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Biomedical subjects

G Remuzzi

Publications and source records attributed to G Remuzzi.

At least 469 records · Page 26Linked to original sources
PubMed1982

Platelet function in patients on maintenance hemodialysis: depressed or enhanced?

Uremic patients on long-term hemodialysis show a paradoxical association of hemorrhages on the one hand and thrombotic complications or atherosclerosis on the other. Platelet function has been found to be depressed in some cases but enhanced in others. In 19 patients, both platelet aggregation and prostaglandin formation appeared to be significantly enhanced in response to low concentrations of arachidonic acid but significantly reduced with high concentrations. It is suggested that this double functional abnormality of uremic platelets may contribute to the complex vascular disturbances of hemodialyzed patients.

Arachidonic Acids↗
PubMed1981

Plasmatic regulation of vascular prostacyclin in pregnancy.

Activity of prostacyclin-stimulating factor was measured in six normal, non-pregnant women, six women in early normal pregnancy, six in late normal pregnancy, and six in late pregnancy complicated by severe pre-eclampsia. The activity was lower in the women in late pregnancy than in those in early pregnancy and the controls but was about normal in those with severe pre-eclampsia. These results may be relevant to the physiology of pregnancy and the pathogenesis of pre-eclampsia.

Adolescent↗
PubMed1980

Reduced umbilical and placental vascular prostacyclin in severe pre-eclampsia.

Prostacyclin production was significantly depressed in foetal and placental vascular tissues from five patients with severe pre-eclampsia in comparison to vascular tissues from women with uncomplicated pregnancy. Such an abnormality may be responsible for a reduced blood flow and defective fetal nutrition thus playing a major role in the pathogenesis of this syndrome.

Adolescent↗
PubMed1980

Intermittent heparin treatment does not induce hypercoagulability in haemodialysed patients.

Antithrombin-III (AT-III) and factor VIII coagulant (F VIII:C) and antigenic (F VIII:RA) activities have been studied in nine conservatively treated and 26 dialysed uraemic patients. AT-III levels were not significantly different from those of controls in either group. Among dialysed patients, those who had experienced thrombotic occlusions of the vascular accesses could not be distinguished from the remaining patients on the basis of their AT-III levels. Both F VIII:C and F VIII:RA were slightly higher than in controls in conservatively treated patients, but significantly higher in haemodialysed patients, especially in those who had never experienced thrombotic complications of the vascular accesses. No acute changes were observed in either the AT-III or F VIII:C/F VIII:RA ratio in five patients given heparin therapy during a dialytic session or in the interdialytic period. Thus repeated intermittent heparin treatment does not induce a hypercoagulable state in haemodialysed patients.

Adult↗
PubMed1980

Haemolytic uraemic syndrome: report of a case and new pathogenetic concepts.

Haemolytic uraemic syndrome (HUS) is a severe clinical condition characterised by thrombocytopenia, microangiopathic haemolytic anaemia and renal impairment [1]. At histological examination hyaline microthrombi occluding terminal arterioles and capillaries are generally found. Other syndromes share major clinical and histological diagnostic criteria with HUS. In particular, there is no method at present which clearly differentiates HUS from thrombotic thrombocytopenic purpura (TTP) [2]. We propose therefore the term thrombotic microangiopathy (TMA) to discuss both syndromes. The pathogenesis of TMA is unclear and many forms of therapy have been attempted without definitive proof of efficacy. The recently reported [3] successful results with exchange transfusion and plasma infusion represented a consistent advance in the management of these diseases. The beneficial effect of these procedures was attributed to replacement of an unknown 'missing' factor in plasma. This finding generated recent observations possibly relevant in understanding the pathogenesis of these diseases.

Adult↗
PubMed1979

Plasmapheresis in the treatment of acute renal failure in multiple myeloma.

Three patients with multiple myeloma and severe acute renal failure were treated by repeated plasmapheresis. Recovery of renal function was observed in all. The pathogenetic role of light chains and the possible mechanisms responsible for renal damage are discussed. It is suggested that the removal of light chains by plasmapheresis may be of therapeutic value in this condition.

Acute Kidney Injury↗
PubMed1979

Prostacyclin and human foetal circulation.

Tissues from human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels from normal adults. High prostacyclin generation could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation in which blood pressure is low despite very high cardiac output.

Adolescent↗
PubMed1979

Vascular prostacyclin and plasminogen activator activity in experimental and clinical conditions of disturbed haemostasis or thrombosis.

In several experimental and clinical conditions associated with thrombotic tendency, or complicated by thrombotic episodes, either prostacyclin (which inhibits platelet aggregation) or plasminogen activator (which promotes fibrinolysis), or both, appear to be decreased in the vessel wall. In other conditions, however, either activity may not change or even be increased. Possibly, vascular damage is followed by an early stimulation of both activities (a defence mechanism?) which may be subsequently reduced or exhausted. While the role of vascular plasminogen activator in haemorrhagic conditions is apparently unknown, prostacyclin activity appears to be markedly enhanced both in experimental animals and in patients with uraemia and bleeding complications. There is a suggestive evidence that uraemic plasma powerfully stimulates vascular prostacyclin generation.

Arteriosclerosis↗