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 defining host resistance factors in uremia, experiments were designed to assess the effect of renal failure serum upon the reactivity of normal human lymphocytes to phytohemagglutinin in vitro. Normal buffy coat cells were resuspended in sera obtained from normal subjects and from 14 patients with renal failure, then stimulated with phytohemagglutinin M and the cellular response measured by the increase in thymidine or uridine uptake. The mean thymidine uptake by stimulated cells in normal sera was 14,389 +/-1695 (SEM) cpm per 2 x 10(6) lymphocytes. Uridine uptake under the same conditions was 12,540 +/-1887 cpm. Compared to these are a mean thymidine uptake of 2740 +/-457 cpm and uridine uptake of 3928 +/-667 cpm in renal failure sera. Both differences are significant at P<0.01 level. For controls representing "chronic illnesses," sera from patients with pneumococcal meningitis, cirrhosis of the liver without jaundice, rheumatoid arthritis, and paraplegia with urinary tract infection did not cause suppression. No single drug had been taken by all the renal failure patients; three patients were taking no drugs. The serum from one patient with acute renal failure suppressed thymidine uptake while her serum obtained after recovery from her illness supported a normal lymphocyte response. Improvement of lymphocyte response was also noted in 9 of 10 sera obtained from patients immediately after hemodialysis. These observations plus the inhibition of stimulated cells by normal serum mixed with renal failure serum indicate the presence of a dialyzable inhibitory factor rather than the absence of a supporting factor in the renal failure sera. Lymphocytes preincubated for 24 hr in renal failure serum responded normally when transferred to normal serum and stimulated. Cells stimulated in normal serum and transferred to renal failure serum within the initial 24 hr of incubation demonstrated depressed thymidine uptake. Also, cell survival for 72 hr incubation as judged by trypan blue exclusion and chromium-51 release was similar in normal and renal failure sera. Thus, the suppressive effect of renal failure serum does not depend upon the initial phytohemagglutinin-cell interaction nor upon a significant cytotoxic effect. These studies demonstrate that a dialyzable factor(s) in the serum of patients with renal failure can greatly suppress one parameter by which an immune function of circulating lymphocytes is assessed and provides at least, a partial explanation for delayed homograft rejections in renal failure as well as the susceptibility of such patients to various infections.
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PMID:Defective cellular immunity in renal failure: depression of reactivity of lymphocytes to phytohemagglutinin by renal failure serum. 557 33

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

Acute respiratory failure had occurred in 89 of 1594 patients in a medical intensive care unit (5.6%), 26.8% of all patients (332) on long-term mechanical ventilation. Compared with the other chronically ventilated patients those with acute respiratory failure averaged a lower age, the proportion of women was higher and the duration of ventilation longer. The death rate was significantly higher (78.7% compared with 58.3%). The important prognostic factors included the underlying disease, additional abnormal organ function, severity of pulmonary gas exchange abnormality, and advanced age. If there was septicaemia, peritonitis, liver cirrhosis with bleeding oesophageal varices or polytrauma with acute renal failure the death rate was over 80%; after hypovolaemic shock, pancreatitis or postoperative pulmonary failure it was less than 65%. Patients who had abnormal function of at most one other organ in addition and an inspiratory arterial pO2 difference below 250 mm Hg, measured 12 hours after onset of mechanical ventilation, had a relatively favourable prognosis with a death rate of 33%, while in the other groups of patients it was 86-100%.
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PMID:[Acute respiratory failure in a medical intensive care unit. Incidence and prognosis]. 636 69

A series of 46 patients with obstructive disease of the bile ducts complicated by acute renal failure (ARF) is presented. The patients exhibited obstructive jaundice with prevalence of conjugated bilirubine. In 80% of the cases biliary obstruction was associated with cholangitis. Disturbances of the liver function (from mild cholestasis to biliary cirrhosis) were also present. The renal damage was due to biliary disorders and was either present on admission (33 cases) or developed postoperatively (13 cases). Most of the patients presented nonoliguric ARF as well as poor perfusion resulting from decreased circulating blood volume (dehydration and electrolyte loss). Among the criteria used to determine the type of ARF, the urinary/plasma creatinine ratio less than 10 and urinary/plasma osmolarity ratio less than 1.1 were the most valuable. Management of ARF by dialysis alone was not satisfactory. Attention is called to the surgical treatment of the biliary disorder as being essential to prognosis. Patients not treated by radical surgery died in proportion of 87 to 100%. From the rest of 18 patients in whom the operation provided an adequate biliary drainage, in 15 the renal function was restored and 12 survived. Better prognosis in these patients was dependent not only on the ability to cure the cholestasis and infection, but on the early surgical treatment. The ultimate prognosis depends on the improvement of the liver function.
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PMID:Acute renal failure in obstructive diseases of the extrahepatic biliary ducts. 649 68

Vasodilatory prostaglandins function to maintain renal perfusion in patients with cirrhosis and ascites. To evaluate the potential contribution of the vasodilator prostaglandin E2 and the vasoconstrictor metabolite thromboxane B2 to the development of the hepatorenal syndrome, we measured urinary excretion of these products in 14 patients with hepatorenal syndrome and in control populations with acute or chronic liver or kidney failure. Radioimmunoassay measurements were confirmed by bioassay and by mass spectrometry. Prostaglandin E2 was decreased compared with healthy controls (2.2 +/- 0.3 vs. 6.3 +/- 0.8 ng/h, p less than 0.01) and compared with acute renal failure (9.6 +/- 2.1 ng/h) and with alcoholic hepatitis (9.2 +/- 3.3 ng/h). Thromboxane B2 concentration was normal in patients with alcoholic hepatitis (0.12 +/- 0.02 vs. 0.15 +/- 0.03 ng/ml) and minimally increased in acute renal failure (0.18 +/- 0.15 ng/ml), but markedly elevated in hepatorenal syndrome (0.69 +/- 0.15 ng/ml, p less than 0.001). Urinary thromboxane B2 concentration fell with improved renal function in 3 patients who survived. These data suggest an imbalance of vasodilator and vasoconstrictor metabolites of arachidonic acid in patients with the hepatorenal syndrome.
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PMID:Urinary thromboxane B2 and prostaglandin E2 in the hepatorenal syndrome: evidence for increased vasoconstrictor and decreased vasodilator factors. 657 62

In a prospective study (from April, 1980 to April, 1981) of 110 patients with moderately severe to severe pneumonia 11 were found to have 12 manifestations of Legionnaires' disease. Diagnosis was proven by indirect immunofluorescence tests, either a quadruple titre rise to 1 : 128 or a single titre of at least 1 : 256. The clinical picture in all 11 patients was the typical one of severe pneumonia, usually involving the lower lobes, high fever between 39 and 40.4 degrees C, as well as WBC counts between 6.8 and 28.9 X 10(9)/l. In nine cases artificial ventilation was required, in four there was acute renal failure requiring dialysis, in four other definite renal insufficiency. All patients had underlying disease, in some severe, such as chronic obstructive lung disease, diabetes mellitus, heart failure, liver cirrhosis, renal transplantation or extensive operations. Eight patients died, four of them of Legionnaires; disease. The relatively high infection rate (10%) indicates that in patients with risk factors, as well as those with a pneumonia unresponsive to the standard treatment within five to seven days, Legionnaires' disease should be considered in the differential diagnosis.
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PMID:[Legionnaires' disease: prospective study of its incidence, clinical features and prognosis. (author's transl)]. 706 Apr 96

Prerenal acute renal failure is defined as a reduction in the glomerular filtration rate due to a primary disturbance in renal hemodynamics in the absence of any structural kidney damage. In case of moderate hypotension or hypovolemia, a number of adaptative systemic and intrarenal responses preserve renal perfusion and filtration rates, particularly by inducing a marked reduction in preglomerular arteriolar resistance and an increase in postglomerular resistance. However, these mechanisms are inherently limited. In the presence of advanced circulatory failure or iatrogenic pharmacologic interventions compromising these renal defense mechanisms, prerenal failure becomes evident. Therefore, prerenal failure may occur during acute hemodynamic disturbances due to hypovolemia or systemic vasodilatation, in severe cardiac failure, in cirrhosis with ascites, and in certain clinical situations following administration of nonsteroidal antiinflammatory agents or angiotensin converting enzyme inhibitors. The treatment depends on the underlying cause.
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PMID:[Functional acute kidney failure]. 756 89

To identify the demographic, clinical, and pathologic features and the prognosis of renal disease in a series of patients with infectious or postinfectious proliferative glomerulonephritis (GN), data were collected from records of 76 adult patients admitted from 1976 to 1993 to 2 neighboring suburban hospital nephrology units, whose catchment population consists of patients living in a suburban borough of Paris with a below-average socioeconomic status. Thirty-four patients (45%) were alcoholics, diabetics, or intravenous illicit-drug users. Sixty-six patients presented with acute nephritic and/or nephrotic syndrome. Acute renal failure was present in 56 (76%) and required dialysis in 14. The diagnostic workup comprised at least 1 renal biopsy in each case. The patient's background, site of infection, clinical course, laboratory variables, and, when available, bacteriologic findings were analyzed in each case to interpret the evolution of the disease. Initial renal biopsy disclosed endocapillary GN in 44 patients, crescentic GN in 26, and membranoproliferative GN in 6. Ten patients had endocarditis. Staphylococci and Gram-negative strains, not streptococci, were the most common bacteria identified. The origin of sepsis was mainly the oropharynx (21), the skin (19) and the lung (14); 19 cases involved multiple sites of infection. Eight patients died (11%), and 20 (26%) recovered renal function, but GN followed a chronic course in 38 (50%), rapidly requiring maintenance dialysis in 6. Poor prognostic factors included age over 50 years, purpura, endocarditis, and glomerular extracapillary proliferation. Twenty-six patients underwent repeat renal biopsy 1 month to 11 years after the initial presentation. The main finding, irrespective of the interval since the first biopsy, was that ongoing or new iatrogenic infection acquired during hospitalization was almost invariably acquired during hospitalization was almost invariably associated with developing glomerular proliferative changes. This study shows that infectious proliferative GN remains common, but that its epidemiology has changed from what was observed until 2 decades ago. The responsible bacteria, when identified, now comprise a majority of staphylococci and Gram-negative strains, in contrast to the streptococci which predominated 3 decades ago. Infectious GN affects with increasing frequency patients with an underlying condition responsible for immunosuppression, especially alcoholism, even in the absence of cirrhosis. Destructive glomerular proliferation persists, especially but not exclusively until infection has been eradicated, and despite rescue treatment with corticosteroids and/or cytostatic drugs. Thus, the prognosis is poor, and infectious GN often ends in renal death. Infection continues in this decade to represent a frequent and probably often overlooked cause of end-stage renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The current spectrum of infectious glomerulonephritis. Experience with 76 patients and review of the literature. 789 44

In cirrhosis of the liver structural distortion of the sinusoidal vessels is the major factor responsible for the increase in portal venous pressure and the development of abdominal ascites. The mechanisms by which advanced cirrhosis of the liver leads to widespread changes in the systemic circulation including vasodilatation, increased cardiac output and expanded plasma volume, together with activation of a range of antinatriuretic and natriuretic factors, are unclear. Several hypotheses have been proposed to explain these pathophysiological consequences, including underfilling of the systemic arterial system, overflow and peripheral vasodilatation, with a decrease in effective arterial blood volume. The evidence for and against these hypotheses is critically examined. In patients with hepatic cirrhosis complicated by ascites, increased intrarenal release of vasodilating prostaglandins may assist in sustaining renal blood flow and glomerular filtration rate by counteracting the vasoconstrictor effects of noradrenaline and angiotensin II. In advanced stages of the syndrome, cirrhotic ascites may become refractory to medical treatment. In this situation renal function becomes progressively impaired and eventually acute renal failure, so-called hepatorenal syndrome, supervenes due to intense renal vasoconstriction and opening of intrarenal arteriovenous shunts. The progressive renal vasoconstriction may also be accentuated by the reduced synthesis of renal vasodilating prostaglandins. The medical treatment of ascites is based on bed-rest, a low-sodium diet and administration of aldosterone antagonists and loop diuretics. Patients who are refractory to such therapy may be further treated by paracentesis or by the LeVeen shunt, though the long-term results of these physical therapies are unsatisfactory.
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PMID:Pathogenesis and treatment of ascites in hepatic cirrhosis. 795 48

Acute renal failure in liver disease includes prerenal renal failure, acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Patients with liver cirrhosis are susceptible to prerenal renal failure because of gastrointestinal bleeding, diuretics and paracentesis etc. ATN is more common in patients with obstructive jaundice but it also develops as a result of prolonged prerenal renal failure. HRS is a functional form of oliguric acute renal failure, occurring in patients with advanced liver disease in the absence of known cause of renal failure. Intrarenal vasoconstriction, attributable to a decrease in effective arterial blood volume, induced by peripheral arterial vasodilation, is proposed to play a causative role. Central hemodynamic monitoring is useful to distinguish HRS from other reversible conditions with renal failure in liver disease.
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PMID:[Renal damage in liver cirrhosis: pathophysiology and management]. 811 86


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