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Platelet aggregation is reduced and ADP release is inhibited leading to
increased capillary fragility and prolongation of bleeding time.


  • Increased fibrinolytic activity of the blood because fibrinolysin is
    normally eliminated by the kidney.

  • Anaemia:
    This bleeding tendency is corrected by dialysis, correction of anaemia
    or administration of DDAVP or oestrogen.


c- Hypertension:
Hypertension in uraemic patients is either due to high renin
secretion or salt and water retention. It occurs in about 80% of cases. In
uraemics, hypertension is characterised by resistance to drug treatment and
by tendency to develop malignant hypertension more than in other forms
of hypertension. Hypertension aggravates the renal disease which further
increases the blood pressure and a vicious circle is produced.


d- Uraemic pericarditis:
This occurs due to deposition of urea on the smooth inner surface
of the pericardial sac changing it into rough surface. Continuous friction
between the visceral and parietal pericardium during cardiac systole and
diastole results in dry pericarditis which manifests by pericardial pain and
pericardial rub on auscultation. Later, haemopericardium develops which
progresses to cause cardiac compression (tamponade). This manifests
clinically by a triad of:



  1. progressive systemic venous congestion with congested neck veins,
    congested liver, and anasarca.

  2. Progressive hypotension due to reduction of stroke volume as
    venous return is progressively decreasing.

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