Role of the Kidney in Fibrinolytic Activity of Blood

Menon, I. S.; Dewar, H. A.; Newell, D. J.

doi:10.1016/s0140-6736(68)92230-7

Cited by 28 publications

(16 citation statements)

References 19 publications

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“…It has been observed by others that the antifibrinolytic effect of serum resides largely with the a2-globulin fraction (7). It has further been shown that the kidney plays a role in the regulation of fibrinolysis (8)(9)(10) and that this system can become impaired with renal damage (11). Antifibrinolysin studies are unfortunately unavailable in our cases.…”

Section: Pathologic Criteriamentioning

confidence: 95%

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Intraglomerular fibrin, platelet aggregation, and subendothelial deposits in lipoid nephrosis

Duffy¹,

Cinque²,

Grishman³

et al. 1970

J. Clin. Invest.

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Section: Pathologic Criteriamentioning

confidence: 95%

“…Under high magnification this material appeared very finely granular and did not resemble fibrin. It occasionally contained what appeared to be remnants of sub- [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. This was observed apparently unassociated with platelet aggregation in nine cases.…”

Section: Pathologic Criteriamentioning

confidence: 99%

Intraglomerular fibrin, platelet aggregation, and subendothelial deposits in lipoid nephrosis

Duffy¹,

Cinque²,

Grishman³

et al. 1970

J. Clin. Invest.

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“…When this was compared to the euglobulin-lysis times (table II) in arterial blood of age-matched subjects without renal disease [3,4,7,8] no statistically significant difference between the two groups was observed (p > 0.3 n.s. ).…”

Section: Resultsmentioning

confidence: 92%

“…Recently M e n o n et al [3,4] have shown that kidneys of subjects without renal disease make a significant contribution of plasminogen activator to the circulation. On the basis of the above findings and in view of the fact that all the patients on RDT had diseased kidneys it is tempting to speculate whether a decrease in the fibrinolytic activity of the blood may be a factor in the pathogenesis of clotting episodes of arteriovenous shunts.…”

mentioning

confidence: 99%

Fibrinolytic Activity of Shunt Arterial Blood in Patients on Regular Dialysis Treatment

Rastogi¹,

Menon²

1970

J Vasc Res

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When fibrinolytic activity of arterial blood from arteriovenous shunts in patients on regular dialysis treatment was compared with arterial blood of age-matched subjects without renal disease no statistically significant difference was observed. It is suggested that this may be due either to the damaged kidneys continuing to produce plasminogen activator or to the smaller amount of activator produced by the diseased kidneys being compensated by a reduced removal of it in the lungs.

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“…53 The kidney is a well-known source of fibrinolytic factors, 54 and if local fibrinolysis was impaired in the malignant phase, coagulation would tend to spread unimpeded within the kidney. With the exception of renal artery stenosis, the fibrinoid lesions of malignant hypertension and of MHA in other states are usually found within the kidney, particularly in the afferent glomerular arteriole, 8 -25 -26 and there is evidence that the fibrinolytic enzymes are to be found in high concentration in this zone.…”

Section: -139mentioning

confidence: 99%

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

Gavras¹,

Brown²,

Brown³

et al. 1971

Circ Res

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Evidence of microangiopathic hemolytic anemia (MHA) was found in 14 of 22 patients with malignant phase hypertension, and in one of these, a patient with proliferative glomerulonephritis, MHA and malignant hypertension developed together during a three-month period of observation.Among 61 rats subjected to unilateral nephrectomy, injected with DOCA, and given 1% saline to drink, 42 developed evidence of MHA, Eighty-four per cent of these also had fibrinoid necrosis and/ or plasmatic vasculosis in the remaining kidney at autopsy. Blood pressure rose to 150 mm Hg or more in 72% of these DOCA-injected animals. In 29 control rats subjected to unilateral nephrectomy only, blood pressure rose to 150 mm Hg or more in 2135, MHA developed in 14%, and fibrinoid lesions were found in none.The significance of these observations is discussed in relation to the possibility that MHA is either a consequence of malignant hypertension or a contributory factor in its pathogenesis. KEY WORDSmicroangiopathic hemolytic anemia DOCA malignant hypertension fibrinoid lesions bilateral nephrectomy renal failure intravascular coagulation glomerulonephritis• An association between malignant phase hypertension and microangiopathic hemolytic anemia (MHA) is now well recognized. 1 " 5Since the association appears relatively common and since MHA, when it occurs in other states, is characterized by features similar to those of malignant hypertension, it seemed possible to us that MHA might at least contribute to the development of the malignant phase. 6 If this is so, MHA should be demonstrable when (or before) the malignant phase appears. Our earlier studies threw little light on this particular question since, by the time most patients presented, both the conditions were well established.

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Role of the Kidney in Fibrinolytic Activity of Blood

Cited by 28 publications

References 19 publications

Intraglomerular fibrin, platelet aggregation, and subendothelial deposits in lipoid nephrosis

Intraglomerular fibrin, platelet aggregation, and subendothelial deposits in lipoid nephrosis

Fibrinolytic Activity of Shunt Arterial Blood in Patients on Regular Dialysis Treatment

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

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