Pericarditis in renal disease

Kumar, Sudarshan; Lesch, Michael

doi:10.1016/0033-0620(80)90028-6

Cited by 22 publications

(10 citation statements)

References 68 publications

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“…Since subepicar dial myocarditis is rare in uremic pericarditis [16][17][18], it is unlikely that these abnormal findings were due to changes related with pericarditis. Although the exact mechanisms leading to altered basement membranes with perturbation of anionic sites in the membranes remain unclear, unfavorable metabolic processes result ing from uremia [28-32] are postulated to be implicated as factors responsible for the alterations of basement membranes.…”

Section: Discussionmentioning

confidence: 99%

“…seemed more often observed in patients with longer duration of uremia. It should be noted that sub epicardial myocarditis is rare in uremic pericarditis [16][17][18]. Furthermore, preliminary studies on sarcolemmal complex of myocardial cells and capillaries have been extensively performed in pericarditis of varying etiologies in this laboratory.…”

Section: Ultrastructure and Anionic Molecular Organization In The Capmentioning

confidence: 99%

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lterations of infrastructure and Anionic Molecular Organization in the Basement Membranes of Chronic Uremic Myocardium

Lee¹

1986

Am J Nephrol

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Ultrastructural and cytochemical studies on the basement membranes of chronic uremic myocardium which was obtained in vivo in 6 uremic patients with severe-grade pericarditis were carried out with special reference to the investigation of anionic molecular organization in the basement membranes of myocardial cells and capillaries. Irregular thickening of the basement membranes of myocardial cells and capillaries was consistently observed in chronic uremic heart. The central electron-lucent surface coat of the sarcolemmal complex and the inner lamina lucida of the capillary basement membrane were often absent with only a thick, dense zone comprising the membranes. In addition, focal splitting of myocardial basement membranes into two layers separated by clear spaces was occasionally demonstrated. The anionic binding sites characterized by cationic polyethyleneimine (PEI) were irregularly and loosely distributed in the basement membranes of chronic uremic myocardium, particularly in the abnormal basement membranes. Apparent increase of PEI deposition in the surface coat of myocardial basement membranes was present in chronic uremia in comparison to that in the controls. Furthermore, the PEI particles were not infrequently observed to be distributed in the intercalated discs and even in the interior of myocardial cells. From the aforementioned results we disclosed the ultrastructural alterations of the basement membranes associated with disorganization of anionic binding sites in the membranes in chronic uremic myocardium. Thus, the present study provides the ultrastructural and molecular basis for the explanation of many clinical manifestations and pathologic findings in the chronic uremic heart. It is suggested that altered membrane permeability of myocardial cells and capillaries resulting from their basement membrane changes in the chronic uremic state appears to play a relevant role in the pathogenesis of uremic cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Section: Ultrastructure and Anionic Molecular Organization In The Capmentioning

confidence: 99%

lterations of infrastructure and Anionic Molecular Organization in the Basement Membranes of Chronic Uremic Myocardium

Lee¹

1986

Am J Nephrol

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“…' Laboratory Tests for Pericardial Fluid Specific Forms of Pericardial Disease Uremic Pericarditis. The success of peritoneal and hemodialysis in extending life for years in endstage renal failure has led to a dramatic increase in the number of patients with uremic pericarditis [53]. The causative agent in this syndrome has not been well established.…”

Section: Diagnostic Testsmentioning

confidence: 98%

Pericardial Disease in the Intensive Care Setting

Thomas

LeWinter

1987

J Intensive Care Med

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Pericardial disease commonly occurs in the intensive care setting, but its timely diagnosis may be missed. The normal pericardium serves as a lubricated sac within which the heart may beat with minimal friction. The effect of the pericardium on cardiac filling at normal diastolic pressures is not clear; however, it may limit cardiac dilation in states of acute volume overload such as mitral regurgitation and right ventricular infarction. Pericardial disease may be divided into two catego ries : those cases that result from inflammation of the pericardium (pericarditis), and those cases in which a pericardial effusion or the thickened pericardium itself causes hemodynamic changes (tamponade and constric tion). Simple pericarditis should not lead to any hemo dynamic alteration other than tachycardia. In both tam ponade and constriction, the jugular venous pressure is elevated with low forward cardiac output; tamponade typically shows pulsus paradoxus, whereas constric tion more frequently shows Kussmaul's sign. The electrocardiogram may show diffuse ST segment elevation with PR segment depression in pericarditis; a large pericardial effusion, even with early tamponade, may not by itself cause any changes in the electrocar diogram. The echocardiogram is invaluable in diagnos ing the presence of a pericardial effusion and recogniz ing tamponade physiology (diastolic collapse of the right ventricular outflow tract and invagination of the right atrium). In selected patients, simple pericarditis may be managed outside of the hospital. Anyone suspected of having a hemodynamically significant pericardial effu sion should be hospitalized, usually in an intensive care unit. Pericardiocentesis should be performed under op timal monitoring conditions, although in an emergency, blind pericardiocentesis may be attempted. Recognition of the cause of the pericardial process will guide its treatment. Management of selected pericardial syn dromes is discussed later in this review.

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“…The correlation has not been high between the incidence of serositis and plasma levels of small or middle molecules [4,7,8,11,12]. Some indirect data suggest that very large molecules, circulating immune complexes (CIC) might be responsible for serositis in patients with renal failure.…”

Section: Introductionmentioning

confidence: 99%

“…Since serositis develops fre quently in well-dialyzed patients [13][14][15], an alleged toxin may not be readily dialyzable. An occurrence of serositis 1-3 weeks after bacterial or viral infection without detect able organisms in an exudate [3,4,12,13] resembles the sequence of events in glomerulonephritis, rheumatic fever, serum sickness, and other immune complex-induced dis eases. One of the functions of healthy kidneys is the removal of CIC with slight antigen excess [16,17], thus CIC levels may be elevated in patients with renal failure.…”

Section: Introductionmentioning

confidence: 99%

Circulating Immune Complexes: Possible Toxins Responsible for Serositis (Pericarditis, Pleuritis, and Peritonitis) in Renal Failure

Twardowski¹,

Alpert²,

Gupta³

et al. 1983

Nephron

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In 71 patients (41 men, 30 women) with advanced renal failure maintained on hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), or within 8 weeks after the commencement of dialysis therapy (ED), studies were performed searching for evidence of serositis and the blood levels of circulating immune complexes (CIC), measured by the polyethylene glycol precipitation method. Mean CIC levels were elevated in these patients compared to the 58 healthy subjects (mean ± SEM 725 ± 40, and 260 ± 34 µg/ml, respectively). Serositides were significantly more prevalent in ED patients compared to both remaining groups, and tended to occur less frequently in CAPD than in HD patients. CIC levels were significantly lower in CAPD than in ED patients. The levels of CIC were significantly higher in patients with serositis compared to those without evidence of serosal inflammation (mean ± SEM 868 ± 71 and 677 ± 53 µg/ml, respectively). In addition, immune complex-like materials were found in all of 4 effusate samples and in 10 of 27 peritoneal dialysates. It is suggested that immune complexes may be the ‘uremic toxins’ responsible for the serositis of renal failure, and may be secreted into serous effusions. Immune complex-like material can be removed in peritoneal dialysate, which may contribute to the lower CIC levels and lower incidence of serositis in the CAPD patients.

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Pericarditis in renal disease

Cited by 22 publications

References 68 publications

lterations of infrastructure and Anionic Molecular Organization in the Basement Membranes of Chronic Uremic Myocardium

lterations of infrastructure and Anionic Molecular Organization in the Basement Membranes of Chronic Uremic Myocardium

Pericardial Disease in the Intensive Care Setting

Circulating Immune Complexes: Possible Toxins Responsible for Serositis (Pericarditis, Pleuritis, and Peritonitis) in Renal Failure

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