Albumin, Fibrinogen, Prothrombin and Antithrombin III Variations in Blood, Urines and Liver in Rat Nephrotic Syndrome (Heymann Nephritis)

Girot, Robert; Jaubert, Françis; Léon, Martine; Bellon, B; Aiach, Martine; Josso, F; Lepelletier, O; Béguin, S.; Jp, Monnet

doi:10.1055/s-0038-1657305

Cited by 27 publications

(12 citation statements)

References 12 publications

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“…Rats with Heymann nephritis had also no evi dence of fibrinogenuria which has been attributed to the high molecular weight [21 ]; however, in humans with NS. fibrinogenuria has been reported in some cases [35].…”

Section: Discussionmentioning

confidence: 98%

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Cruz

Juárez-Nicolás

Tapia

et al. 1994

Nephron

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The human nephrotic syndrome is accompanied by important alterations of the coagulation system related proteins. The purpose of the present study was to examine the activity of coagulation- and fibrinolysis-related proteins in plasma and urine of control and puromycin aminonucleoside injected rats on days 2 (prenephrotic stage) and 10 (nephrotic stage). We measured the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the activities of (1) the coagulation factors (CFs) I, II, V, and VII-XII; (2) the inhibitor of coagulation antithrombin III (ATIII), and (3) the component of the fibrinolytic system α₂-antiplasmin (α₂-APL). PT and aPTT and the activities of CF, ATIII, and α₂-APL were not measurable in the urine of control and puromycin aminonucleoside injected rats on day 2. On this same day, plasma ATIII and CF VIII decreased. On day 10 (1) PT and aPTT decreased in plasma and were not measurable in urine; (2), plasma CFs I, II, V, VII, VIII, X, and XI increased; (3), plasma ATIII decreased; (4), plasma CFs IX and XII and α₂-APL did not change, and (5) ATIII and CFs II, VII, VIII, IX, X, XI, and XII, but not CFs I and V and α₂-APL, appeared in urine on day 10. ATIII deficiency was secondary probably to the urinary losses; however, the plasma activity of CFs II, VII, VIII, X, and XI increased and that of CFs IX and XII remained unchanged in spite of their urinary losses which suggests that other mechanisms such as deranged catabolism and altered hepatic synthesis may be involved. This model may be useful to study the pathophysiology of the abnormalities of coagulation in humans with nephrotic syndrome.

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Section: Discussionmentioning

confidence: 98%

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Cruz

Juárez-Nicolás

Tapia

et al. 1994

Nephron

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“…Fibrinogen gene expression is induced in nephrotic rats, high levels of fibrinogen mRNA and plasma concentration [35] are detected in the nephrotic stage, however, the urinary excretion of this protein is not increased in nephrotic rats [36] . This also indicates that neither urinary losses of the specific protein nor proteinuria are involved in the expres sion of this gene.…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation in the Expression of Hepatic Genes in Nephrotic and Pair-Fed Rats

Ibarra-Rubio¹,

Pedraza‐Chaverrí²,

Panduro³

1993

Nephron

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The messenger ribonucleic acid (mRNA) levels of albumin, fibrinogen, α1-acid glycoprotein (pAGP) and transferrin were analyzed in puromycin aminonucleoside (PAN)-treated (nephrotic) and in pair-fed (PF) rats with the Northern and dot blot hybridization techniques. Albumin mRNA levels in nephrotic and PF rats were 2- and 1.5-fold higher, respectively, than in ad-libitum-fed control (C) rats 6 days after PAN treatment. On day 11, this mRNA in PAN-treated rats was 2.5-fold higher than in PF and 4-fold higher than in C rats. A differential expression at the level of specific mRNAs was also detected for fibrinogen, pAGP, and transferrin in nephrotic and PF rats. On day 6, the fibrinogen and transferrin mRNA levels were significantly higher (p < 0.05) in nephrotic than in PF rats. In contrast, pAGP mRNA levels were normal or low in nephrotic rats and increased 2-fold in PF rats. These studies indicate the differential expression of hepatic genes in nephrotic and PF rats and show that albumin gene expression is only partially regulated by diet during the nephrotic stage of the disease.

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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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Albumin, Fibrinogen, Prothrombin and Antithrombin III Variations in Blood, Urines and Liver in Rat Nephrotic Syndrome (Heymann Nephritis)

Cited by 27 publications

References 12 publications

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Differential Regulation in the Expression of Hepatic Genes in Nephrotic and Pair-Fed Rats

Plasma Composition in the Nephrotic Syndrome

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