Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present three cases of benign prostatic hypertrophy associated with chronic renal failure for three years from 1982 to 1984. Endogenous 24-hour creatinine clearance (Ccr) on admission ranged from 8.7 to 29.4 ml/min. Temporary hemodialysis treatment was required in one patient at the beginning of hospitalization. Indwelling intraurethral catheterization for 3 months or more improved the renal function in one patient, but brought troublesome complications of gross hematuria, intractable urethral pain or recurrent pyelonephritis in the other patients. These complications might arise from strong uninhibited detrusor contractions triggered or accelerated by stimuli and/or urinary tract infection induced by urethra-indwelt catheters. Intermittent self catheterization reduced these complications in one patient. In two patients, Ccr increased beyond 30 ml/min as a desirable standard level for safe operations. Suprapubic prostatectomy was successfully performed in all the patients. However, severe gastric ulcer or fatal duodenal ulcer occurred in two patients. Hypoproteinemia and/or urinary tract infection was thought to be highly related to ulceration. In conclusion, we would like to emphasize that a Ccr of more than 30 ml/min is needed for safe operations concerning renal function in patients with benign prostatic hypertrophy associated with chronic renal failure.
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PMID:[A pre- and post-operative clinical study in three patients with benign prostatic hypertrophy and implicated chronic renal failure]. 243 7

A case is reported of a 72-year-old woman who presented with severe vertigo, vomit, and mild neck and occipital pain. She had a medical history of hypertension, angina pectoris, cholelithiasis, gastric ulcer, pyelonephritis and periodical mild dizziness. Neuroimaging revealed right vertebral artery occlusion, right cerebellar stroke and basilar impression. The therapeutic approach chosen in our patient was conservative, with non-steroid anti-inflammatory drugs and neck collar. Although our patient's prior risk factors for stroke supported a diagnosis of vertebrobasilar stroke, it is possible that the vertebral artery occlusion was the result of changes in the atlantoaxial anatomy and that cerebellar infarction was secondary to craniocervical anomaly. Although the presence of vertebral artery occlusion, cerebellar stroke and basilar impression in our patient may have been coincidental, we suggest that patients with basilar impression and craniocervical anomalies in general may be at an increased risk of vertebrobasilar vascular disease and vertebrobasilar stroke.
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PMID:Basilar impression as a possible cause of cerebellar stroke: case report. 2264 89