Spousal renal donor transplants in India.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S C Dash.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Seroconversion rate following hepatitis B vaccination in patients of chronic renal failure (CRF) has been in the range of 10%-82% in various studies. Different approaches have been tried to improve seroconversion rate. We studied two schedule of hepatitis B vaccination, 0,1,2 (Group A) and 0,1,2,6 (Group B) in mild (creatinine 1.5 to 3.0 mg%), moderate (creatinine 3.0 to 6.0 mg%) and severe CRF (creatinine > 6.0 mg%). Between Oct. 93 to Oct. 95, 117 patients with CRF who were negative for HBsAg and anti-HBs were included in the study. Forty micrograms of recombinant vaccine "ENGIREX" (20 micrograms in each deltoid region) was given in both the groups. Number of cases of mild, moderate and severe CRF were 18, 15 and 42 in group A and 12, 13 and 17 in group B, respectively. One month after the last dose of vaccination, anti-HBs was measured using ELISA kit (Abbot Laboratories, India). Anti-HBs titres of > 10 IU/L were taken as criteria of positive seroconversion. In group A seroconversion rate was 87.5%, 66.6% and 35.7% in mild, moderate and severe CRF respectively while same results in group B were 100%, 77% and 36.36%, respectively. We conclude that patients of chronic renal failure should be vaccinated at very early stage of the disease using 40 micrograms of vaccine. Four doses schedule of 0,1,2,6 give better results than three doses schedule in early CRF.
Explore the source record for details and available documents.
BACKGROUND: Hepatitis C viral (HCV) infection is a major cause of hepatitis during haemodialysis after the control of hepatitis B following vaccination and isolation measures. Magnitude of this problem in India has not been studied and there are only few reports of HCV infection during haemodialysis from this country. This study was conducted to find out the incidence of HCV infection in patients of end stage renal disease (ESRD) and haemodialysis (HD), along with its source and to find out the clinical course of HCV positive patients. METHODS: HCV infection was diagnosed by detecting anti-HCV antibodies using the IIIrd generation ELISA kits. RESULTS: Of the 208 consecutive patients of ESRD accepted for the study, HCV prevalence was 4.3% at the time of start of study. Of the all risk factors studied, past history of jaundice and number of blood transfusion (BT) were significantly higher in HCV positive patients as compared to HCV negative patients. Of the 208 patients, 20 (9.6%) died, 119 (57.2%) lost follow-up and 69 (33.2%) got renal transplant (RT). Incidence of HCV in patients who died, lost follow-up and got RT was 10%, 3.4% and 36.2% while prevalence was 15%, 4.2% and 42% respectively. In these groups, duration of HD was 8.4, 5.2 and 22.7 weeks respectively while the mean blood transfusion (BT) was 1.2, 0.8 and 5.4 in number respectively. Mean age of patients in these groups was 37.85, 37.9 and 32.53 years and percentage of males were 65%, 75% and 89.9% respectively. At no stage of follow-up, patients with HCV infection had any symptoms or high serum bilirubin. Major abnormality was fluctuating ALT in these patients. HCV in 512 units of blood transfusions given to these patients and healthy volunteers was 1.17% and 0.66% respectively. Marked increase of HCV infection while patients were on HD is likely to be due to nosocomial spread. Blood transfusion was not found to be important source of HCV infection. Longer the patients remain on HD; more will be chance of HCV infection. CONCLUSION: It is concluded that HCV is a major cause of concern in haemodialysis patients in India and the predominant source of spread of infection is nosocomial. In our set-up, blood transfusion is not an important source of infection. Majority of these patients remains asymptomatic at least for the short terms follow-up.
BACKGROUND: Prolonged dialysis is associated with acquired cystic kidney disease (ACKD) and also higher incidence of renal cell carcinoma. Relationship among dialysis, tubular cell proliferation, development of cystic change and neoplastic transformation is not clearly known. Whether dialysis causes additional stress on tubular cells is also conjectural. Study of heat shock protein (HSP) expression which are rapidly synthesized in cells in response to a variety of stresses may be helpful in this regard. METHODS: To evaluate dialysis induced early changes in end stage renal disease (ESRD), kidneys from eight adult autopsied patients were examined (group I) who were on weekly maintenance haemodialysis for 3-12 months. The heat shock protein (HSP 72/73) expression of tubular epithelial cells and their proliferating cell nuclear antigen (PCNA) labelling index (LI) were studied by immunohistochemistry using monoclonal antibodies. For comparison similar study was carried out in 10 cases of ESRD (Group II) of similar age and sex distribution who were not dialysed. The atrophic tubules were subtyped morphologically into (1) classic, (2) thyroid, (3) endocrine and (4) super tubules. RESULTS: In the dialysed group (I) the percentage of hyperplastic super tubules (10.6 +/- 4.1%) was significantly higher than in the non-dialysed group (II) (5.2 +/- 1.3%) with a higher PCNA LI (6.8 +/- 2.04%) (group II 4.9 +/- 1.9%) (P < 0.01 to < 0.001). Though grossly not detected, but microscopic cysts and microadenoma like areas were seen in all the cases in group I with a mean diameter of 522.66 +/- 315.25 microns and 494.85 +/- 262.46 microns respectively. They were seen in one case of group II. PCNA LI of the cells in microadenoma (7.2 +/- 3.1%) and microcysts (6.6 +/- 2.6%) were similar to that of super tubules in group I. Quantitation of HSP expression by image analysis (optical density 2.309 +/- 0.155) showed a positive correlation (r = 0.7555) (P < 0.001) with PCNA LI in super tubules indicating a higher induction in the dialysed group. CONCLUSIONS: This study suggests that haemodialysis may cause injury to tubular cells and aggravate stress on an already compromised situation of ESRD leading to increased cell proliferation and more hyperplastic supertubule formation which may be the forerunner of cyst formation as well as neoplastic transformation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a prospective study of 200 non-cirrhotic portal fibrosis (NCPF) patients, 7% had mild proteinuria and their renal biopsies showed mild mesangial proliferative glomerulonephritis (mes-PGN). The remaining 93% biopsies were normal. However, following the insertion of a spleno-renal shunt (SRS) for portal hypertension 32% of these patients developed nephrotic syndrome in five years. Renal histology revealed mesangiocapillary glomerulonephritis (MCGN) (18.5%), mes-PGN (9%), minimal change nephropathy (3%), and chronic sclerosing GN (1.5%). Immunofluorescence showed granular deposition of IgA and C3. IgA2 was the predominant form of Ig in the glomerular deposits, indicating that IgA in the immune complexes was derived from the gastrointestinal tract. Electron microscopy revealed electron dense deposits in the mesangium. In contrast to the NCPF patients who underwent a SRS for portal hypertension, the 200 patients in our study who underwent spleno-renal shunting because of extra hepatic portal obstruction did not have renal disease, nor did they develop renal disease during the five-year post-operative follow-up. Fifty percent of the glomerulonephritis (GN) in the NCPF group progressed to renal failure in five years; 46.6% continued to have proteinuria. Low serum complement, C3 (40%) and circulating immune complexes (14.8%) were detected in the glomerulonephritis group. Our study shows that: (i) there is a high rate of the occurrence of GN following SRS in NCPF patients, but not in those with normal livers; (ii) the type of GN is primarily IgA nephropathy; and (iii) the GN could be the result of defective hepatic reticuloendothelial function in the NCPF group that is worsened by the shunting procedure.
We present our experience on the comparison of three different modes of steroid therapy, oral prednisolone (OP), intravenous dexamethasone (IVDX) and intravenous methylprednisolone (IVMP) in the treatment of acute rejection (AR) in renal allograft recipients. Between January 1980 and January 1992, 206 patients underwent live related renal transplantation. Before 1990, all received prednisolone (PRED) and azathioprine (AZA) only. After 1990, patients were given PRED, AZA and cyclosporine (CsA). After 1 year, CsA was stopped and patients were converted to a two-drug regimen only. Of the 206 patients, 180 (87.4%) were male and mean age was 30.3+/-8.7 years (range 14-63). During the mean follow-up of 43.5 months, 178 episodes of AR were seen in 121 patients. Each episode was considered as a separate entrant in the study. Conventional immunosuppression was given in 151 episodes and 27 episodes were on triple-drug therapy. Diagnosis of AR was made by clinical, sonography, nuclear scan with or without graft biopsy evidence. Of the 178 AR, 110 (61.8%) were within 3 months, 36 (20.2%) were between 3 months and 1 year and 32 (18%) were after 1 year. OP was given in 11 cases while IVDX and IVMP were given in 48 and 119 cases respectively. Overall, 154 (86%) showed either a complete or partial response to antirejection therapy. Response to therapy was 91, 90 and 85% in OP, IVDX and IVMP groups respectively. There was no statistical difference in response rate in different groups. There was also no difference in side effects in three different groups. Our data suggest that it is the high dose of steroid rather than mode of therapy which is responsible for therapeutic benefit in treatment of AR.
Differentiation between glomerular and non-glomerular haematuria by observation of the changes in red cell morphology using phase-contrast microscopy is a well established technique. However, the method is not widely accepted in clinical practice because of controversy regarding the minimum percentage of dysmorphic red cells required to diagnose glomerular aetiology, as well as the need for specialized microscopes. Recently, a glomerular-specific morphological alteration of red cells has been described, which has the form of a doughnut shape with one or more blebs and which is termed the "G1" cell. In the present double-blind prospective study 250 urine samples were examined without any knowledge of diagnosis. Haematuria was detected in 122 cases. The type of haematuria was characterized by counting dysmorphic cells and G1 cells separately, in each case using a phase-contrast microscope as well as an ordinary bright-field microscope with and without staining of urinary sediments. The results were later correlated with the confirmed diagnosis. The study showed that the G1 cell is more specific than the dysmorphic cell for the diagnosis of glomerular haematuria. Evaluation of both dysmorphic red cells and G1 cells can be done using bright-field microscopy with 100% specificity and sensitivities of 82 and 100%, respectively. It has been concluded that the ordinary bright-field microscope can be used for the diagnosis of glomerular haematuria with an efficiency similar to that of a phase-contrast microscope.
Explore the source record for details and available documents.
The incidence of post-transplant diabetes mellitus (PTDM) was evaluated in 250 patients who underwent live-related renal transplantation at our hospital between 1978 and 1992. Twelve (4.8%) patients developed PTDM requiring drug therapy. PTDM occurred in 4 of 197 (2%) patients on conventional prednisolone-azathioprine immunosuppression as compared to 8 of 53 (15.1%) patients receiving cyclosporine in addition (triple-therapy). Three patients (25%) developed PTDM during or immediately following anti-rejection therapy with intravenous methylprednisolone. Eight patients (66.6%) developed PTDM within six months of transplantation. Majority of our patients (66.6%) could be managed successfully with oral hypoglycemic agents. Two patients (16.6%) showed spontaneous resolution of hyperglycemia within six months of onset of PTDM. Eleven patients (91.6%) were symptomatic for their hyperglycemia with two patients presenting as 'pseudorejection' and one with diabetic ketoacidosis. Females were more predisposed to develop PTDM in our study (10% vs. 4.1%). HLA-B15 and DR 3 were the commonest phenotypes in our PTDM patients. No other known predisposing or triggering factors associated with PTDM were found in our patients. The current study suggests, that addition of cyclosporine to the conventional immunosuppression in live-related renal allograft recipients has contributed to an increased incidence of post-transplant diabetes mellitus. Close and regular blood sugar monitoring is thus recommended in post-transplant patients especially those on triple drug immunosuppression.
Results of 34 recipients of living related renal allografts initially treated with cyclosporine, azathioprine, and prednisolone and later electively converted to AZA and PRED are presented. Thirteen (group A), 14 (group B), and 7 (group C) patients were converted before 9 months, between 9 and 12 months, and after 12 months, respectively. Thirty-four patients who were on AZA and PRED and had never received CsA served as controls. Of the 34 patients, 33 were HLA haploidentical with their donors and 1 was HLA identical. All patients received a mean 8.62 +/- 7.39 third-party blood transfusions. In the control group, 29 patients received haploidentical grafts. The number of blood transfusions given to this group was 7.09 +/- 9.13. Of the 34 patients receiving triple-drug therapy, 9 (26%) had acute rejection within 3 months after conversion, as compared with 5 (14.7%) in the control group (P > 0.05). Although 1 case had acute rejection before conversion, all recipients had stable graft function at the time of conversion. Of these 9 recipients, 7 had conversion over 4-7 weeks, while 2 had rapid conversion. Following treatment of the rejection episodes, 4 patients in the study group responded to therapy, as compared with 3 cases in the control group (P > 0.05). After a mean follow-up of 18.62 +/- 10.31 months (range 3-41 months) following conversion, 4 patients were normal, 4 had chronic rejection (mean serum creatinine = 3.0 mg/100 ml), and 1 was back on regular dialysis. Eventually, of the 34 patients who were converted from triple-drug to double-drug therapy, 25 were normal, 5 had stable chronic rejection, 2 were back on regular dialysis, 1 was retransplanted, and 1 died due to failed graft. At the end of follow-up, graft survival in the study group was 88.2%, as compared with 85.5% in controls (P > 0.05). We conclude that conversion from triple-drug to double-drug therapy is not without risk, even in living related primary renal transplantation. Degree of HLA matching, number of pretransplant blood transfusions, and rejection before conversion did not have any significant effect on rejections following conversion, and the graft loss following conversion is unpredictable.
Explore the source record for details and available documents.
Explore the source record for details and available documents.