Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pretransplant cellular immune responsiveness of 90 renal failure patients was correlated with subsequent allograft survival. Patients were subdivided in two bases: whether the pretransplant immune parameter values were above (strong responder) or below (weak responder) the group median, and whether they were responsive or anergic to recall skin test antigens. In a group of 72 cadaveric renal allograft recipients, treated with only Imuran and prednisone, the overall 1-year graft survival was 48%. Pretransplant immunocompetence correlated with graft survival: factors predicting longer allograft survival (P < 0.01) included: percentage of active T rosette-forming cells (A-T RFCs) < 36.5%, anergy to microbial skin test (ST) antigens, in vitro spontaneous blastogenesis (SB) < 14,600 cpm, and response to a panel of five donors in mixed lymphocyte culture (PMLC) < 28,000 cpm. In the two groups, weak and strong responders, the 1-year graft survival rates differed: 63% versus 32% when segregated by the A-T RFC parameter, 63% versus 33% for ST, 57% versus 36% for SB, and 63% versus 35% for PMLC. There were no significant differences in the number of HLA mismatches between the two groups. An additional group of 18 patients was treated with adjuvant immunosuppressive therapy by prophylactic administration of antithymocyte globulin (ATG; Upjohn Co.). Strong, but not weak, responders treated with ATG displayed a significantly improved (P < 0.01) 1-year graft survival over that of the untreated group. Thus, pretransplant immunological assessment may guide the selection of adjuvant immunosuppressive therapy to improve renal allograft survival in strong immune responders at high risk of rejection.
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PMID:Improved allograft survival of strong immune responder-high risk recipients with adjuvant antithymocyte globulin therapy. 700 94

Idiopathic mesangial glomerulonephritis with IgA deposits was observed in two relatives, father and son, in a family of 5 members. In the father the disease started at age 43 with relapsing macroscopic hematuria, proteinuria, renal failure and hypertension, with a progressive course in the ensuing four years. The affected son, the oldest of three brothers, developed relapsing macroscopic hematuria at age 16; two years later renal function was normal and there was no hypertension, but microhematuria persisted without proteinuria. The mother and the other two brothers had no clinical or biological signs of renal disease. Serum immunoglobulins (IgG, IgA, and IgM) and complement (C3, C4, C3 proactivator) were normal in the patients and their relatives. Histocompatibility typing demonstrated the presence of HLA-Bw35 in the father and the two unaffected sons, being negative in the mother and the affected son. The analysis of HLA-Bw35 in 23 patients with IgA mesangial glomerulonephritis gave positive results in 30% of them, while the control group had a positivity of 15% (p non significant with the X2 test). The present observations suggest that IgA mesangial glomerulonephritis is a potentially familial and hereditary renal disease. HLA-Bw35 antigen appears not to be a genetic marker of the disease in our geographical area.
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PMID:[Familial and hereditary mesangial glomerulonephritis with IgA deposits (author's transl)]. 701 69

More than 50% of patients with chronic renal failure will be suppressed in their cell-mediated immune response to 2,4-dinitrochlorobenzene (DNCB). This applies in renal failure attributable to juvenile onset diabetes as well as other types of end stage renal disease. Significantly better kidney survival of both living related and cadaver grafts is seen in diabetic patients who are non-responsive to DNCB. Twelve-month kidney survival for DNCB-negative patients receiving living related allografts is 71% compared with 25% for DNCB-positive patients. Twelve-month kidney survival in cadaver recipients is 39% in DNCB-negative compared with 9% for DNCB-positive patients. Successful second grafts were done in DNCB-negative diabetic patients, however, all second grafts in DNCB-positive patients failed in less than 3 months. DNCB skin test reactivity as a measure of cell-mediated response is a valuable predictor of immunological outcome of transplantation in patients whose renal disease results from juvenile onset diabetes. Patient survival in DNCB nonresponders is nearly twice that of DNCB responders. Differences in outcome following transplantation could not be accounted for by HLA disparity, transfusion history, or other variables known to effect transplant outcome. Kidney and patient survival in DNCB-positive diabetic patients receiving either cadaver or living related allografts is sufficiently low as to identify them as a subpopulation of renal failure patients who should be treated by dialysis, or selected for special protocols which might provide immunological manipulation prior to transplantation to improve their treatment outcome.
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PMID:Dinitrochlorobenzene skin test reactivity as a predictor of outcome in transplantation of juvenile onset diabetics. 703 53

The HLA haplotype A 10,B18 has been associated with hereditary deficiency of the second component of complement(C2). In an effort to detect individuals homozygous for C2 deficiency, a thorough audit of HLA serotyping results in 3,100 individuals was performed, and a single patient homozygous for the A10, B18 haplotype was identified. Detailed complement studies in this patient's serum and plasma revealed previously undetected selective absence of C2 antigen and haemolytic activity, and a hereditary basis for this deficiency was indicated by half-normal levels of C2 haemolytic activity in both of his children. The patient was of special interest in that he had previously developed renal failure which was treated by cadaver kidney transplantation. C2 antigen was undetectable in serum and plasma samples taken prior to and up to 9 months following transplantation. This experience suggests that HLA serotyping can be a valuable screening technique for the detection of individuals with C2 deficiency, and that renal transplantation does not reconstitute normal levels of C2.
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PMID:Renal transplantation in a patient with hereditary deficiency of the second component of complement. 703 90

Renal transplantation was performed in 25 patients for renal failure secondary to nephrotic syndrome and histologically proven segmental glomerulosclerosis (FSGS). They received 33 allografts, 13 from cadaveric (CAD) and 20 from living related donors (LRD) including 6 HLA-identical siblings. All have been followed for at least 1 year with none lost to follow-up. Overall, functional graft survival of the 33 grafts was 68.7% at 12 months and 60.5% at 48 months, similar to controls matched for age, sex, time of transplant, and donor source. Recurrent FSGS was documented histologically in 9 (5 CAD and 4 LRD) of 33 grafts (27.3%) and resulted in loss of graft function in 3 (9.9%). The presence and extent of mesangial proliferation (MP) in conjunction with or preceding typical lesions of FSGS in native kidneys was predictive of recurrent disease. Age at onset, duration of disease, and donor source were not. Sixteen patients with only FSGS on multiple biopsies of native kidneys received 22 allografts and recurrent disease occurred in 4 (18%) but did not cause loss of graft function in any. Six patients with focal areas of MP as well as FSGS underwent eight transplants, in which recurrent FSGS developed in two (25%) and caused graft loss in one. All three grafts transplanted to the patients with diffuse MP and FSGS developed recurrent disease, this resulting in graft failure in two. This study demonstrates the importance of a thorough histological evaluation by multiple biopsies of all patients with steroid-nonresponsive nephrotic syndrome. Only in this manner does it appear possible to define that subgroup of patients with FSGS who are at greatest risk of clinically significant recurrent disease.
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PMID:Incidence and significance of recurrent focal segmental glomerulosclerosis in renal allograft recipients. 704 54

The preliminary results of a pediatric renal transplantation program started two years ago are presented. Fourteen children aged four to 13 years received a renal transplantation from April 1979 through March 1981. In eight patients renal graft was obtained from a living related donor (father-mother) and six from corpse donor. Recipients body weight ranged from 11 to 40 kg. (mean, 25 kg.). The previous time on hemodialysis was between three and 13 months (mean, seven months). In all cases a transfusion protocol prior to renal transplantation was followed (five transfusions minimum). Donor-recipient compatibility ranged zero-three HLA compatibilities. The patients were coordinately managed by pediatric specialists. The follow-up of the transplanted children ranges from one to 24 months (mean, 10 months). All of the patients are alive and the graft is functioning in all but one. A chronic rejection episode begun five months after renal-transplantation caused in one patients a graft loss. Plasma creatinine is lesser than 1.50 mg/100 ml. in 11 cases and inferior to 2 mg./100 ml. in the other two patients. The non-immunological complications presented have been unremarkable and no repercussions on the patients evolution have been detected. Even though the follow-up period is short, the results are highly encouraging, supporting that renal transplantation is the election treatment in children with terminal renal failure.
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PMID:[Renal transplantation in children: preliminary report (author's transl)]. 704 8

The results achieved by treating patients with end-stage renal failure with allotransplantation have improved dramatically since the 1950s when immunosuppression was induced by total body irradiation and there was a lack of HLA typing. Although long-term hemodialysis offers prolonged survival and partial rehabilitation for many individuals with end-stage renal disease, the technique is inconvenient and time consuming. Patients are restricted by necessary proximity to the machine, dietary limitations, potential failure of access sites, and complications of various organ systems. Despite the availability of dialysis and the federal funds to partially pay for treatment, long-term dialysis still remains a costly process for the individual in need of care. During the same period when dialysis techniques improved and became widely available, transplantation of the human kidney became an established and justified treatment for some patients with end-stage renal disease. Those with successful kidney allografts may achieve remarkable recovery and are often able to return to normal lives. One of the more striking improvements in the results of renal transplantation in recent years had been the decline in morbidity and mortality. Mortality by the end of the first year after transplantation during which time most deaths occur, is currently less than 5 percent in a number of major medical units. In part, this decline represents a change in philosophy by transplant teams, who now tend to decrease immunosuppression and sacrifice the kidney rather than the patient in instances of inexorable rejection. In addition, declining mortality is directly attributable to improved methods of preventing, discovering, and treating patients with potential or real infections. More recently, in some centers, the rate of successful engraftment has shown gratifying improvement due to refinements in tissue typing, improved cross matching, new immunosuppressive therapies, and pretransplant conditioning with blood products. These recent improvements are the primary focus of this review. Unfortunately, until very recently, rates of functional survival of allografts have not been satisfactory.
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PMID:The improving utility of renal transplantation in the management of end-stage renal disease. 704 37

Three of five siblings developed a steroid-resistant nephrotic syndrome with focal segmental glomerulosclerosis within a four-month period. Two of the siblings with nephrotic syndrome (Patients 1 and 2) also have sickle cell anemia; the third (Patient 3) carries the thalassemia trait. The dizygotic twin brother of Patient 2 has sickle cell anemia, but does not have the nephrotic syndrome. The nephrotic syndrome of patient 1 was resistant to corticosteroid and cyclophosphamide therapy and she developed severe renal failure 14 months after onset. The nephrotic syndrome of Patients 2 and 3 was steroid resistant but was partially responsive to cyclophosphamide therapy. They have persistent proteinuria with mild elevation of serum creatinine concentration and hypertension 5 1/2 years after diagnosis. In this family, the nephrotic syndrome appeared unrelated to the specific hemoglobinopathy, HLA type or mixed lymphocyte culture responsiveness despite the similarity of the renal disease.
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PMID:Familial nephrotic syndrome and focal segmental glomerulosclerosis. 719 18

Diabetic nephropathy with renal failure is a major cause of death among juvenile diabetics. It is as yet unknown why some diabetics suffer from this serious renal complication while others do not, in spite of long duration of diabetes. For therapeutic reasons it is of the utmost importance to find out which patients are at risk long before the manifestation of renal insufficiency. Juvenile diabetics are know to have an increased frequency of some HLA antigens. The relationships between the HLA-A, HLA-B and HLA-C antigens and diabetic end-stage nephropathy were therefore evaluated in the present study. The study comprised 121 insulin-dependent diabetics with renal failure (mean age at onset of diabetes 13.4 leads to 7.6 (SD) years, mean pre-uraemic duration of diabetes 21.7 leads to 4.7 years), and 36 insulin-dependent diabetics (mean age at onset of diabetes 16.5 leads to 8.4 years) without renal failure despite long mean duration of diabetes (32.5 leads to 5.1 years). We found the expected significant increase in B8 and B15 and a decrease in B7 frequencies in the diabetics compared with the non-diabetic population, but no difference was found between uraemic and non-uraemic diabetics. Neither the early onset of diabetes nor the rapid appearance of renal failure was associated with any HLA frequency. The data therefore do not provide evidence of the involvement of B8 or B15 allele-associated mechanisms in the disease process leading to diabetic nephropathy with renal failure. There was a significant difference (p corrected less than 0.01) between the frequency of Bw22 in uraemic diabetics (14%) and that in non-diabetics (5%) while the frequency was near normal in non-uraemic diabetics. Further data are needed to confirm the possible association of Bw22 with diabetic nephropathy.
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PMID:HLA-antigen distribution in juvenile diabetics with end-stage nephropathy. 723 15

Glomerulonephritis with mesangial deposition of IgA was diagnosed in 31 patients. In Spain this disease is the second more frequent primary glomerulonephritis, representing 27% of them. One out of every four patients with IgA mesangial glomerulonephritis ends the clinical course in renal failure. Such bad evolution might be predicted by the existence of arterial hypertension, severe proteinuria, degree of glomerular sclerosis, presence of HLA Bw35, and increased polymeric IgA in serum. The present pathogenetic concepts are reviewed.
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PMID:[IgA mesangial glomerulonephritis (author's transl)]. 725 41


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