Decreased platelet counts and decreased platelet serotonin in poststreptococcal nephritis.

Mean platelet survival time in patients with acute poststreptococcal glomerulonephritis (APSGN) is reduced to 50-60% of the control values, and glomerular deposits of platelet factor 4 are found in these patients. In order to investigate further systemic platelet changes of pathogenic, clinical or prognostic significance, we measured the platelet serotonin (5-HT) content and the blood platelet counts during the 1st week of the disease in 27 patients with APSGN. Platelet 5-HT was significantly reduced in patients with APSGN as compared with patients with impetigo without glomerular involvement (785 +/- 54 vs. 1,329 +/- 94 ng 5-HT/10(9) platelets; p < 0.001). Similarly, the mean blood platelet count was reduced to 247 +/- 16 x 10(3) as compared with 303 +/- 14 x 10(3) in the controls (p < 0.05). Thirteen (48%) of these patients had individual values of platelet 5-HT lower than the 95% confidence interval calculated in the control group. No significant correlation was observed between the concentration of 5-HT and either the severity of the disease judged by the amount of urinary protein excretion and the serum creatinine value or the presence of circulating immune complexes. Significant correction of the platelet 5-HT content (to 1,180 +/- 111 ng/10(9) platelets; p < 0.01) and of the platelet counts (to 309 +/- 21 x 10(3); p < 0.01) were observed in the longitudinal study at least 2 weeks later. Platelet activation, with secretion of granular content and increased consumption, may explain these findings. Additionally, the reduced mean age of the circulating platelets could contribute to their decreased 5-HT levels.(ABSTRACT TRUNCATED AT 250 WORDS)

A study on the antigenic nature of circulating immune complexes in hemolytic uremic syndrome: no evidence of platelet membrane glycoprotein antigens.

Circulating immune complexes (CIC) have been described in the hemolytic uremic syndrome (HUS) in children. They may represent an epiphenomenon or could be related to the platelet activation and endothelial damage observed in this disease. In an attempt to define this relationship, we investigated the CIC isolated in 17 patients with the classic form of HUS, by means of monoclonal antibodies against platelet surface glycoprotein Ib and IIb-IIIa complex. The negative results obtained do not support the possibility of platelet antigens being constituents of CIC and make an antibody-induced platelet activation in HUS very unlikely.

Detection of platelet-activating factor in plasma of patients with streptococcal nephritis.

The purpose of this study was to evaluate whether platelet-activating factor (PAF) is released in the plasma of patients with acute poststreptococcal glomerulonephritis, because previous studies have shown an involvement of platelets in the active phase of this disease. The results of this study indicate that PAF bioactive material is released in significant amounts in the plasma of 49 out of 50 patients with acute poststreptococcal glomerulonephritis. The observed release of PAF was not a direct consequence of the bacterial infection, because it was minimal or absent in patients with streptococcal infection without glomerular involvement. PAF bioactive material extracted and purified from the plasma of patients was shown to be chemically and biologically identical to the synthetic C-16 PAF (1-O-hexadecyl-2-acetyl-sn-glyceryl 3-phosphorylcholine).

Idiopathic membranous nephropathy, associated with HLA-DRw3 and not related to monocyte-phagocyte system Fc receptor dysfunction, in father and son.

Familial idiopathic membranous nephropathy, an immune-complex-associated glomerulopathy, has not been previously reported in father and son, despite its striking immunogenetic correlation, especially with HLA-DR3. As a dysfunction of the monocyte-phagocyte system (MPS), it has been observed linked to DR3 antigen, so we studied the MPS Fc receptor function in a father and his son with a histologically proven membranous nephropathy, associated with the haplotype A9-B35-DR3-DQw2. The Fc receptor function of the MPS was examined by measuring the clearance of IgG-sensitized, 51Cr-labeled erythrocytes and by measuring the ability of isolated monocytes to ingest autologous red blood cells coated with IgG anti-Rh (D) antibody. Immune clearance and in vitro phagocytosis was normal in both patients and not related to their levels of immune complexes (as measured by ELISA C1q and Conglutinin solid-phase binding assay). This report suggest that genetic factors may play an important role in the development of membranous nephropathy, and it seems not to be related to a dysfunction of MPS as measured by these tests.

Presence of circulating immune complexes in the classic form of hemolytic uremic syndrome: a constant finding.

In an attempt to further study the possible contribution of circulating immune complexes (CIC) in the pathogenesis of the classic form of hemolytic uremic syndrome, 9 patients were studied during the acute phase of the diseases. C1q solid-phase ELISA and conglutinin solid-phase ELISA, were used to measure the levels of immune complexes. All 9 were positive in one or both assays. No correlation was found between the levels of CIC and the clinical severity of the disease. The constant finding of positive CIC in these patients might represent an epiphenomenon, point out the postinfectious nature of this disease but also suggest a possible pathogenic role.