[Basis of a therapeutic protocol of nephrotic syndrome with minimal glomerular lesions in adults (proceedings)].
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Biomedical subjects
Publications and source records attributed to A Meyrier.
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In 3 cases, total parathyroidectomy, with graft of fragments of one of the glands into the forearm gave rapid correction of the clinical and biological disorders associated with secondary hyperparathyroidism. The secretion of parathyroid hormone by the autograft was confirmed by radioimmunoassay on brachial vein samples. This technique appears to be more satisfactory than 7/8 parathyroidectomy, the postoperative course of which is not always free of complications, which involves a risk of necrosis of the gland fragment left in place and in which reoperation is difficult.
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Renal transplantation was performed in five adult patients with thrombotic microangiopathy, three of whom had had a bilateral nephrectomy prior to transplantation. The graft remained functional in three patients 72, 18, and 12 months after transplantation. One patient developed a thrombosis of the renal artery and one patient died from infection. There was no clinical or histological evidence of recurrence of thrombotic microangiopathy in the five patients after transplantation. Immunological investigations were performed in four of five patients before transplantation: C3 and C1q levels were low in two patients; serum C3-splitting activity and circulating immune complexes were present in all four patients and remained unchanged on haemodialysis and/or after bilateral nephrectomy. Complement abnormalities and immune complexes were not detected in the three patients with successful renal transplantation.
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In five patients with chronic renal failure, rapid correction by dialysis of hypertension and/or high blood urea levels provoked acute neurological disorders, followed by slowly reversible neuropsychiatric disturbances. Focal EEG alterations were noted in three patients with normal carotid angiograms. Our cases differed from those usually described as suffering from the dialysis disequilibrium syndrome because of their duration, the severity of mental disturbances, and the asymmetrical pattern of EEG abnormalities. We propose that the symptoms observed could be due to cerebral ischemia. This possibility emphasizes the importance of limiting the duration and efficiency of the first dialyses in patients with severe hypertension and high nitrogen retention, especially if high performance dialyzers are used.
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Two patients are reported in whom early and irreversible renal allograft rejection was associated with passage of necrotic papillary material in the urine. Evidence is presented for a causal relationship between rejection and medullary necrosis. Passage of a papilla is regarded as a definite indication for graft exploration.
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Three patients with chronic renal failure treated by haemodialysis developed acute asymmetrical sensory and motor neuropathies when ultrafiltration was induced to treat oedema. The neuropathies were characteristic of acute mononeuritis multiplex rather than uraemic polyneuritis, and we give our reasons for believing that they were not caused by toxic uraemic metabolites but by an ischaemic process due to vasoconstriction resulting from ultrafiltration.
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