An open letter to my mother's nephrologist.
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Biomedical subjects
Publications and source records attributed to V Mazzarella.
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We have studied complement activity, total leukocyte counts, PO2 and acid-base balance during a single hemodialysis with cuprophan membranes in a patient with hereditary angioedema and C3NeF-positive chronic membranoproliferative glomerulonephritis. Before, during and after the dialytic procedure plasma complement activity (total hemolytic complement, classical and alternative pathway activities) was not detectable and no C3-conversion occurred, while profound leukopenia (from 8,500 to 1,800 leukocytes/microliter) and hypoxemia (from 101.8 to 86 mmHg PO2) were found within 20 min from the initiation of hemodialysis. Similar results were obtained by studying the same parameters during two additional hemodialytic procedures. In vitro experiments showed that the patient's C3 could not be converted, either by cuprophan or zymosan, a specific and potent complement activator, even under optimal experimental conditions. Our data demonstrate that complement activation is not the only possible mechanism responsible for early leukopenia (as well as hypoxemia) during dialysis with cuprophan membranes.
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BACKGROUND: The management of patients suffering from Amanita Phalloides poisoning (APP) may be very challenging. Furthermore, the treatment often includes depurative techniques and Orthotopic Liver Transplantation (OLTx) must be started timely to be effective. We report our experience in severe APP treatment. PATIENTS AND METHODS: We retrospectively evaluated five patients suffering from APP and hospitalized within our Intensive Care Unit, assessing different kinds of treatment: two different dialytic techniques, namely Continuous Renal Replacement Therapy (CRRT), and Charcoal Plasmaperfusion (CRRT+CPP), and OLTx. RESULTS: Two patients treated with CRRT+CPP, one patient treated with CRRT only and the patient treated by OLTx recovered. One patient, undergoing CRRT only, died after 14 days of treatment. During the CRRT+CPP treatment no relevant complication occurred. The transplanted patient received dialytic treatment for 7 days after transplantation in order to support renal function impairment and to enhance liver function recovery. CONCLUSIONS: Clinical management of patients suffering from APP requires multi-disciplinary intervention; therefore it is recommended to treat these patients in an Intensive Care Unit with specialized nephrological and toxicological consultancy, in collaboration with an organ transplantation team. In the near future we wish to associate dialytic treatment with a bioartificial liver device, which could bridge the time gap to liver transplantation.
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In evaluating biocompatibility, haematological changes induced by ACCM in vivo and in vitro were studied. Twenty minutes after the start of haemoperfusion a significant fall in white blood cell number was found. After 60 minutes the leucopenia still occurred. In a previous work we suggested that complement activation is at least one of the possible mechanisms responsible for these phenomena. Moreover, our data showed a significant decrease in platelet number after 60 minutes of haemoperfusion. During the in vitro study, we found, using citrated blood, a significant correlation between aggregation response to ADP and collagen, either at different ACCM doses or at various periods of incubation. Our results suggest that the fall in platelets is due to platelet aggregation. The haemocoagulation study may have clinical importance in high-risk patients when haemoperfusion is required.
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