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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As calcium oxalate stones are the most important component in urolithiasis, an experimental model has to be designed to clarify the pathogenesis and aid in their prevention. Hyperoxaluria as well as hypercalciuria were produced in rats by administering ethylene glycol (0.5%, in drinking water administered ad libitum) and 1-alpha (OH) D3 (0.5 micrograms/rat given every other day), respectively, for three to four weeks. Neither drug alone produced stones efficiently as did the combination regimen of these two compounds. The occurrence of stones was 77.3%, and with only a moderate degree of renal functional impairment. Biochemical and histological data were obtained using this model.
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PMID:[Experimental and clinical studies on calcium urolithiasis: (I) Animal model for calcium oxalate urolithiasis using ethylene glycol and 1-alpha (OH) D3]. 403 34

The relationships between urinary oxalate, calcium and magnesium were investigated in 81 patients with idiopathic calcium oxalate urolithiasis on their regular diets. A significant relationship was established between calcium and oxalate excretion in the analysis of recurrent stone-formers (n = 44, P less than 0.01), though there was no significant difference between the two in the analysis of the patients overall or in single stone-formers. This suggests that recurrent stone-formers may have some abnormality of oxalate absorption in relation to calcium absorption. The role of calcium-oxalate interaction in the gut as a cause of mild hyperoxaluria is discussed.
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PMID:Comparison of urinary oxalate excretion in urolithiasis patients with and without hypercalciuria. 406 29

Pyridoxilate is a salt formed from glyoxylic acid and pyridoxine. It has been used therapeutically as an antianoxic drug in the treatment of various arterial complaints. Its use is based theoretically on its ability to block the conversion of glyoxylic acid into oxalic acid. The following cases suggest, however, that pyridoxilate can cause stones. Intraperitoneal injection of glyoxylate in doses of 130 mg/kg will cause oxalate stones in rats. The same effect results from injection of 427 mg/kg pyridoxilate (i.e. an equivalent dose of glyoxylate). In human subjects, intravenous injection of 200 mg of pyridoxilate results in a fourfold increase in the urinary oxalic acid content in the two hours following the injection. Thirteen cases of chronic progressive oxalate stone disease have recently been reported in patients receiving a prolonged course of pyridoxilate at 450 to 600 mg daily. Eight of these patients had no previous history of lithiasis. Oxaluria levels of 80 to 100 mg daily are observed in all cases of lithiasis in patients receiving pyridoxilate. The levels fell after cessation of the pyridoxilate treatment, and reverted to normal (30 mg/24 hours) in all but three patients. These three patients maintained levels of close to 50 mg and all three had a previous history of urolithiasis.
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PMID:[Calcium oxalate stones and hyperoxaluria secondary to treatment with pyridoxilate]. 408 39

The authors report a case of acute renal failure with hyperoxaluria and intratubular deposits of oxalate crystals, following a massive ingestion of piridoxilate. Cases of calciumoxalate urolithiasis have also been reported after chronic administration of piridoxilate.
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PMID:[Acute renal failure caused by acute oxalosis after massive ingestion of pyridoxilate]. 409 37

In a group of 112 patients with ulcerative colitis, eight patients (7.1%) developed the complication of urolithiasis. A higher incidence was found in those with total colitis (15.4%) and in postoperative patients (20%). The mean period between the onset of colitis and the initial urinary symptoms was 5.4 yr. All the analyzed stones contained oxalate and seven of eight patients had hyperoxaluria, which was believed to be one of the important lithogenic factors. Increased urinary Ca/Mg ratio, steroid, and sulfasalazine are suggested as the other lithogenic factors in patients with ulcerative colitis.
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PMID:Clinical and urinary characteristics of urolithiasis in ulcerative colitis. 612 77

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.
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PMID:Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. 624 14

The pattern of oxalate uptake in various segments of the bowel has been studied after 80% small bowel resection and antiperistaltic colon interposition in Rhesus monkeys. The levels of urinary oxalate excretion were significantly raised in the immediate postoperative period, with progressive reduction at six and 12 months. None of the animals developed renal calculi. The possible benefit of the colon interposition after massive small bowel resection, in the prevention of hyperoxaluria and urolithiasis is suggested. Improvement in the fat malabsorption, formation of insoluble calcium oxalate in the bowel lumen, leading to reduced net intestinal absorption of oxalates is the possible mechanism.
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PMID:Absorption and urinary excretion of oxalates following massive small bowel resection and colon interposition in rhesus monkeys. 651 51

The purpose of this study was to determine and to compare the frequency of hypercalciuria, hyperoxaluria and hyperuricosuria in 49 patients with a pure or mixed calcium oxalate urolithiasis. During this study, all patients were on a normal diet and had no special disease or medication. We noted that hypercalciuria (35%) and hyperoxaluria (24%) were more often associated (18%) than isolated (8 and 2%). They were more frequent in mixed stones (44% et 39%) than in pure one (29% and 16%). Hyperuricuria (39%) had a same frequency wathever the renal stone type may be. A same frequency was noted when hyperuricuria was associated with hypercalciuria and hyperoxaluria (12%) or isolated (14%). None of these three biologic disturbances was observed in 45% of our patients.
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PMID:[Comparative study of urinary calcium, oxalate and uric acid in calcium oxalate lithiasis]. 653 Oct 54

The pathophysiologic consequences of renal function impairment and chronic renal failure among others result from the loss of excretory and regulatory functions of the kidneys. The role of the exchange of cellular hydrogen ions of tubular fluid in the reabsorption of bicarbonate and in the urinary excretion of titratable acid and ammonia (acid-base regulation) is outlined. The effects of decreased glomerular filtration rate on calcium and phosphorus homeostasis are discussed. De novo urolithiasis in these patients is uncommon. However, it is well recognized that they may form matrix stones with calcium oxalate inclusions. Of greater significance is the prophylaxis in those patients, in whom urolithiasis has been the cause of chronic renal failure. In these patients it is of importance to modify the drug dosage or to abandon the prophylaxis when it interferes with the metabolic changes of renal function impairment. Some agents require no modification, others minor or major modifications. Some are even contraindicated. Hazards of stone prophylaxis in chronic renal failure: Acidification - cave metabolic acidosis! Cave RTA! Antibiotic agents - special rules to prevent accumulation. Thiazides - contraindicated! Hypokalemia; hyperuricemia; cave HPT! Triamterene - contraindicated! Acetazolamide (cystinuria) - contraindicated. Spironolactone - contraindicated. Sodium-cellulose-phosphate - Hyperoxaluria, hypomagnesiuria , hyperphosphatemia, cave HPT. Orthophosphate - cave urinary infection, cave poor renal function, cave obstruction. Allopurinol - dose reduction advisable. Brenzbromaron - contraindicated.
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PMID:[Prevention of calculus recurrence in impaired kidney function]. 653 25

The 75% of the renal stone formers have a so-called idiopathic calcium urolithiasis. The majority of these patients, however, do have a detectable biochemical disorder such as hypercalciuria, hyperuricosuria or hyperoxaluria. A high fluid intake unequivocally represents the first step in the therapeutic approach to these patients. Nevertheless, the detection of any type of biochemical disturbance is of great importance since the addition of a specific therapy will then become possible. Patients with absorptive idiopathic hypercalciuria will be advised to decrease their intake of dairy products as a function of the degree of calcium hyperabsorption, and simultaneously the major dietary sources of oxalate such as chocolate, spinach, rhubarb and asparagus will be eliminated; neutral orthophosphates (3-4 times 500 mg/d) or a thiazide, resp. an analogue as chlorthalidone (50 mg/d) are reasonable alternatives. Renal idiopathic hypercalciuria should be treated, according to the authors, with chlorthalidone (50 mg/d), with or without allopurinol (300 mg/d) depending on the presence of concomitant hyperuricosuria. Patients with dietary idiopathic hypercalciuria should be advised to better equilibrate the various components of their dietary intake. Finally, patients with isolated idiopathic hyperuricosuria whose disease would remain active despite a high fluid intake should receive allopurinol (300 mg/d). The treatment of isolated idiopathic hyperoxaluria is not yet well established. Two main arguments favor this so to say "tailored" approach to the idiopathic stone former: first, some metabolic disturbances are causally related to a particularly active and severe urolithiasis, whereas others are less so; second, the lack of efficacy of some types of treatment appears more and more to be due to insufficient screening of the patients before starting a given treatment.
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PMID:[Idiopathic calcium nephrolithiasis: therapeutic aspects]. 665 21


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