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

Although urolithiasis is common in spinal cord injury patients, it is presumed that the predisposing factors for urinary stones in spinal cord injury patients are immobilization-induced hypercalciuria in the initial period after spinal injury and, in later stages, urine infection by urease-producing micro-organisms, e.g., Proteus sp., which cause struvite stones. We describe a patient who sustained C-7 complete tetraplegia in a road traffic accident in 1970, when he was 16 years old. Left ureterolithotomy was performed in 1971 followed by left nephrectomy in 1972. Probably due to adhesions, this patient developed volvulus of the intestine in 1974. As he had complete tetraplegia, he did not feel pain in the abdomen and there was a delay in the diagnosis of volvulus, which led to ischemia of a large segment of the small bowel. All but 1 ft of jejunum and 1 ft of ileum were resected leaving the large bowel intact. In 1998, suprapubic cystostomy was performed. In 2004, this patient developed calculus in the solitary right kidney. Complete stone clearance was achieved by extracorporeal shock wave lithotripsy. Stone analysis: calcium oxalate 60% and calcium phosphate 40%. Metabolic evaluation revealed hyperoxaluria, hypocitraturia, and hypomagnesiuria. Since this patient had hyperoxaluria, the stool was tested for Oxalobacter formigenes, a specific oxalate-degrading, anerobic bacterium inhabiting the gastrointestinal tracts of humans; absence of this bacterium appears to be a risk factor for development of hyperoxaluria and, subsequently, calcium oxalate kidney stone disease. DNA from the stool was extracted using the QIAamp DNA stool Mini Kit (Qiagen, Chatsworth, CA). The genomic DNA was amplified by polymerase chain reaction using specific primers for oxc gene (developed by Sidhu and associates). The stool sample tested negative for O. formigenes. The patient was prescribed potassium citrate mixture; he was advised to avoid oxalate-rich food, maintain recommended levels of calcium in his diet, and take live bio-yogurt. Two months later, 24-h urinary oxalate decreased from 0.618 to 0.411 mmol/day; 24-h urine citrate increased from 0.58 to 1.10 mmol/day. Six months later, an oxalate absorption test was performed. The patient swallowed a capsule, soluble in gastric juice, containing 50 mg (0.37 mmol) sodium [13C2]oxalate corresponding to 33.8 mg of [13C2]oxalic acid. The amount of labeled oxalate, excreted in urine, was measured by a gas chromatographic-mass spectrometric assay. Oxalate absorption, expressed as the percentage of the labeled dose recovered in the 24-h urine after dosing, was 8.3% (reference range: 2.3-17.5%). In addition to other conventional measures, oral administration of O. formigenes or lactic acid bacteria mixture to promote bacterial degradation of oxalate in the gut, and thus combat hyperoxaluria, may play a role in prevention of calcium oxalate kidney stones.
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PMID:Hyperoxaluria, hypocitraturia, hypomagnesiuria, and lack of intestinal colonization by Oxalobacter formigenes in a cervical spinal cord injury patient with suprapubic cystostomy, short bowel, and nephrolithiasis. 1761 9

In a large population of animals, it is normal to have some die each day from causes not related to disease, which is often referred to as natural causes. In poultry production, this phenomenon is commonly referred to as daily mortality. In egg-producing chickens, many of the natural causes of death are associated with making an egg. The causes of normal mortality in commercial egg-laying chicken flocks have been described very little to date. A commercial chicken egg farm, housing approximately two million single-comb white leghorn chickens (Gallus gallus domesticus) in 16 egg-producing flocks, was visited on a monthly basis to monitor bird health, body conditioning, skeletal integrity, and causes of daily mortality in an attempt to provide early detection of health abnormalities. A representative sample of daily mortality from each flock was necropsied to determine the cause of death. Reported herein is a summary of visits for a period of 38 mo from June 2011 to July 2014. The top 15 causes of normal mortality, in rank order of prevalence, were determined to be the following: egg yolk peritonitis, hypocalcemia, gout, self-induced molt, salpingitis, caught by spur, intussusception or volvulus (twisted intestine), cannibalism (pick out), tracheal plug, septicemia, fatty liver syndrome, internal layer, layer hepatitis, persecution, and prolapsed vent. Other causes noted were hyperthermia (during summer), trauma, coccidiosis, ovarian neoplasia, being egg bound, urolithiasis, peritonitis (not egg yolk induced), leg fracture, caught in the structure, tumor (other than ovarian origin), wing fracture, exsanguination, and cardiomyopathy.
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PMID:Causes of Normal Mortality in Commercial Egg-Laying Chickens. 2895 10