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)

The pathophysiology of ascites in patients with cirrhosis is complex and includes increases in hepatic sinusoidal pressure, the formation of hepatic and splanchnic lymph, renal sodium retention, and hypoalbuminemia. However, the role of hypoalbuminemia in ascites formation is controversial. Evaluating ascites in hypoalbuminemic patients with nephrotic syndrome could add to our understanding of the role of hypoalbuminemia in ascites development. We conducted a retrospective analysis of 52 adults and 21 children with nephrotic syndrome who were hospitalized in the Hadassah University Hospital on Mount Scopus during 1981-1994. There was a significant difference in the prevalence of ascites between pediatric (52%) and adult patients (23%) (p = 0.024). Pediatric patients had lower serum albumin levels than adults (1.70 +/- 0.08 g/dl vs. 2.10 +/- 0.07 g/dl, p = 0.001). Adult patients with ascites had lower serum albumin levels than adult patients without ascites (1.80 +/- 0.13 g/dl vs. 2.20 +/- 0.07 g/dl, p = 0.01). This difference was not found in pediatric patients. Temporary fluctuations in liver enzymes (up to four times the upper limit of normal for transaminases) were evident in five patients from the pediatric group with ascites, whereas all pediatric patients without ascites had completely normal liver enzymes (p = 0.035). Among the 12 adult patients with ascites, seven had liver disease (three with cirrhosis and four with amyloidosis), and two had right-sided congestive heart failure. Among the 40 adult patients without ascites, only four had liver disease (amyloidosis). The plasma albumin levels of the patients with amyloidosis without ascites were higher than patients with amyloidosis with ascites (1.90 +/- 0.10 g/dl vs. 1.50 +/- 0.07 g/dl, p = 0.03). Two patients with nephrotic syndrome and ascites (one without liver disease) had episodes of spontaneous bacterial peritonitis. Ascites in nephrotic syndrome is more common in children than in adults. Although in most pediatric patients ascites formation is probably a common manifestation of the general fluid retention, in most adult patients with nephrotic syndrome ascites can be attributed to both hypoalbuminemia and the presence of liver disease or congestive heart failure, with increased hepatic sinusoidal pressure.
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PMID:Ascites in Nephrotic syndrome. Incidence, patients' characteristics, and complications. 877 92

Diuretic resistance is encountered in a number of disease states, such as chronic renal failure, nephrotic syndrome, congestive heart failure (CHF) and cirrhosis. Diuretic stratagems which produce sequential nephron segment blockade, and thus a synergistic diuretic response, are frequently necessary and are regularly employed in these conditions. Pharmacokinetic determinants of diuretic response, including dose administered, absolute bioavailability, and tubular transport capacity and transport rate, are reviewed here. Pharmacodynamic factors are perhaps more important to overall response, and often result in modification of the dose-response relationship; these are also reviewed here. Stratagems used to maximise the diuretic response to loop diuretics include correcting abnormal haemodynamic parameters, utilising larger doses or constant intravenous infusions, and using albumin as a vehicle to deliver the loop diuretic to the site of tubular secretion. If these measures fail, then diuretic combinations are useful. Perhaps the most effective is the combination of metolazone (a thiazide-type diuretic) and a loop diuretic. The rationale for and use of various diuretic combinations, with particular emphasis on the metolazone-loop diuretic combination, is reviewed here and applied to the major disease states associated with diuretic resistance.
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PMID:Diuretic combinations in refractory oedema states: pharmacokinetic-pharmacodynamic relationships. 888 3

Zone electrophoresis of serum proteins is still widely performed as a routine procedure in clinical laboratories. It is used in the diagnosis and management of many disorders, e.g. monoclonal gammopathies, cirrhosis, nephrotic syndrome, acute-phase reaction, immunoglobulin deficiency and others. The aim of this work is to evaluate the analytical performance of zone electrophoresis of serum proteins carried out in the Helena Laboratories Rapid Electrophoresis analyser (REP) comparing the results with those obtained in the Olympus Hite System 200 (HS-200). The REP system employs agarose gel as support medium, the HS-200 system employs cellulose acetate and it is the routine method in our laboratory. To date, we have not found any paper that deals with the assessment of a system for performing zone electrophoresis of serum proteins in terms of comparison with another.
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PMID:Evaluation of zone electrophoresis of serum proteins performed on the Helena Laboratories rapid electrophoresis analyser. 890 43

Glomerular pathology in liver cirrhosis is common in autopsies but is underdiagnosed antemortem. The most common pathologic findings are mesangial disease with immunoglobulin A deposits, and membranoproliferative glomerulonephritis. The latter is associated, most frequently, with hepatitis C infection and cryoglobulinemia. We describe a patient with longstanding liver cirrhosis who presented with a nephritic and nephrotic syndrome. Membranoproliferative glomerulonephritis was diagnosed on kidney biopsy. There was no clinical, laboratory or histologic evidence of hepatitis C infection or cryoglobulinemia. The different aspects of "cirrhotic glomerulonephritis" are discussed and the need for searching for this underdiagnosed condition in patients with chronic liver disease is emphasized.
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PMID:Cirrhotic glomerulonephritis: an underdiagnosed condition. 900 58

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

Diuretic therapy in edematous diseases often yields an inadequate natriuretic response ("diuretic resistance"). To study the functional changes in patients with congestive heart failure, liver cirrhosis with ascites, and nephrotic syndrome, characterized by a reduced effective arterial blood volume (EABV), different diuretic strategies were studied. It was shown that monotherapy with hydrochlorothiazide or furosemide was followed by an inadequate natriuretic response. Correlation of diuretic response with pretreatment fractional sodium excretion of the patient revealed a clear-cut interdependency: Those patients were resistant whose FENa+ was greatly below normal (<0.2%). In addition, it was found that the coadministration of the carboanhydrase inhibitor acetazolamide to diuretic therapy was very effective. We therefore conclude that an increase in proximal-tubular Na+ reabsorption is the major ("pharmacodynamic") determinant for diuretic resistance in edematous diseases with functional "underfilling" of the vascular tree. This alteration of the kidney can easily be overcome by coadministration of a carboanhydrase inhibitor (e.g., acetazolamide).
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PMID:Sequential nephron blockade breaks resistance to diuretics in edematous states. 912 75

Atrial natriuretic peptide (ANP) produced in the heart and prostaglandin E2 (PGE2) synthesised in the kidneys facilitate renal excretion of sodium and water, and thus oppose the actions of angiotensin II, aldosterone, arginine vasopressin (AVP), endothelin, and the renal sympathetic nerves. In the present work we studied the contributions and interactions of these substances in the regulation of blood volume (BV), renal haemodynamics, renal sodium and water handling and blood pressure (BP) in patients with glomerulonephritis and cirrhosis. The aim was through a better understanding of the pathophysiology to improve the treatment of fluid retention in these patients, which occurs as development of the nephrotic syndrome and accumulation of ascites, respectively. Normotensive patients with glomerulonephritis but without the nephrotic syndrome had normal baseline BV values measured as the sum of plasma volume and red cell volume; they responded to BV expansion after infusion of albumin and BV depletion after administration of furosemide with appropriate counterregulatory hormonal changes. However, they tended to hold more fluid within the intravascular phase after both manipulations than did the healthy subjects. The acutely induced increase in BV did not affect the BP, which was likely attributable to the changes in plasma values of angiotensin II and ANP shown. ANP could be expected to be a tool in the management of fluid accumulation in patients with the nephrotic syndrome and cirrhosis. The non-renal effects of high-dose ANP were studied for the first time in dialysis patients without excretory kidney function. A reversible shift of fluid away from the intravascular phase was demonstrated. The BV was maximally reduced 30 min after ANP had been given. The BP was reduced before fluid displacement occurred and to the same extent in patients and healthy subjects. The reduction in the BV was negatively correlated to the reduction in BP. From that study it is inferred that the BP reducing effect of ANP is not mediated by its diuretic effect or ability to displace fluid from the intravascular to the interstitial fluid compartment. As a pharmacological dose of ANP was given, it can only be suggested that endogenous ANP, by altering transcapillary Starling mechanisms, assists in buffering intravascular fluid expansion until renal excretion or dialysis can take place. The same dose of ANP was given to patients with the nephrotic syndrome and cirrhosis. The ability of ANP to increase sodium excretion through inhibition of sodium reabsorption in the distal tubules and to increase the glomerular filtration rate (GFR) was blunted in both patient groups, but the BP was reduced to the same extent as in the healthy controls. Patients with the nephrotic syndrome tended to have a slightly elevated BP. We only studied patients with normal or slightly reduced GFR. They had a normal BV, reduced renal filtration fraction, suppressed aldosterone, increased ANP, but normal plasma values of angiotensin II, endothelin, and AVP, and normal urinary excretion of PGE2. Thus, neither haemodynamic nor hormonal factors can easily explain the spontaneous sodium retention or the resistance to the effects of ANP and furosemide. An interesting finding, not previously reported in nephrotic humans, was the low cyclic guanosine 3'5'-monophosphate (cGMP) in plasma and urine in relation to ANP, both before and after administration of ANP. It is hypothesised that renal resistance to ANP, exaggerated renal cGMP degradation, or preponderance of clearance receptors in nephrotic kidneys may contribute to sodium retention and the low filtration fraction. Elevation of ANP in these patients is connected with increased albuminuria, and probably an increase in intraglomerular capillary pressure. The resistance to furosemide could not be attributed to delayed passage of fluid from the interstitial to the intravascular fluid phase, but is most likely due to renal tubular resistan
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PMID:Regulation of renal sodium and water excretion in the nephrotic syndrome and cirrhosis of the liver. 915 Oct 12

What I have tried to describe in these brief introductory statements are the key elements stimulating renal sodium retention mediated by arterial underfilling, as illustrated by the volume repletion reaction (Fig. 3). They may be summarized by saying that edematous states characterized by underfilling-most notably systolic pump failure-represent, in fact, suicidal arterial filling. This point of view is illustrated in Figure 8. Essentially, as shown in Figure 8, the original reduction in filling of the arterial tree, by provoking both hemodynamic changes and diminished sodium avidity, has the net effect of increasing end diastolic volume and, for a time, cardiac output, but at two great expenses: an increased afterload and a an increased preload. In the end, these latter two effects produce a reduced ejection fraction which obviously propagates the syndrome of systolic failure. Thus, suicidal arterial filling represents a vicious cycle in which homeostatic mechanisms set into play an attempt to compensate for inadequate arterial filling, which inevitably leads to increasing degrees of cardiac dysfunction and, hence, to deterioration of the patient. I have enjoyed presenting these introductory remarks. I am certain that subsequent talks in this Conference will consider more explicitly the provocative issue of the "overfilling" hypothesis as a mechanism for sodium retention in edematous states such as the nephrotic syndrome and cirrhosis.
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PMID:Edematous states: an overview. 918 96

Albumin infusions are given far from always on the correct indications, and often there are alternatives that are cheaper and equally suitable. In septic or hypovolaemic shock, crystalline fluids are cheaper and equally efficacious for volume therapy. It is only in sporadic patients with a nephrotic syndrome that colloidal solutions such as albumin are indicated in hypovolaemia. Albumin infusion has no place in the combating of oedema. In decompensated hepatic cirrhosis with ascites, it appears useful to combine paracentesis with albumin infusion, to prevent renal insufficiency and hyponatraemia, but other colloidal fluids are probably equally suitable. Combating hypoalbuminemia as such is not useful in seriously ill patients; it is the underlying disease that should be treated.
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PMID:[Clinical application of albumin: a closer look at indications]. 938 Jan 82

The current treatment of hyponatremia is unsatisfactory and can be associated with significant morbidity. Vasopressin is inappropriately elevated in the majority of patients with hyponatremia and causes free water retention by stimulating V2-receptors in the collecting ducts. Recently, orally active, nonpeptide, selective vasopressin V2-receptor antagonists have been characterized and offer an exciting prospect for the treatment for hyponatremia. V2-receptor antagonists are effective aquaretic agents, that are capable of increasing free water clearance and plasma sodium and might be useful in the treatment of hyponatremia caused by syndrome of inappropriate secretion of antidiuretic hormone, heart failure, cirrhosis, and nephrotic syndrome. The rationale for their use and evidence from animal and human studies are discussed.
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PMID:Vasopressin V2-receptor antagonists: panaceas for hyponatremia? 932 5


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