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

Bile salts are formed from cholesterol and conjugated in the liver, excreted via the biliary system into the duodenum, reabsorbed in the ileum, stored temporarily in the hepatic bile salt pool, and reexcreted into the biliary system. This normal enterohepatic circulation of bile salts is both efficient and rapid. Interruption of the enterohepatic circulation of bile salts may cause cholesterol cholelithiasis or oxalate urolithiasis. Clinical and radiologic features of pediatric patients with gallstones and urolithiasis secondary to abnormalities of the ileum are reported. The pathophysiology of lithiasis due to interruption of the enterohepatic circulation of bile salts is discussed. This enteric cause is included in the differential diagnosis of cholelithiasis and urolithiasis in infants and children.
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PMID:John Caffey Award: lithiasis due to interruption of the enterohepatic circulation of bile salts. 11 96

Magnesium influences mineral metabolism in hard and soft tissues indirectly through hormonal and other modulating factors, and by direct effects on the processes of bone formation and resorption and of crystallization (mineralization). Its causative and therapeutic relationships to calcium urolithiasis (CaUr) are controversial despite an association between low urinary Mg and CaUr. Recent studies have also found a tendency to low serum and/or lymphocyte Mg levels in CaUr. Despite earlier studies demonstrating an inhibitory effect of Mg supplementation on experimental CaUr in animals and in spontaneous CaUr in humans, at least two properly controlled clinical trials of Mg supplementation have failed to demonstrate a beneficial effect on CaUr frequency. With regard to the skeleton, experimental studies have shown that Mg depletion causes a decrease in both osteoblast and osteoclast activity with the development of a form of 'aplastic bone disease'. At the same time, bone salt crystallization is enhanced by Mg deficiency. Conversely, Mg excess impairs mineralization with the development of an osteomalacia-like picture, and may also stimulate bone resorption independently of parathyroid hormone. Whether or not Mg depletion may be a causal factor in human osteoporosis is also controversial, and there are conflicting reports as to the Mg content of osteoporotic bone. Small decreases in serum and/or erythrocyte Mg in osteoporotic patients have been reported, and one author has noted improved bone mineral density with a multinutrient supplement rich in Mg. The extant data are sparse and indicate a clear need for more rigorous study.
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PMID:Relation of magnesium to osteoporosis and calcium urolithiasis. 184 60

Almost all segments of the gastrointestinal tract have been used as urinary tract substitutes. The specific nutritional and gastrointestinal complications depend on the particular portion of bowel that is removed from the alimentary tract. The use of stomach theoretically may predispose the patient to hypergastrinemia and peptic ulcer disease, hypocalcemia, and iron deficiency or megaloblastic anemia. Resection of a large amount of jejunum causes malabsorption. Limited use of colon segments usually is well tolerated, but loss of large parts of the colon directly decreases available absorptive area, resulting in diarrhea. Resection of the ileum and ileocecal valve can lead to several disease states. One is mixed secretory-osmotic diarrhea. Decreased ileal reabsorption of bile salts results in fat malabsorption and steatorrhea. The presentation of increased amounts of bile salts and fatty acids to the colon decreases water absorption and stimulates active chloride and water secretion, producing a cholera-like high-volume secretory diarrhea. The loss of the ileocecal valve and ileum segment accelerates intestinal transit time, which does not allow for complete digestion and absorption of food. Water and electrolytes remain associated with undigested food particles and may overwhelm the absorptive capacity of the colon, resulting in an osmotic diarrhea. A second problem is vitamin B12 deficiency. Surgical reduction of sites in the terminal ileum for active and exclusive uptake of vitamin B12 might lead to hypovitaminosis. If this is unrecognized, patients may develop irreversible neurologic injury. A third problem is cholelithiasis. Derangements in bile salt metabolism can occur when as little as 10 cm of ileum is resected, and the propensity to form gallstones is increased. Pigment gallstones appear to be the predominant stone associated with ileal resections. The fourth possible problem is urolithiasis, the etiology of which is multifactorial in patients with ileal resections. With decreased availability of bile salts, fat malabsorption occurs. Fatty acids bind with calcium and magnesium to form soaps, resulting in increased levels of free oxalate available for absorption. Moreover, fatty acids directly increase colonic permeability to oxalate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional and gastrointestinal complications of the use of bowel segments in the lower urinary tract. 194 6

Dietary excesses in animal protein and/or salt have been implicated as risk factors in calcium oxalate urolithiasis. The underlying physicochemical mechanism is, however, not known. Eight healthy men were given four different diets varying in animal protein and in sodium content for 1 week each. On a high protein intake (2 g/kg.day) significant changes in urinary calcium, uric acid, and citrate excretion rates were found. Similar changes in calcium and citrate were induced by a high sodium intake (310 mmol/day). The changes were more pronounced when a high protein was combined with a high sodium diet. Urinary calcium increased from 3.79 +/- 0.31 to 6.42 +/- 0.61 mmol/24 h and urinary uric acid from 4.69 +/- 0.26 to 8.0 +/- 0.47, whereas urinary citrate decreased from 3.93 +/- 0.53 to 2.79 +/- 0.34 mmol/24 h. All three dietary regimens induced a significant decrease in the ability of urines to inhibit calcium oxalate monohydrate crystal agglomeration, which was most marked during the combined diet (from 345 +/- 39 to 205 +/- 28 min). The ability of urines to inhibit crystal agglomeration was related to their citrate content (r = 0.69, P less than 0.0001). These results show that high animal protein and/or sodium intake decrease the ability of urines to inhibit the agglomeration of calcium oxalate crystals and provide a possible physicochemical explanation for the adverse effects of dietary aberrations on renal stone formation.
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PMID:The effects of dietary excesses in animal protein and in sodium on the composition and the crystallization kinetics of calcium oxalate monohydrate in urines of healthy men. 240 15

Citrate is a normal constituent of urine which combines with calcium to form a soluble salt. Urinary citrate excretion was examined in patients with urolithiasis and normal subjects by a specific enzymatic technique. There was a considerable overlap in the urinary citrate excretion between normal subjects and stone-formers, but the citrate-creatinine ratio, the citrate-calcium ratio and the citrate-magnesium-calcium ratio, which were all highly significantly lower (p less than 0.001) in stone-formers than in controls, proved most reliable in discriminating between these groups.
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PMID:Urinary citrate excretion in patients with urolithiasis and normal subjects. 277 9

Relationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium was analyzed in 93 ambulatory patients with urolithiasis. There was a significant correlationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate (only in male stone formers), phosphate and magnesium, respectively. Under a salt restricted diet (NaCl 3-5 gm/day) for 3 days, urinary sodium excretion of 16 inpatients with urolithiasis was reduced remarkably together with significant reduction of urinary excretion of calcium, uric acid and oxalate. Urinary excretion of phosphate and magnesium showed no change. From these findings we conclude that restriction of sodium intake is an effective treatment for prevention of stone recurrence.
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PMID:[Clinical studies of the recurrence of urolithiasis (3). Influence of sodium intake on urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium]. 321 89

A semiquantitative method is presented for the determination of cysteine in urine, based on the formation of a red cysteine/nitroprusside salt. The method is suitable as a rapid test for checking the progress of ascorbic acid therapy of cystinuria and cystine urolithiasis. It guarantees acceptable reproducibility of values and can be easily carried out in any clinical chemical laboratory. With the K2CO3/nitroprusside test described and an additional colorimetric determination of cystine (CN-/nitroprusside), a separate semiquantitative differentiation of cysteine and cystine in fresh (!) urine is possible.
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PMID:[A semiquantitative rapid test for cysteine: possible use for monitoring the ascorbic acid therapy in cystinuria and cystine lithiasis]. 340 89

Kidneys from broiler chicks receiving 300 micrograms of oosporein K salt per gram of feed continuously from 0 to 21 days of age were examined by light and electron microscopy. Chicks that died at 3 days had nephrosis of initial proximal tubular segments with an early pyogranulomatous interstitial response. Macula densa cells had cytoplasmic accumulations of periodic-acid-Schiff-positive granules. Kidneys from chicks surviving 21 days had hypercellular or atrophic glomeruli and hyperplastic dilated proximal tubules. Centrilobular distal tubules were dilated and filled with hyaline basophilic casts. Interstitial fibrosis was prominent in cortical and medullary zones. These findings indicate that oral oosporein is a severe nephrotoxin which can cause visceral urate deposition and severe nephrosis of initial proximal tubular segments. The histopathology of this mycotoxicosis was compared with those of infectious-bronchitis-induced nephrosis and avian urolithiasis syndrome.
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PMID:Microscopic and ultrastructural renal pathology of oosporein-induced toxicosis in broiler chicks. 344 38

In this paper a method of semiquantitative cysteine determination is presented, which is based on the formation of a red cysteine-Na-nitroprusside salt. The method is a suitable rapid test for checking the process of ascorbic acid therapy in cystinuria and cystine urolithiasis patients. It guarantees acceptable reproducibility of values and can be easily carried out in every clinicochemical laboratory. With the K2CO3/nitroprusside test described and an additional cystine rapid test (Ni2+/S2O4(2-) tablet reagency) a separate semiquantitative differentiation of cysteine and cystine in fresh (!) urine is possible.
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PMID:[Simple rapid test with carbonate/nitroprusside for the semiquantitative determination of cysteine in the urine--possible use for control of ascorbic acid therapy in cystine urolithiasis]. 367 61

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


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