Browsing by Author "OLAVARRIA, F"

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    A STUDY ON THE ANTIGENIC NATURE OF CIRCULATING IMMUNE-COMPLEXES IN HEMOLYTIC-UREMIC SYNDROME - NO EVIDENCE OF PLATELET MEMBRANE GLYCOPROTEIN ANTIGENS
    (KARGER, 1994) OLAVARRIA, F; PEREIRA, J; MEZZANO, S; KUNICK, M; CASTILLO, A
    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.
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    DECREASE IN MEAN PLATELET SURVIVAL-TIME IN ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
    (1990) MEZZANO, S; LOPEZ, MI; OLAVARRIA, F; ARDILES, L; MEZZANO, D
    In an attempt to study further the possible participation of platelets in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), we studied the platelet survival time, as an index of platelet activation, in 22 patients with APSGN. Mean platelet survival time was computed from the disappearance of radioactivity from blood, sampled serially after injection of autologous 51Cr-labelled platelets. Clq solid phase ELISA and conglutinin (K) solid phase ELISA were used to measured the serum level of immune complexes. The platelet survival time in APSGN patients was 113 .+-. 10 h vs 197 .+-. 10 h in the control group (p < 0.001); 68% of the patients had a shortened platelet survival, lower than 95% confidence limit. There was a significant increase in the platelet survival in the six patients that were studied after recovery from acute nephritic syndrome. There was no significant association between the mean platelet time survival and CICs (circulating immune complexes). Similarly, no significant correlation was found between the mean platelet lifespan and the severity of the glomerular disease, as assessed by the serum creatinine level and the proteinuria. These results support evidence of platelet activation and consumption in APSGN and we suggest that this activation occurs in the glomeruli capillary wall, due to platelet-vascular wall interaction.
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    DECREASED PLATELET COUNTS AND DECREASED PLATELET SEROTONIN IN POSTSTREPTOCOCCAL NEPHRITIS
    (KARGER, 1995) MEZZANO, S; KUNICK, M; OLAVARRIA, F; ARDILES, L; ARANDA, E; MEZZANO, D
    Mean platelet survival time in patients with acute poststreptococcal glomerulo-nephritis (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 Ist 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+/-16x10(3) as compared with 303+/-14x10(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+/-21x10(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. The reduced platelet counts are not of clinical significance, but serial measurements of platelet 5-HT may be useful in predicting active glomerular inflammation.
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    GLOMERULAR LOCALIZATION OF PLATELET FACTOR-IV IN STREPTOCOCCAL NEPHRITIS
    (1992) MEZZANO, S; BURGOS, ME; ARDILES, L; OLAVARRIA, F; CONCHA, M; CAORSI, I; ARANDA, E; MEZZANO, D
    Since platelet factor 4 (PF4), a cationic (pI 7.6) platelet secretory protein, binds avidly to glomerular polyanions both in vitro and in vivo, and is implicated in neutrophil chemotaxis, we studied by indirect immunofluorescence microscopy the presence of PF4 deposits in glomeruli of patients with poststreptococcal nephritis (APSGN).
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    KALLIKREIN EXCRETION - RELATIONSHIP WITH MATURATION AND RENAL-FUNCTION IN HUMAN NEONATES AT DIFFERENT GESTATIONAL AGES
    (1987) VIO, CP; OLAVARRIA, F; KRAUSE, S; HERRMANN, F; GROB, K
    Kallikrein excretion and renal function were studied on 37 one-day-old newborn infants (14 fullterm and 23 preterm infants). Preterm infants excreted less kallikrein (p < 0.001), had lower creatinine clearance (p < 0.02) and urinary osmolality (p < 0.01). They had higher values on urinary volume (p < 0.001), FENa (p < 0.001), FEk (p < 0.02), and free water clearance (p < 0.01) than fullterm infants. The excretion of kallikrein correlated directly with gestational age (p < 0.01) and body weight (p < 0.01). No correlations were found with FENa, urinary volume, FEk or free water clearance. The values of kallikrein excretion were very low when compared with a young adult population. As kallikrein is synthesized in the distal nephron we advance as an hypothesis that the low levels of kallikrein excretion observed in newborns could be a reflection of immature distal tubular mass, and to the relative unresponsiveness of the distal nephron to hormones known to stimulate renal kallikrein such as aldosterone and antidiuretic hormone.