In a variety of renal disorders, including SLE and transplantation, in vivo platelet activation is present. This is in part a result of the nephrotic syndrome, but is also observed in patients with g.n. who are not nephrotic. As a result, intraplatelet concentrations of serotonin and other amines are depleted in patients with active nephritis. The functional capacity of such amine-depleted platelets has been little studied; Pareti et al (1980) reported defective aggregation to ADP, adrenaline and collagen in such “acquired storage pool deficiencies”. We studied aggregation thresholds to ADP, collagen and AA in 25 patients with SLE nephritis, none of whom had a nephrotic syndrome or reduced renal function. In these patients platelet activation is due principally to circulating factors. Sixteen transplant recipients were also studied. In them, activation is principally within the renal microvasculature of the allograft. We also measured intraplatelet serotonin concentrations, which were low or zero in the great majority of patients in both groups. Bleeding times were normal in all, as were platelet aggregation thresholds to ADP and collagen. AA thresholds, however, were markedly depressed (<0.32 mmol) in all transplant recipients and most patients with SLE. This specific hyperaggregability may be responsible for both persistence of disease and the thrombotic tendency observed in some patients, including those with circulating anticoagulant.
Bone histology in patients with nephrotic syndrome and normal renal function