Nine patients undergoing regular dialytic treatment (RDT) for more than 60 months (mean 125 +/- 33 months) showed clinical and radiological evidence of non-infective destructive spondyloarthropathy (DSA). The cervical spine was the skeletal segment most affected (100% of cases). Three patients were found also to be suffering from discal and bone alterations of the dorsal column, and in two other patients the vertebral bodies L4-L5 were changed. Typical radiological pictures showed a narrowing of intervertebral spaces with the destruction or sclerosis of adjacent subchondral bones, erosions of vertebral body plates and cavitations. CT studies of the altered spines confirmed discal lesions and osteolytic areas with bone condensation at each level. Ligamentous lesions resulting in severe disorders of spinal statics were discovered during autopsy of three patients. Histological study of disc and peridiscal ligaments indicated the presence of large amyloid deposits containing beta-2-microglobulin (B2-m). It is possible that the minor biocompatibility of the cuprophan membrane of dialyzers is the most significant factor responsible for the hyperproduction of B2-m and thus of the osteo-articular deposition of a new type of amyloidosis.
The clinical usefulness of serial assays of urinary N-acetyl-β-D-glucosaminidase (NAG), γ-glutamyltransferase (GGT) and β2-microglobulin (β2M) were tested to evaluate and follow up the nephrotoxicity resulting from the prolonged administration of ciclosporin (CS). Three groups of patients were studied for 18 months: group A: functioning renal transplant patients (n = 13) on maintenance therapy from 12-31 months with CS and prednisone; group B: functioning renal transplant patients (n = ll) treated with prednisone and azathioprine; group C: patients (n = 10) affected by autoimmune steroid-unsensitive uveitis, free from previous renal disorder and treated with CS (for 8-16 months) at progressively decreasing doses. In groups A and B, the urinary enzymes and β2M underwent overlapping increases, so that these parameters cannot be considered reliable indices of CS-induced nephrotoxicity. This is due to the fact that transplanted kidneys are already altered by concomitant or preexisting affections, or by persistent immunologic injury. Conversely, in patients with uveitis, the serial assays of such urinary parameters prove to be quite reliable to evidence clinically yet unrecognizable kidney involvement due to prolonged CS administration. High enzymuria has been shown to be an earlier marker of nephrotoxicity only in nephropathy-free patients; on the other hand, the regression of elevated β2Muria into normal ranges indicates complete tubule cell recovery.
Both the plasma determinations of erythropoietin (EPO) and transferrin receptor (TfR) would provide a good characterization of anemia especially when mixed erythron disorders underlie, such as in renal failure. Immunologic assays of EPO and TfR, as well as standard hematologic determinations (hematocrit, reticulocyte count, serum iron, transferrin, ferritin) were performed in patients with chronic renal failure (CRF), in regular dialysis treatment (RDT) and in transplanted (TX) patients. In nonanemic TX patients both EPO and TfR ranged normally, whereas in anemic TX ones (Hct < 40%) both values were increased suggesting the physiologic response both of the kidney and of the erythron to decreased red cell mass. In transitory posttransplant erythrocytosis the increased values of TfR, with normal EPO values, would hypothesize a defective feedback to EPO release. Both EPO and TfR values were found increased in TX patients with adult polycystic kidney disease with persistent erythrocytosis (Hct > 50%), thus confirming previous observations. In CRF and RDT patients, all anemic, both EPO and TfR were normal, even though significantly low with respect to the degree of anemia. In RDT seriously anemic patients, the administration of recombinant human EPO induced different patterns of bone marrow response. We conclude that the determination of TfR would provide further information on renal anemia since the receptor increase mostly preceded the rise of Hct, evidencing those patients who will not have an effective bone marrow response to the therapy.
The administration of calcium channel antagonists to renal-risk patients during surgery and immediately before and after it has failed to prevent the onset of postoperative ARF. Nevertheless this procedure has been shown to somehow reduce surgery-mediated lesions of the tubule cells, as demonstrated by the finding of elevated urinary enzymes only in the untreated group.
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