a patient who had hyperparathyroidism due to a parathyroid adenoma and enteric hyperoxaluria resulting from a small bowel bypass and who had severe stone-related complications. This combination of stone-generating factors has heretofore not been reported. The pathophysiology of these entities is discussed.
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PMID:Nephrolithiasis due to primary hyperparathyroidism and enteric hyperoxaluria: a case report. 865 Aug 79

The first episode of nephrolithiasis provides an opportunity to advise patients about measures for preventing future stones. Low fluid intake and excessive intake of protein, salt and oxalate are important modifiable risk factors for kidney stones. Calcium restriction is not useful and may potentiate osteoporosis. Diseases such as hyperparathyroidism, sarcoidosis and renal tubular acidosis should be considered in patients with nephrolithiasis. A 24-hour urine collection with measurement of the important analytes is usually reserved for use in patients with recurrent stone formation. In these patients, the major urinary risk factors include hypercalciuria, hyperoxaluria, hypocitraturia and hyperuricosuria. Effective preventive and treatment measures include thiazide therapy to lower the urinary calcium level, citrate supplementation to increase the urinary citrate level and, sometimes, allopurinol therapy to lower uric acid excretion. Uric acid stones are most often treated with citrate supplementation. Data now support the cost-effectiveness of evaluation and treatment of patients with recurrent stones.
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PMID:Prevention of recurrent nephrolithiasis. 1059 18

When hypercalcemia is detected in a kidney stone formation, an intact parathyroid hormone measurement should be made. Detection of hyperparathyroidism (HPT) is important to prevent further stone episodes and to avoid the complications of high serum calcium in other organ systems. Stones in patients with HPT often contain apatite salts in addition to calcium oxalate because parathyroid excess may create a renal tubular acidosis. The calculi seen in patients with sarcoidosis, another hypercalcemic state that may cause stone formation, however, are usually pure calcium oxalate. Excess generation of 1,25-dihydroxyvitamin D results in intestinal hyperabsorption of calcium and secondary hyperoxaluria.
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PMID:Kidney stones as a manifestation of hypercalcemic disorders. Hyperparathyroidism and sarcoidosis. 1077 70


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