Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the plasma of healthy subjects, 4 fractions of immunoreactive glucagon are found. The first has a molecular weight of about 160000, the second of 9000, the third 3500 and the fourth about 2000. The third probably corresponds to the intact hormone glucagon. In cirrhosis of the liver and diabetes mellitus, a statistically significant rise in the third fraction has been found. In patients with tumors of the pancreatic A-cells, in addition to the third fraction the second in particular was also increased: it may be a precursor of the glucagon molecule. In chronic renal insufficiency, fractions 2 and 3 were as markedly increased as in glucagonoma, which suggests a role for the kidney in the decomposition of glucagon. The pathophysiologic significance of the four immunoreactive fractions of glucagon cannot yet be assessed with certainty.
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PMID:[Circulating types of human glucagon (author's transl)]. 30 29

The consequences of chronic renal insufficiency relevant to hepatic failure are not well appreciated. We describe a patient with chronic cirrhosis and marked porto-systemic shunting who, after the onset of chronic renal failure, developed intractable encephalopathy which improved markedly during an eight month period of maintenance hemodialysis.
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PMID:Exacerbation of hepatic encephalopathy by chronic renal failure: response to maintenance hemodialysis. 66 27

Following a single oral dose of 20 mg nifedipine combined with 2 mg co-dergocrine to 24 subjects, the pharmacokinetics of this drug were studied. 8 normotensive subjects had normal renal and hepatic function, 8 patients had chronic renal insufficiency (creatinine clearance less than 30 ml.min-1) and 8 patients had liver cirrhosis which was confirmed by liver biopsy. The area under the plasma level time curve (AUC infinity) of co-dergocrine increased from 0.59 +/- 0.41 ng.ml-1. (mean +/- SD) in the normals to 1.24 +/- 0.95 ng.ml-1.h in liver cirrhosis (P less than 0.05) and to 1.81 +/- 0.9 ng.ml-1.h in renal failure (P less than 0.05 compared with the control group). Corresponding values for the nifedipine AUC infinity were 564.5 +/- 268 ng.ml-1.h, 1547.5 +/- 1134 (P less than 0.05) and 929 +/- 533 ng.ml-1.h (P less than 0.05; gas chromatographic method). The incidence of adverse effects was lower in patients with renal failure than in subjects with normal renal and liver function as well as in those with liver cirrhosis.
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PMID:Clinical pharmacokinetics of the nifedipine/co-dergocrine combination in impaired liver and renal function. 149 95

We have assessed the effects of acute and chronic administration of etodolac, ketoprofen, and indomethacin on renal function in patients with mild to moderate chronic renal insufficiency (CRI). We studied 18 normal volunteers and 24 patients with CRI due to hypertension and/or diabetes mellitus with creatinine clearances between 19 and 83 mL/min/1.73 m2. Clearance studies were performed with the first dose of nonsteroidal antiinflammatory drug (NSAID) to compare acute effects of the agent with a no-drug control. Subjects then received the NSAID for three to five days and, on the last day of study, underwent another clearance study to assess the effects of a single dose of NSAID superimposed on chronic dosing. With each dose of each NSAID, inulin and paraaminohippurate (PAH) clearances and fractional excretion of NA+ decreased. However, the baseline control collections after chronic dosing did not differ from the no-drug control periods. Hence, the decline in renal function with each dose is transient, and no overall adverse effect on renal function occurred with chronic dosing. In five patients with cirrhosis, we assessed the renal sparing effects of sulindac. After equilibration on a fixed sodium intake, they received a 200-mg dose of sulindac. In one patient, no adverse effect occurred; the remaining patients suffered declines in creatinine clearance of 29%, 87%, 37%, and 37%, respectively. This effect was transient and returned to control values six to eight hours after sulindac administration. At the time of maximal depression of renal function, serum concentrations of sulindac sulfide were comparable to those in subjects with normal hepatic function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nonsteroidal antiinflammatory drugs on renal function in patients with renal insufficiency and in cirrhotics. 294 56

Basing on the data obtained at 10433 autopsies performed from 1972 to 1981, cases of secondary kidney cirrhosis (chronic pyelonephritis, glomerulonephritis and interstitial nephritis) and renal pelvis cancer were thoroughly analysed. Analgetic nephropathy was found in 13.5% of all chronic interstitial and tubulo-interstitial inflammatory renal diseases, and in cases of bilateral lesions--in 17.2%. The conclusion was made on the basis of morphologic criteria ("chronic" papillary necroses and capillarosclerosis of renal pelvis). There was 41 patient with analgetic nephropathy, who died of chronic renal insufficiency, i.e. 10.6% out of the total number of patients deceased of the same reason for the period mentioned. In the biopsy material reviewed for the same period, that mainly consisted of cases with renal pelvis cancer, analgetic nephropathy was found in 15.7%.
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PMID:[Morphology of analgesic nephropathy and its incidence in Czechoslovakia]. 356 46

Irreparable late lesions after a malaria infection are rare. They occur mainly after infection of tropical malaria. As ascertained late lesions are regarded cerebral disturbances, e.g. epilepsy after cerebral tropical malaria, cardiac disturbances, e.g. arrhythmia after cardiac tropical malaria and chronic renal insufficiency after quartan malaria. Chronic liver diseases, e.g. cirrhosis, are not known as ascertained late lesions of malaria. Bodily lesions may be recognized by experts as malaria-depending, when kind and form of the course of malaria may be considered as cause meanwhile appearing symptoms anticipate a connection and other causes were excluded with regard to these lesions.
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PMID:[Assessment of late complications of malaria in travelers to the tropics]. 688 Mar 14

The renal effects of aspirin and acetaminophen are minor. With a major overdose of acetaminophen, uncommonly renal failure may occur that cannot be ascribed to hepatic failure; its mechanism is unknown. Aspirin may cause a transient shedding of renal tubular cells, alterations in urate excretion, inhibition of spironolactone action, and, in certain clinical settings, a reversible decline in renal function manifested as a fall in glomerular filtration that may be accompanied by mild water, sodium, and potassium retention. Active systemic lupus erythematosus, advanced cirrhosis, and chronic renal insufficiency seem to predispose patients to the effects on renal function, and there is direct or indirect evidence in those conditions that prostaglandin synthesis is an important part of the body's attempt to preserve renal blood flow. Study of these effects has provided new insight into the way in which the kidneys may use prostaglandins to preserve renal function when it is threatened.
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PMID:Acute effects of aspirin and acetaminophen on renal function. 700 35

In the last decade our knowledge on vitamin D has grown considerably due to the identification of numerous steps of the vitamin D metabolism and to the isolation and synthesis of active metabolites. Therefore a lot of progress had been made in the understanding of the physiological mechanism of regulating blood calcium homeostasis and of the pathogenesis of many related diseases. The diseases connected to the calcium-phosphate metabolism requiring treatment with vitamin D and its metabolites are numerous. The basis for a rational therapeutic approach is provided by the new concepts on the pathogensis of the various diseases and on the pharmacology of vitamin D metabolites. Pure vitamin D depletion may be controlled with physiological doses of vitamin D. Administration of 25-OHD3 is advisable in chronic hepatitis or cirrhosis accompanied by a defect of 25-hydroxylation and/or intestinal loss of the metabolite. A defect in the synthesis of 1,25-(OH)2D3, the metabolite of renal origin, is present in an interesting and wide group of diseases. These are: chronic renal insufficiency, hypoparathyroidism, hypocalcemic D-resistant rickets and senile or post-menopausal osteoporosis. In the treatment of this group of diseases, which sometimes is of a preventive nature, it is preferable to administer the dihydroxylated metabolites of vitamin D. The results of treatments and prevention in a few selected conditions are reported.
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PMID:[Physiopathological and therapeutic aspects of vitamin D (author's transl)]. 724 90

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

From January 1991 to May 1994, we have operated on 15 cases of Type B aortic dissection. In 10 of these patients, thoracoabdominal repair was performed. According to Crawford's classification, 2 patients fell into Type I, 6 patients into Type II, and 2 patients into Type III. The aneurysms were exposed through a left thoracotomy extending into the retroperitoneum with the hemidiaphragm divided circumferentially. The operations were performed under femoro-femoral partial cardiopulmonary bypass. In 6 of these cases selective perfusion of the visceral branches was used. The celiac axis was reconstructed in 10 patients, superior mesenteric artery in 9, right renal artery in 7, left renal artery in 6. Abdominal vessels were reconstructed by the "inclusion" technique described by Crawford in 2 patients, by "beveling" the distal prosthetic end in 6 and by the "interposition" technique in 4 patients. Vessels arising from the false lumen were reconstructed by the "interposition" technique. To prevent paraplegia, the evoked spinal cord potentials by direct stimulation of the cord (ESPs-dsc) were monitored perioperatively and the aneurysms were repaired sequentially in segments. In all patients except 2 with Crawford type III aneurysms, spinal cord ischemia was detected by ESPs-dsc. In 7 of these patients, 2 to 8 pairs of intercostal/lumbar arteries (I/L aa.) that arose from the "responsible" aortic segment were reconstructed. Reconstruction techniques included the "inclusion" technique in 2 patients, the "beveling" technique in 1, the "interposition" technique in 1 and the "on lay grafting" technique in 3 patients. One hospital death occurred in a patient who had chronic renal insufficiency and liver cirrhosis preoperatively. Spinal cord injury occurred in 5 patients, including 4 paraparesis and 1 delayed-onset paraplegia. In 2 of these patients, responsible I/L aa., were not reconstructed correctly despite ESPs changes, and injury might have been prevented if reconstruction of the "responsible" arteries had been performed. Thoracoabdominal repair for chronic Type B aortic dissection could be performed safely with an acceptable mortality rate. Spinal cord injury remains an unsolved problem.
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PMID:Operative results of thoracoabdominal repair for chronic type B aortic dissection. 920 Nov 25


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