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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

The autopsy report of Ludwig van Beethoven written by Dr Johann Wagner in 1827 reveals that he had renal calculi that had not been diagnosed during his lifetime, together with perirenal fibrosis. The most comprehensive interpretation of this autopsy finding is that the regular calcareous deposits in every one of his renal calices represented calcified necrotic papillae. Severe urinary obstruction or diabetes as possible causes of papillary necrosis were not present. Analgesic abuse because of headaches, back pain, and attacks of rheumatism or gout may be presumed on the basis of Beethoven's uncontrolled way of taking medication. Salicin, a commonly used analgesic substance of that time (dried and powdered willow bark), is able to cause papillary necrosis. Perirenal fibrosis may be due to chronic infection or drug intake. Beethoven's other well-known diseases are deafness caused by otosclerosis of the inner ear, relapsing attacks of diarrhea as the symptoms of irritable bowel syndrome, and liver cirrhosis following viral hepatitis and chronic alcohol consumption. Liver cirrhosis also may cause papillary necrosis. In Beethoven's case, renal papillary necrosis was most probably the consequence of analgesic abuse together with decompensated liver cirrhosis. The autopsy report of Beethoven is the first case of papillary necrosis recorded in the literature.
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PMID:Beethoven's renal disease based on his autopsy: a case of papillary necrosis. 850 20

We present the first case report of bilateral renal papillary necrosis developing in a patient on hemodialysis. A 37-year-old hypertensive male with chronic glomerulonephritis had a normal retrograde pyelogram one year prior to initiation of hemodialysis. After two years of maintenance dialysis, he presented with gross hematuria and was found to have extensive bilateral renal papillary necrosis. His only predisposing factor was hepatic cirrhosis. It is postulated that recurrent hypotensive episodes associated with hemodialysis may lead to renal papillary necrosis in predisposed individuals. This diagnosis should be considered in hemodialysis patients who develop hematuria.
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PMID:Renal papillary necrosis in a hemodialysis patient. 851 6

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
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PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25

While the relative incidence of serious nephrotoxicities in the population consuming nonsteroidal anti-inflammatory drugs (NSAIDs) is very low, the frequency of adverse events in patients at risk has considerably increased due to the rising popularity of the use of the drugs in recent years. Under normal conditions, NSAIDs have relatively little effect on the kidney because of low renal production of prostaglandins. However, in the presence of renal hypoperfusion in which local synthesis of vasodilator prostaglandins is increased to protect the glomerular hemodynamics and to maintain appropriate renal tubular transport of fluid and electrolytes, inhibition of prostaglandin synthesis by NSAIDs can lead to vasoconstrictive acute renal failure as well as fluid and electrolyte disorders such as sodium retention and resistance to diuretics, hyponatremia and hyperkalemia. Conditions that increase the risk for NSAID-induced nephrotoxicities include volume depletion from diuretics and other causes, edematous states such as congestive heart failure and cirrhosis of the liver, old age and underlying renal disease, especially in the presence of renal functional impairment. In addition, renal parenchymal diseases may develop in susceptible patients taking NSAIDs. These include acute tubulointerstitial nephritis, frequently associated with nephrotic syndrome, and chronic progressive renal disease, with or without renal papillary necrosis. Rare cases of vasculitis and glomerulonephritis have also been reported. Finally, NSAIDs may aggravate hypertension by interacting with antihypertensive drugs, especially with diuretics and beta-blockers. Withdrawal of NSAIDs in patients at risk can frequently reverse or improve the nephrotoxicities. It is recommended that physicians be aware of the clinical settings that increase the risk for NSAID-induced nephrotoxicities and take preventive or therapeutic measures accordingly.
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PMID:Nephrotoxicities of nonsteroidal anti-inflammatory drugs. 908 Jul 53

Ludwig van Beethoven had a number of medical conditions, including deafness and chronic liver disease, for which there are contemporary descriptions. An autopsy was performed on the day after his death. Physicians and historians have tried to reinterpret original sources to determine the causes of his deafness and systemic illnesses. We have reviewed the differential diagnoses that have been proposed by otologists and physicians. Clinical and post-mortem findings point to renal papillary necrosis and liver cirrhosis of unknown aetiology. In the absence of further histological examination, there is no definitive answer to the cause of his deafness and gastro-intestinal symptoms.
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PMID:Deafness and liver disease in a 57-year-old man: a medical history of Beethoven. 1117 70

There is dispute about the cause of Beethoven's death; alcoholic cirrhosis, syphilis, infectious hepatitis, lead poisoning, sarcoidosis and Whipple's disease have all been proposed. In this article all primary source documents related to Beethoven's terminal illness and death are reviewed. The documents include his letters, the report of his physician Andreas Wawruch, his Conversation Books, the autopsy report, and a new toxicological report of his hair. His terminal illness was characterised by jaundice, ascites, ankle oedema and abdominal pain. The autopsy data indicate that Beethoven had cirrhosis of the liver, and probably also renal papillary necrosis, pancreatitis and possibly diabetes mellitus. His lifestyle for at least the final decade of his life indicated that he overindulged in alcohol in the form of wine. Alcohol was by far the most common cause of cirrhosis at that period. Toxicological analysis of his hair showed that the level of lead was elevated. During the eighteenth and early nineteenth centuries, lead was added illegally to inexpensive wines to sweeten and refresh them. These findings strongly suggest that liver failure secondary to alcoholic cirrhosis, associated with terminal spontaneous bacterial peritonitis, was the cause of death. This was complicated in the end stages by renal failure. If the presence of endogenous lead was verified by analysis of Beethoven's skeletal remains, it would suggest that the lead was derived from wine that he drank. Lead poisoning may account for some of his end-of-life symptoms. There is little clinical or autopsy evidence that Beethoven suffered from syphilis.
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PMID:Beethoven's terminal illness and death. 1721 30