Tissue-Type Plasminogen Activator (t-PA) and Dilute Blood Clot Lysis Time in Nephrotic Patients

Abstract

SummaryWhen compared to normal weight normolipidemic control subjects, dilute blood clot lysis time was found to be obviously (p <0.001) prolonged in hypertriglyceridemic patients without proteinuria and slightly (p <0.05) accelerated in hyperlipidemic nephrotic patients in spite of their very high levels of plasma fibrinogen. As a result the ratio plasma fibrinogen (mg/dl) per clot lysis time (minutes) was 1.241 ± 0.08 (X ± SEM) in control subjects, 0.574 ± 0.07 in hypertriglyceridemic patients and 2.69 ± 0.172 in nephrotic patients. This finding suggesting that a larger amount of fibrin is rather readily dispersed from dilute blood clots of nephrotic patients was associated with higher levels of plasma t-PA: Ag (9.45 ng/ml ± 1.18 in nephrotic patients versus 5.8 ng/ml ± 1.23 in controls before venous occlusion and respectively 33.1 ng/ml ± 3.83 versus 20.3 ± 3.40 in controls after venous occlusion). Plasminogen activator activity of the euglobulins as assessed by the bovine fibrin-agarose plate was significantly higher in nephrotic patients only after venous occlusion. Plasma samples of nephrotic patients exerted a more potent inhibition of fibrinolysis in a urokinase activated system. This effect was, however, mainly due to the high levels of α2 macroglobulin in nephrotic plasma which apparently have little influence on dilute blood clot lysis time.

Occupational risk factors for chronic kidney disease in Andhra Pradesh: ‘Uddanam Nephropathy’

“…CKD was defined following the KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease [ 12 ] of impaired kidney function or kidney damage. Impaired kidney function was defined as an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m 2 using the CKD-EPI equation [ 13 ].…”

α2-Antiplasmin, Plasminogen Activator Inhibitor (PAI) and Dilute Blood Clot Lysis Time in Selected Disease States

“…2). Previous investigations (16) however emphasized that in nephrotic patients a larger amount of t-PA antigen is released from their endothelia and euglobulins obtained from their plasma exert a higher lytic activity on fibrin plates. As PAl activity is not increased in these patients one may presume that a relatively higher proportion of free t-PA would overcome the resistance to fibrinolysis of a clot rich in fibrin, factor XIII and a2AP.…”

“…For example plasma PAl levels are increased not only in atheroscle~otic hyperlipidemic patients (10) who also display a retarded dilute blood clot lysis (11) but also in many cases with severe hepatic cirrhosis (12,13) in whom clot lysis was found to be accelerated (11) probably in relation to their reduced plasma levels of u2AP (14) and factor XIII (15). On the other hand in spite of the high plasma levels of fibrinogen and factor XIII the dilute blood clot lysis was not retarded but rather accelerat;d in patients with the nephrotic syndrome (15,16).…”