Split products of fibrin in human renal disease

Stiehm, E. Richard; Trygstad, Carl W.

doi:10.1016/0002-9343(69)90028-x

Cited by 81 publications

(27 citation statements)

References 31 publications

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“…Fibrin deposition in the renal glomerulus is believed to be important in the pathogenesis of lupus nephritis (22)(23)(24). The deposition of antigen-antibody-complement complexes in the glomerulus may result in localized intravascular coagulation with consequent fibrin deposition (25). Evidence for the occurrence of low-level DIC in SLE has been provided by studies based chiefly on the detection of fibrinogen/fibrin degradation products in serum (22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

“…A drop of mixed methyl red indicator (15) was added, and the samples were titrated to neutrality by adding 10 N NaOH with a syringe microburet equipped with a finely pulled glass tip. Neutralization of the extract of a 2-ml plasma sample required [25][26][27][28][29][30] /Al of 10 N NaOH, and resulted in dilution of the sample by about 0.01 vol or less. The samples were heated to 500C in a water bath, then removed from the bath and placed under water aspirator vacuum until they began to boil.…”

Section: Methodsmentioning

confidence: 99%

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Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus.

Cronlund¹,

Hardin²,

Burton³

et al. 1976

J. Clin. Invest.

108

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A B S T R A C T A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 1"I introduced into tyrosine-FPA synthesized in our laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA.In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml).A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus.

Cronlund¹,

Hardin²,

Burton³

et al. 1976

J. Clin. Invest.

108

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“…disease [9,15]. Although chronic intravascular coagulaSince a-2-macroglobulin, the major antiplasmin in tion is not regularly found in the nephrotic syndrome serum, is markedly elevated in the nephrotic syndrome [27], several coagulation abnormalities have been de- [12,16,22,25], we have investigated the fibrinolytic scribed which suggest a hypercoagulable state with a system in patients with the nephrotic syndrome, inthromboembolic potential [2,4]. Deficient fibrinolysis eluding three patients with thromboembolic disease.…”

Section: Introductionmentioning

confidence: 99%

Fibrinolytic Studies in the Nephrotic Syndrome

Scheinman

Stiehm

1971

Pediatr Res

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“…Received for publication 20 September 1973 and in revised form 12 December 1973. experimental renal diseases (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). In addition, fibrin degradation products have appeared in the blood and urine of patients with glomerulonephritis and in renal transplant recipients (11,12). How fibrinogen is deposited and fibrin degradation products are produced in renal disease have not yet been established; and the precise role of coagulation proteins in the pathogenesis of renal failure is still unknown.…”

mentioning

confidence: 99%