Ischiemic Heart-Disease as a Complication of Nephrotic Syndrome

Berlyne, G.M.; Mallick, N. P.

doi:10.1016/s0140-6736(69)90110-x

Cited by 129 publications

(46 citation statements)

References 3 publications

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“…however, it should be noted that persistence of the nephrotic syndrome results in a normal serum HDL-cholesterol level with further increases in the LDL-and VLDL-cholesterol levels (manuscript submitted), which might become a risk factor of atherosclerosis. The present results help to explain why reports about the atherogenicity of the nephrotic syndrome are conflicting (Berlyne and Mallick 1969;Alexander et al 1974;Gilboa 1976;Wass et al 1979). …”

Section: Discussionsupporting

confidence: 61%

“…Because of the atherogenicity of such hyperlipidemias (Carison and Bottiger 1972), persistence of the nephrotic syndrome could be a cause of atherosclerosis, as suggested in some reports (Alexander et al 1974;Berlyne and Mallick 1969). For the formation of atheromatous lesions, not only serum factors but also the response of vessels to serum factors are very important (Morisaki and Saito 1981).…”

mentioning

confidence: 99%

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Lipid metabolism in the aorta of daunomycin-induced nephrotic rats.

Morisaki

Matsuoka

Shinomiya

et al. 1983

Tohoku J. Exp. Med.

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Several enzyme activities involved in lipid hydrolysis (acid and neutral cholesterol esterase and lipase) or synthesis (aryl-CoA synthetase, acyl-CoA: cholesterol acyltransferase and cholinephosphotransferase) were assayed in the aortas of rats with nephrosis induced by daunomycin and of rats fed on high cholesterol diet. In nephrotic rats activities of some enzymes involved in lipid hydrolysis, but not in synthesis, were increased. On the contrary, in rats fed on high cholesterol diet, the activities of all enzymes involved in lipid synthesis were significantly increased, with some increase in those involved in lipid hydrolysis. In nephrotic rats fed on high cholesterol diet all enzyme activities were markedly increased. From the view point of accumulation of cholesterol ester (CE), the ratio of hydrolysis of CE in lysosomes to CE incorporated from the blood and the ratio of hydrolysis of CE to reesterification of free cholesterol in microsomes were considered to be important. From this point of view, nephrotic hyperlipidemia was not so atherogenic as hyperlipidemia induced by the diet. The role of serum high density lipoproteins in lipid metabolism in the aorta was discussed. ----daunomycin; aorta; nephrotic rat; hyperlipidemia; cholesterol esterase

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Section: Discussionsupporting

confidence: 61%

mentioning

confidence: 99%

Lipid metabolism in the aorta of daunomycin-induced nephrotic rats.

Morisaki

Matsuoka

Shinomiya

et al. 1983

Tohoku J. Exp. Med.

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“…Alterations in plasma lipoprotein concentration would be anticipated to increase the likelihood of atherosclerosis [134,135], although the association between nephrotic hyperlipidemia and atherogenesis remains controversial [136], The plasma concentration of fibrinogen is in creased [ 10,11,14] …”

Section: Consequences Of Altered Plasma Compositionmentioning

confidence: 99%

Plasma Composition in the Nephrotic Syndrome

Kaysen¹

1993

Am J Nephrol

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The nephrotic syndrome is a consequence of urinary loss of intermediate sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Intermediate sized proteins, including albumin, transferrin, IgG, hormone binding proteins, and low molecular weight inhibitors of the clotting cascade, are lost in the urine and their concentration in plasma reduced. Synthesis of many proteins secreted by the liver is increased either at the level of transcription or posttranscriptionally. Synthesis of several liver-derived proteins is increased in the absence of their urinary loss, suggesting that hypoalbuminemia or reduced plasma oncotic pressure (Π) stimulates the production or reduces the rate of catabolism of these proteins. Their plasma levels, including those of lipoproteins and elements of the coagulation cascade, are increased. Plasma Πfalls and plasma viscosity increases because of the replacement of intermediate sized plasma proteins by larger ones. The plasma concentration of several proteins lost in the urine but not secreted by the liver, such as erythropoietin and IgG, are not defended by increased synthesis, suggesting that increased synthesis of plasma proteins is primarily confined to the liver. Loss of both liver-derived and non-liver-derived proteins may cause reduced immunity, anemia, and deficiency syndromes. Urinary loss of albumin alone is not responsible for decreased plasma Π. The relationship between plasma protein concentration and Πis greatly disturbed in nephrotic rats. In contrast, the relationship between Πand plasma protein concentration is nearly the same in rats with hereditary analbuminemia (NAR) and normal rats, despite the absence of albumin from the plasma of NAR. When proteinuria is induced in NAR the relationship between plasma protein concentration and Πbecomes identical to that in nephrotic animals, although no albumin was lost in the urine of NAR.

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“…Since that time various other instances of thromboembolic complications involving different organs have been re ported in NS. These included pulmonary thromboembo lism [2][3][4][5][6], mesenteric artery thrombosis with small bowel and omental necrosis [5,6], inferior vena cava thrombosis [7], femoral artery thrombosis [8][9][10], axil lary and subclavian artery thrombosis [11], iliac vein thrombosis [5], right ventricular mural thrombosis with massive pulmonary embolism [5], coronary artery thrombosis [9,12], ischemic necrosis of the foot [5], and most commonly renal vein thrombosis [13][14][15][16][17][18][19][20][21][22][23][24], Because of these observations NS has been considered a hypercoagulable state. Although generally associated with hyper coagulability, various clotting deficiencies can also occur in this setting.…”

mentioning

confidence: 99%

Nephrotic Syndrome and Coagulation and Fibrinolytic Abnormalities

Vaziri¹

1983

Am J Nephrol

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Ischiemic Heart-Disease as a Complication of Nephrotic Syndrome

Cited by 129 publications

References 3 publications

Lipid metabolism in the aorta of daunomycin-induced nephrotic rats.

Lipid metabolism in the aorta of daunomycin-induced nephrotic rats.

Plasma Composition in the Nephrotic Syndrome

Nephrotic Syndrome and Coagulation and Fibrinolytic Abnormalities

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