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

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.
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PMID:Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease. 48 60

In a selected material of 228 patients with chronic inflammatory bowel disease (CIBD) the incidence of urolithiasis was 15% (95% confidence limit 11-21). The tendency to urolithiasis is significantly correlated to small-bowel resection and its extent and to obstruction in the urinary tract. On the other hand, there is no definite correlation to the duration or extent of the bowel disease. The significant correlation between urolithiasis and ileal resection is in agreement with the hyperabsorption of oxalate as an important cause of stone formation demonstrated by others. That local factors too play an essential role in the formation of urinary calculi is apparent from the increased incidence of urolithiasis in obstruction of the urinary tract. The incidence of urolithiasis was particularly high (22-25%) among patients with ileostomies. The few and negligible symptoms of and sequelae to, urolithiasis in CIBD encourage a conservative attitude.
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PMID:Urolithiasis in chronic inflammatory bowel disease. 67 52

Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
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PMID:Magnesium and inflammatory bowel disease. 329 19

Inflammatory bowel disease affects the genitourinary tract not infrequently, either by way of direct extension of the gastrointestinal inflammatory process or through metabolic interrelationships between the two organ systems. The abnormalities that most frequently result include retroperitoneal abscess, ureteral obstruction, cystitis, enterovesical fistula, and urolithiasis. Some of these may be sufficiently symptomatic to draw attention to their presence, even, on occasion, overshadowing or preceding gastrointestinal disease symptoms. Other urinary lesions are clinically silent and require periodic uroradiologic evaluation for purposes of discovery.
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PMID:Genitourinary complications of inflammatory bowel disease. 382 92

In up to one-third of patients with calcium oxalate stones, a hyperoxaluria can be detected. Hyperoxaluria can result from increased endogenous production, from excessive oxalate content of the food, or from intestinal hyperabsorption. For a causal therapy, it is important to discriminate between metabolic and hyperabsorptive hyperoxaluria. Our new 13C-oxalate test allows this differentiation. Under standardized conditions, 50 mg of disodium salt of [13C2]oxalic acid was applied. From the amount of labeled oxalate excreted in urine as measured by a gas chromatographic-mass spectrometric assay, the intestinal absorption was calculated. Seventy patients with recurrent calcium oxalate urolithiasis who had no signs of inflammatory bowel disease were tested. Their mean intestinal oxalate absorption was 9.2+/-5.1%. This was significantly higher than the mean absorption of 50 healthy volunteers (6.7+/-3.9%). There was no difference in oxalate absorption between male (n = 25) and female volunteers. Oxalate absorption correlated with the oxalate excretion in the 24-h urine (volunteers: r = 0.46, P < 0.01; patients: r = 0.62, P < 0.001). Oxalate hyperabsorption was defined as an absorption exceeding 10%. According to this definition, 34% of the patients had oxalate hyperabsorption; 20% of the volunteers showed a hyperabsorption, too. The 13C-oxalate absorption test allows reliable determination of intestinal oxalate absorption. Because of the use of a stable isotope, this test may be repeated as often as required. It will allow the control of therapeutic regimens and also help to unravel genetic influences in stone formation.
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PMID:Intestinal hyperabsorption of oxalate in calcium oxalate stone formers: application of a new test with [13C2]oxalate. 1054 Dec 57

Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake. Certain intestinal diseases like short bowel syndrome, chronic inflammatory bowel disease or cystic fibrosis and other malabsorption syndromes are known to increase the risk of secondary hyperoxaluria. Although the urinary oxalate excretion is usually lower than in primary hyperoxaluria, it may still lead to significant morbidity by recurrent urolithiasis or progressive nephrocalcinosis. A clear distinction between primary and secondary hyperoxalurias is important. As correct classification may be difficult, appropriate diagnostic tools are needed to delineate the metabolic background as a basis for optimal treatment. We developed an individual approach for the evaluation of patients with suspected secondary hyperoxaluria. First, 24 h urines are examined repeatedly for lithogenic (e.g. calcium, oxalate, uric acid) and stone-inhibitory (e.g. citrate, magnesium) substances, and the patients are asked to fill in a dietary survey form. Urinary saturation is calculated using the computer based program EQUIL2, and the BONN-Risk-index is determined. The measurement of plasma oxalate and of urinary glycolate helps to distinguish between primary and secondary hyperoxalurias. If secondary hyperoxaluria is suspected, the stool is examined for Oxalobacter formigenes, an intestinal oxalate degrading bacterium, as lack or absence may lead to increased intestinal oxalate absorption. The last diagnostic step is to study the intestinal oxalate absorption using [13C2]oxalate. Depending on the results, various therapeutic options are available: 1) a diet low in oxalate, but normal or high in calcium, 2) a high fluid intake (>1.5 L/m2/d), 3) medications to increase the urinary solubility, 4) specific therapeutic measures in patients with malabsorption syndromes, depending on the underlying pathology, and 5) intestinal recolonization of Oxalobacter formigenes or the treatment with other oxalate degrading bacteria.
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PMID:Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. 1295 11

The incidence of drug-induced stone disease is 0.44%. A 57-year-old woman with ulcerative colitis presented with obstructive nephropathy and pyelonephritis. She underwent cystoscopy, bilateral retrograde pyelography, and bilateral ureteral stent placement. A 6-cm bladder calculus and two 3-mm right distal ureteral calculi were discovered. Later, cystolithotomy was performed. The stone analysis demonstrated sulfapyridine, a sulfasalazine metabolite. Patients with inflammatory bowel disease can develop urolithiasis owing to acidic urine and low-volume urine production. Patients receiving aminosalicylates are at an increased risk of urolithiasis and may benefit from oral hydration and urinary alkalization.
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PMID:Obstructive nephropathy secondary to sulfasalazine calculi. 1455 Apr 62

Urolithiasis is quite rare in pediatric inflammatory bowel disease (IBD) compared with the incidence at 9-18% in adult cases. The diagnosis and treatment of pediatric IBD is challenging. Indeterminate colitis (IC), originally proposed as a subgroup of fulminant IBD, has also been used for patients when the diagnosis of either UC or CD cannot be made with certainty. Such patients should be diagnosed as having "IBD unclassified" based on evidence including mucosal biopsy samples. We report herewith a 9-year-old boy with isolated colitis that reached a diagnosis of IBD unclassified. Infliximab therapy led to a successful remission after the refractory course. However, urolithiases were impacted in the urethral valves and vesico-ureteral junction. Microhematuria was noticed from the onset of colitis. Renal calculi were detected on the X-ray films during the first line treatment. Transurethrally crushed stones consisted of calcium oxalate. Renal calculi are more closely associated with CD than ulcerative colitis in adult patients for the ileal involvement. The oxalate stones and treatment response indicated a CD-like pathophysiology. Nephrolithiasis might be a rare but noticeable extra-intestinal presentation of pediatric IBD. Infliximab therapy could be an option in pediatric refractory colitis to change the critical steroid dependency.
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PMID:Nephrolithiasis as an extra-intestinal presentation of pediatric inflammatory bowel disease unclassified. 2112 80

Acute oxalate nephropathy can occur due to primary hyperoxaluria and secondary hyperoxaluria. The primary hyperoxalurias are a group of autosomal recessive disorders of endogenous oxalate overproduction. Secondary hyperoxaluria may occur as a result of excess dietary intake, poisoning with oxalate precursors (ethylene glycol), or enteric hyperoxaluria. The differential diagnosis of enteric hyperoxaluria includes inflammatory bowel disease, short bowel syndrome, bariatric surgery (with jejunoileal bypass or Roux-en-Y gastric bypass), celiac disease, partial colectomy, and chronic pancreatitis. The common etiology in all these processes is fat malabsorption, steatorrhea, saponification of calcium, and absorption of free oxalate. Hyperoxaluria causes increased urinary oxalate excretion, urolithiasis (promoted by hypovolemia, decreased urinary pH caused by metabolic acidosis, and decreased citrate and magnesium concentrations in urine), tubulointerstitial oxalate deposits, and tubulointerstitial nephritis. We report a rare case of acute oxalate nephropathy due to pancreatic atrophy and exocrine insufficiency caused by newly diagnosed pancreatic cancer.
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PMID:Acute oxalate nephropathy due to pancreatic atrophy in newly diagnosed pancreatic carcinoma. 2661 99