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Biomedical subjects

N R Sridhar

Publications and source records attributed to N R Sridhar.

6 recordsLinked to original sources

Urea kinetics with dialyzer reuse--a prospective study.

UNLABELLED: We performed a prospective study to examine the impact of dialyzer reuse on KT/V under rigidly standardized conditions on 3 membrane types. Heparin dosage was standardized with ACT during an eight week run-in period and remained unchanged through the study. Post dialysis BUN and weight were obtained at five minutes after exactly 80 +/- 0.5 l of blood were processed through the dialyzer. Dialyzers were reused after automated glutaraldehyde processing and after ensuring >80% open fiber bundles. Each membrane type was utilized 3 times on a set of 3 patients; each individual dialyzer was reused 8 times. KT/V was done on the 1st, 2nd, 4th and 8th uses of each dialyzer (36 measurements) starting mid week; BUN measurements were grouped. The KT/V (mean +/- SD) for the 1st, 2nd, 4th, and 8th uses of the cellulose acetate dialyzer were 1.3 +/- 0.2, 1.3 +/- 0.3, 1.3 +/- 0.2, 1.3 +/- 0.2 respectively; the corresponding values of the cuprophane dialyzer were 1.4 +/- 0.3, 1.4 +/- 0.3, 1.3 +/- 0.4, 1.3 +/- 0.3 respectively; and those of the polysulfone dialyzer 1.7 +/- 0.3, 1.6 +/- 0.2, 1.6 +/- 0.2 respectively. By a 3 way ANOVA there were no significant differences between the 1st and subsequent uses of any of the dialyzers tested. CONCLUSIONS: Reuse of dialyzers up to 8 times does not result in a loss of urea clearance. We believe this model is useful for further studies on reuse and quality assurance.

Aged↗

Immunologic aspects of renal disease.

The kidney can become involved in immune-mediated diseases through 3 mechanisms. It can be the primary target of antibody-mediated injury. Good-pasture syndrome, with antibodies directed at the glomerular basement membrane, is an example of this type. The kidney can be injured by immune complexes that are trapped in the kidney and cause local inflammation. Examples include systemic lupus erythematosus and IgA nephropathies. Finally, the kidney can be injured by immune responses initiated in other organs. In Wegener granulomatosis, inflammation begins in the airway but results in glomerulonephritis. Currently available therapies lack efficacy and specificity. New therapies based on pathophysiology are being developed in animal models.

Anti-Glomerular Basement Membrane Disease↗

Post-OKT3 induction therapy CD complex response predicts renal allograft rejection.

CD complex response to cessation of induction with OKT3 may be predictive of rejection. Twenty-seven patients receiving renal allografts and OKT3 induction immunosuppression were retrospectively analyzed for CD complex repopulation and allograft rejection. Flow cytometric monitoring was utilized in all patients. Responder status groups were identified based on CD complex repopulation, with fast responders demonstrating CD complex repopulation above the determined cohort mean. Slow responders had repopulation below this mean. Student's t test yielded P<0.01 (CD2), P<0.02 (CD3), and P<0.01 (CD8). Nonresponder patients were identified with repopulation below the mean, but flat compared with depletion. All nine fast responders lost their graft or were treated for rejection. No slow responder experienced graft loss or rejection episodes. One nonresponder was treated for rejection. CD complex activity following OKT3 cessation correlates with future rejection. Identification of responder status provides insight into propensity to reject, allowing individual tailoring of immunosuppression to patient response.

Antibodies, Monoclonal↗

Evaluation of flowcytometric crossmatching in renal allograft recipients.

Forty-four cadaver renal allograft recipients who had flowcytometric cross-match (FCXM) testing and sequential quadruple immunosuppression were studied with respect to the number of rejection episodes and the functional viability of the graft in the first year after transplantation. Fourteen of these patients had antibodies to donor T cells by FCXM. All were negative by conventional crossmatch. Multiple-regression analysis with HLA mismatches, panel-reactive antibody (PRA) percentage, flowcytometric channel shifts and transplant number as independent variables revealed that transplant number and high PRA (> 50%) impacted (p < 0.05) on serum creatinine at 1 month and 1 year, and graft survival at 1 year. In first transplants, a positive FCXM had no impact on 1-year graft survival rates; however, in retransplants, a positive FCXM and/or high PRA had a significant negative impact on 1-year graft survival. This study indicates that the FCXM should be utilized for retransplant patients, and in patients with a high PRA, in an attempt to improve graft survival for these high-risk recipients.

Antilymphocyte Serum↗

Flow cytometric evaluation of cytotoxic peripheral blood lymphocytes in acute renal graft rejection.

The presence of the S6F1+ epitope on the surface of CD8+ lymphocytes is believed to be uniquely representative of cytotoxic subpopulations. A preliminary study was conducted to evaluate the CD8+ S6F1+ peripheral lymphocytes by flow cytometry in patients undergoing renal allograft biopsy for allograft dysfunction. Lymphocytes, obtained at the time of biopsy, were analyzed by flow cytometry with CD8-FITC/S6F1-RD1 as the test monoclonal antibody and MsIgG-RD1/MsIgG-FITC as internal control. A 100% increase in S6F1+ cells over internal control was considered to be positive result. The results were correlated with the histopathologic findings in 14 instances of allograft dysfunction occurring 26.5 +/- 11.6 days posttransplantation. The histopathologic diagnosis was acute cellular rejection in eight cases, acute tubular necrosis in four, and cyclosporine nephrotoxicity in two. Flow cytometric detection of an increase in S6F1+ cells yielded a sensitivity of 87.5% and a specificity of 83.3% for the diagnosis of acute rejection. It would appear that the use of a monoclonal antibody to detect increases in the number of CD8+ S6F1+ peripheral lymphocytes is a valuable test for the detection of acute allograft rejection in the initial period after transplantation.

Acute Disease↗

Disseminated histoplasmosis in a renal transplant patient: a cause of renal failure several years following transplantation.

A 49-year-old man developed disseminated histoplasmosis 6 1/2 years after transplantation. The organism was initially present in the urine and in a tongue lesion. Treatment with itraconazole was instituted. However, there was further dissemination of the disease and worsening of renal function. Allograft biopsy showed extensive involvement with the organism. Amphotericin B was started, resulting in a rapid resolution of the disease. However, renal function deteriorated, leading to permanent hemodialysis.

Biopsy↗