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T H Mathew

Publications and source records attributed to T H Mathew.

At least 37 records · Page 2Linked to original sources
PubMed1994

Recurrent mesangial IgA nephritis following renal transplantation.

Recurrence of mesangial IgA deposits in renal allografts of patients whose original disease was primary IgA nephropathy (IgAN) has been studied. Forty-six patients with primary IgAN received 51 renal allografts and have been followed for 3-183 months. A prospective study of 11 patients (11 biopsies) and a retrospective analysis of 17 patients (16 biopsies; 2 nephrectomy specimens) have been combined. Seventeen of the 29 allografts had recurrent mesangial IgA deposits and of these three patients have negative urinalysis, normal glomeruli by light microscopy, and stable renal function; six patients have microhaematuria, mesangial proliferative nephritis, but at present stable renal function; and five have mesangial proliferative glomerulonephritis with microhaematuria, heavy proteinuria, hypertension, and progressive allograft failure secondary to IgA disease alone, and one of these is now back on dialysis. Three other grafts with recurrent deposits are failing because of transplant glomerulopathy or rejection. The only predictor identified for recurrence of mesangial IgA deposits was length of time post-transplantation, with allograft tissue being studied at 45.9 +/- 10.0 versus 15.3 +/- 4.8 months (P = 0.008) post-transplantation in patients with and without recurrent deposits respectively. Cyclosporin A did not prevent recurrence. By virtue of a longer follow-up of patients post-transplantation than all other reported series, these results suggest that with increasing time post-transplantation recurrence of mesangial IgA disease will become increasingly important as a cause of progressive allograft dysfunction and failure unless effective treatment is found for the primary disease.

Complement C3↗
PubMed1993

Diltiazem in renal allograft recipients receiving cyclosporine.

Of 113 cyclosporine-treated primary renal allograft recipients, 60 were randomized to receive standard therapy without diltiazem (ND) and 53 received standard therapy plus diltiazem (D). There was no difference in CsA blood levels between ND and D at all intervals between 3 and 24 months follow-up, yet the D group required 35% less CsA than the ND group (measured at 12 months). At all intervals to 24 months there was no difference in blood pressure, renal function (as measured by serum creatinine), or in the number of grafts lost between the 2 groups (ND, 4 lost; D, 3 lost). There was no significant difference in the total number of rejection episodes in the 2 groups (ND, 89 episodes; D, 71 episodes). However, the severity of rejection episodes was greater in the ND group as evidenced by a significant difference in the usage of OKT3 (ND, 17 courses; D, 8 courses of OKT3, P < 0.05). Of the biopsy-proven episodes of rejection, there were more episodes of vascular rejection in the ND group (ND, 14 episodes; D, 3 episodes, P = 0.005). The incidence of primary nonfunction was less in the D group (ND, 16 patients; D, 5 patients, P = 0.05). It was concluded that the use of diltiazem was associated with a markedly reduced requirement for CsA without any adverse effect on graft function or graft outcome. Diltiazem with CsA was associated with fewer episodes of primary nonfunction and less-severe rejection episodes and in particular fewer episodes of vascular rejection.

Adult↗
PubMed1992

Drug-induced renal disease.

OBJECTIVE: To review drug-induced renal disease with emphasis on current issues and practical problems with commonly used agents. DATA SOURCES: English language literature search using MEDLINE, Index Medicus, textbook articles and relevant reviews. STUDY SELECTION: Drugs in common use were reviewed in detail. Uncommonly used drugs or those with only a few reports of nephrotoxicity were excluded from this review. DATA SYNTHESIS: The clinical patterns of nephrotoxicity include an episode of acute deterioration of renal function, chronic renal failure and proteinuria which may be severe enough to cause the nephrotic syndrome. Diagnosis is made by clinical suspicion, distinctive clinical patterns and usually improvement in renal function on drug withdrawal. CONCLUSION: A high index of suspicion is necessary to detect drug-induced renal disease particularly with increasing availability of over-the-counter drugs. Drugs should always be suspected of causing renal disease where no alternative cause is obvious. When any doubt exists the agent in question should be withdrawn.

Acetaminophen↗
PubMed1989

The effect of withdrawal of phenacetin-containing analgesics on the incidence of kidney and urothelial cancer and renal failure.

Incidence data for cancers of the kidney and urinary tract (1973-83) and for end stage renal failure (ESRF) due to analgesic nephropathy (1973-86) were examined by loglinear regression to determine the effect of the withdrawal of phenacetin from analgesic preparations in New South Wales and the Australian Capital Territory. Allowing for the altered age and sex structure of the population, the incidence rate between 1973-83 for ESRF due to analgesic nephropathy, in persons aged between 5 and 54 years, decreased by 4.2% per year while that for ESRF excluding patients with analgesic nephropathy or diabetes increased annually by 1.3%. The incidence rates in persons over 14 years of age for cancer of the renal parenchyma (3.4% per year), renal pelvis (5.5%) and bladder (2.1%) increased significantly more than that for cancer at all sites (1.2%). Thus the decrease in ESRF due to analgesic nephropathy had not, by 1983, been paralleled by a decrease in renal parenchymal or urothelial cancer.

Analgesics↗
PubMed1988

Recurrence of disease following renal transplantation.

The diagnosis of recurrent renal disease after transplantation is dependent on an accurate and complete diagnosis of the initial cause of renal failure and a similar determination of the cause of graft failure. To be classified as recurrent, the disease in the renal graft must be identical to that seen in the native kidneys. Recurrence of disease accounts for less than 2% of all graft failures, but the overall incidence of recurrent disease is probably 5 to 10 times more common. The most frequent cause of recurrent disease is glomerulonephritis, which was first recognized to recur soon after renal transplantation was introduced. It was then recognized that a variety of metabolic disorders would recur, but it has taken 25 years of experience for a clear picture to emerge of recurrence in most conditions. No initial cause of renal failure poses a contraindication to at least one attempt at transplantation, although with Fabry's disease and oxalosis, a special assessment of the risks for the individual recipient is warranted. In some patients, experience has shown the need for a delay in the commitment to transplantation (eg, in those with anti-glomerular basement membrane [GBM] antibody glomerulonephritis or Henoch Schonlein purpura), the need for the choice of a particular immunosuppressive regimen (eg, in hemolytic uremic syndrome [HUS]), the need for avoidance of primary nonfunction (eg, in oxalosis), and the desirability of avoiding live kidney donation (eg, in heterozygote donors in Fabry's disease, high-risk recipients with focal glomerulosclerosis, and in recipients with HUS). Probably all types of glomerulonephritis recur, but with great variation in frequency and severity. In some forms of glomerulonephritis, recurrence may be frequent and definite on histopathological criteria but may only have a minor clinical expression (eg, dense deposit disease, anti-GBM antibody glomerulonephritis, IgA nephropathy), but in others, recurrence is less predictable yet it is clearly associated with premature graft failure (eg, focal glomerulosclerosis, membranous nephropathy). A common theme emerging is that where the initial glomerulonephritis is aggressive and causes kidney failure over a short time, recurrence is more likely, and when present, it will lead to graft failure with an increased frequency. Clinical manifestations, the frequency of recurrence, and the prognosis of the graft are now identified for most conditions. Unexpected observations have included the rarity of recurrent systemic lupus erythematosus (SLE), the immediate return of heavy proteinuria in focal glomerulosclerosis, and the predictable return of dense deposit disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Glomerulonephritis↗
PubMed1986

Typing of intraglomerular mononuclear cells associated with transplant glomerular rejection.

To investigate the pathogenesis of glomerular injury in renal allografts, we have analyzed intraglomerular mononuclear cells from 20 biopsies with typical features of transplant glomerular rejection (TGR) (segmental or global occlusion of capillaries by swollen cells). Ten biopsies showing cellular rejection but no glomerular pathology were selected as controls. Microwave fixation and an avidin-biotin immunoperoxidase technique were used with the following monoclonal antibodies; Leu1 and OKT3 (pan T cell), Leu 3 a + b and OKT4 (helper T cell), OKT8 (cytotoxic T cell), OKB7 (B cell), OKM1 (monocyte) and OKDR (DR positive cell). The results showed a significant increase of T cells, helper T cells, cytotoxic T cells and monocytes in the patients with TGR compared with the controls (all p less than 0.001, Mann-Whitney U test). Of the T cell subsets, cytotoxic T cells outnumbered helper T cells by a mean ratio of 3.2:1. In the interstitium, the distribution of mononuclear cells was not different between the two patient groups. In both, T cells and monocytes were predominant and few B cells were found. The percentage of cytotoxic T cells was similar to that of helper T cells. In this study, there were at least four TGR patients without cytomegalovirus (CMV) infection and the distribution of intraglomerular mononuclear cells in these patients was indistinguishable from that of other TGR patients. There was no significant association of the distribution of mononuclear cells with the severity of glomerular damage. These results suggest that T cells, predominantly of the cytotoxic subset and monocytes are involved in the mediation of TGR.(ABSTRACT TRUNCATED AT 250 WORDS)

B-Lymphocytes↗
PubMed1985

Dialysis 1984.

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Aluminum↗
PubMed1985

Glomerular transplant rejection: a distinctive pattern of early graft damage.

Five hundred seventy-six consecutive biopsy or nephrectomy specimens obtained during the first 6 months of transplantation from 300 grafts in 431 recipients were examined by light microscopy for focal or diffuse endocapillary hypercellularity. Forty-seven (8.2%) of the 576 specimens obtained from 37 (12.3%) of the 300 grafts exhibited segmental or global occlusion of capillaries by swollen cells in 40-100% of glomeruli per biopsy. The lesions occurred at any time after transplantation, but 34 (72.3%) were present by day 60 and 7 (14.9%) before day 10. Immunofluorescence in 39 affected biopsies revealed focal or segmental glomerular staining in 18 (46.2%), among which IgM was found most frequently, and was considered to be non-specific. Electron micrographs of 17 biopsies from 14 grafts revealed that glomerular capillaries were narrowed or occluded by mononuclear cells of uncertain type, possibly monocytes, as well as lymphocytes and a few neutrophils. Complement-fixing antibody titers to cytomegalovirus rose at least fourfold in 10 (45.5%) of the 22 patients studied, but glomerular lesions were no more severe in the seroconverters than in the non-converters, and there was no consistent temporal relationship between the occurrence of glomerular changes and seroconversion. Cellular or vascular rejection was present in most biopsies. One year graft survival was 34% among 35 accessed grafts with glomerular lesions, compared to 55% among 243 biopsied grafts with no glomerular changes. We consider that these lesions do not have a consistent association with cytomegalovirus infection and that they represent a distinctive form of glomerular rejection. Whether they indicate a poor graft survival, as the present results suggest but do not prove, requires further studies of other series of cases.

Cytomegalovirus Infections↗