Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the incidence, risk factors of acute renal failure (ARF) after allogeneic hematopoietic stem cell transplantation (allo-HSCT), and evaluate its effect on the prognosis of patients after allo-HSCT. A retrospective analysis was performed in 86 patients undergoing allo-HSCT at Peking University First Hospital from June 2003 to April 2007. ARF is defined as a doubling of baseline serum creatinine at any time during the first 100 days post-transplant. The risks of ARF and mortality after ARF were examined using univariate analysis and multivariate unconditional logistic regression. The correlation of ARF and survival was examined using Cox regression. The results indicated that 27 patients (31.40%) developed ARF at a median of 59.5 days after transplant (range 1 to 93 days). The univariate analysis showed that elevated risks were severe acute GVHD (OR 6.196; 95% CI 1.121 - 34.249, p = 0.033), sepsis or septic shock (OR 4.184; 95% CI 1.314 - 13.325, p = 0.018) and hyperbilirubinemia (OR 3.709; 95% CI 1.428 - 9.635, p = 0.006). Renal disease before transplant (OR 6.711; 95% CI 1.199 - 37.564, p = 0.027), hypertension (OR 2.067; 95% CI 0.739 - 5.782, p = 0.165), the use of vancomycin (OR 2.133; 95% CI 0.844 - 5.392, p = 0.106) or foscarnet sodium (OR 2.133; 95% CI 0.844 - 5.392, p = 0.106) may be potential risks. Multivariate logistic regression analysis showed that renal disease before transplant (OR 6.288; 95% CI 1.218 - 32.455, p = 0.028), sepsis or septic shock (OR 3.614; 95% CI 1.040 - 12.544, p = 0.043) and hyperbilirubinemia (OR 4.448; 95% CI 1.563 - 12.665, p = 0.005) appear to be independently associated with an increased risk of ARF. Age, gender, baseline serum creatinine level, advanced malignant disease, unrelated-donor, total body irradiation (TBI) and cyclosporine levels were not associated with the development of ARF. Cox regression showed that ARF (RR 2.124; 95% CI 1.016 - 4.441, p = 0.045) was independently associated with survival of patients after allo-HSCT. The mortality of patients with ARF within 6 months post-transplant was significantly higher than that of those without ARF (44.4% vs 8.47%, p < 0.001). It is concluded that the cumulative incidence of ARF after allo-HSCT remains high. Renal disease before transplant, hyperbilirubinemia and sepsis or septic shock are all related factors which can increase the risk of ARF. ARF appears to be independent factor influencing survival of patients after allo-HSCT.
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PMID:[Clinical analysis of acute renal failure after allogeneic hematopoietic stem cell transplantation]. 1954 95

BK virus (BKV) is an important pathogen and cause of nephropathy in renal transplant recipients, but its significance following hematopoetic stem cell transplantation (HSCT) is less well described. We measured blood and urine BKV in 124 allogeneic HSCT patients (67 had undergone prior HSCT [surveillance cohort]; 57 were monitored from transplant day 0 [prospective cohort]). BK viruria was manifest in 64.8% of the patients; 16.9% developed viremia. In the prospective cohort, the median time from transplantation to BK viremia development (128 days) was longer than for viruria (24 days; P < .0001). Among clinical factors (sex, disease, transplant type, alemtuzumab use, cytomegalovirus [CMV] viremia, graft-versus-host disease [GVHD], donor HLA C7 allele), only CMV viremia was more common in patients with BKV infection (P < or = .04). There was a direct relationship between blood and urine BKV levels and the occurrence, and degree, of hematuria (P < or = .03). Finally, BKV infection was analyzed along with other clinical factors in relation to the development of post-HSCT renal impairment. On multivariate analysis, only BK viremia (P=.000002) and alternative-donor transplantation (P=.002) were independent predictors of development of post-HSCT renal impairment, with BK viremia associated with a median 1.62mg/dL rise in creatinine from the pretransplant baseline. Among 8 patients in the surveillance cohort with BK viremia, 2 developed biopsy-proven BKV nephropathy requiring hemodialysis. Investigation of whether prophylaxis against, or treatment of, BKV in the post-HSCT setting mitigates the associated morbidities, especially kidney injury, warrants prospective evaluation.
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PMID:BK virus infection is associated with hematuria and renal impairment in recipients of allogeneic hematopoetic stem cell transplants. 1966 Jul 16

Allogeneic hematopoietic stem cell transplantation (HSCT) is the treatment of choice for a wide range of diseases, but is associated with a significant risk of chronic kidney disease (CKD), affecting up to 25% of survivors with a significant morbidity. The causes of CKD after HSCT vary between different studies. The present study evaluated CKD in patients undergoing allogeneic HSCT. We analyzed the clinical course of 148 patients who received allogeneic HSCT at the University Hospital of St. Louis in Paris between 1999 and 2002 and were alive after 2 years without relapse. CKD was defined as a glomerular filtration rate (GFR) <60 mL/min/1.73 m(2), using the abbreviated modification of diet in renal disease (MDRD) equation for adults and the Schwartz formula for children. Of the 148 relapse-free 2-year survivors, 11 (7%) patients had renal dysfunction. No chronic renal failure was noted in the younger age group (<15 years at transplantation). CKD was associated with total body irradiation (TBI) (odds ratio [OR] = 4.53; 95% confidence interval [CI] 1.15 to 17.9; P = .026) and chronic graft-versus-host disease (cGVHD) (OR = 4.58; 95% CI 1.16-18.1; P = .026). Only 1 additional patient developed CKD between 2 and 5 years of follow-up (cumulative incidence of 0.7% over the 3-year period). In the CKD group, renal function tended to stabilize over the 3-year period (estimated GFR 45 +/- 14 mL/min/1.73 m(2) at 2 years and 46 +/- 14 mL/min/1.73 m(2) at 5 years). A 7% prevalence of CKD was noted in the relapse-free 2-year survivor patients. Renal impairement was correlated with TBI and cGVHD. Minor incidence of CKD and a relative stability of renal function were noted between 2 and 5 years after HSCT.
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PMID:Chronic kidney dysfunction in patients alive without relapse 2 years after allogeneic hematopoietic stem cell transplantation. 1974 32

Recipients of hematopoietic cell transplantation may be at risk for developing acute kidney injury (AKI), and this risk may be increased in patients who undergo transplantation for severe systemic sclerosis (SSc) due to underlying scleroderma renal disease. AKI after transplantation can increase treatment-related mortality. To better define these risks, we analyzed 91 patients with SSc who were enrolled in 3 clinical trials in the United States of autologous or allogeneic hematopoietic cell transplantation (HCT). Eleven (12%) of the 91 patients with SSc in these studies (8 undergoing autologous HCT, 1 undergoing allogeneic HCT, 1 pretransplantation, 1 given i.v. cyclophosphamide on a transplantation trial) experienced AKI, of whom 8 required dialysis and/or therapeutic plasma exchange. AKI injury in the 9 HCT recipients developed a median of 35 days (range, 0-90 days) after transplantation. Ten of 11 patients with AKI received angiotensin-converting enzyme inhibitor (ACE-I) therapy. The etiology of AKI was attributed to scleroderma renal crisis in 6 patients (including 2 with normotensive renal crisis), to AKI of uncertain etiology in 2 patients, and to AKI superimposed on scleroderma kidney disease in 3 patients. Eight of the 11 patients died, one each because of progression of SSc, multiorgan failure, gastrointestinal and pulmonary bleeding, pericardial tamponade and pulmonary complications, diffuse alveolar hemorrhage, pulmonary embolism, graft-versus-host disease, and malignancy. Limiting nephrotoxins, cautious use of corticosteroids, renal shielding during total body irradiation, strict control of blood pressure, and aggressive use of ACE-Is may be of importance in preventing renal complications after HCT for SSc.
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PMID:Acute kidney injury in patients with systemic sclerosis participating in hematopoietic cell transplantation trials in the United States. 2070 86

We present the case of a patient with past medical history of acute mieloblastic leukemia treated with a related, fully match alogenic bone marrow transplantation (BMT). He presented after BMT treatment graft versus host disease (GVHD) and thrombotic thrombocytopenic purpura. He also developed end-stage renal disease that required renal replacement therapy. A preemptive kidney transplant was performed. The haematopoiesis were in complete chimera and the patient developed tolerance to the kidney graft, requiring only minimal immunossupression because of his GVHD.
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PMID:Unresponsiveness to a kidney graft after a fully matched allogenic bone marrow transplantation combined with low-dose tacrolimus therapy: a case report. 2183 67

Graft-versus-host disease (GVHD) is a rare complication after kidney transplantation. We describe a 62-year-old female with end-stage renal disease due to hypertension. She received a kidney with 4 mismatched human leukocyte antigen (HLA) out of 6 HLA - A, B, DR from a deceased donor. After the procedure, the patient showed watery diarrhea on postoperative day (POD) 45. An endoscopic biopsy of the colon revealed some apoptotic cells consistent with GVHD. Thrombocytopenia was gradually developed on POD 54. She received steroid pulse therapy, and thrombocytopenia did not progress. However, pneumonia, renal failure, and cardiac failure occurred. She died due to multiple organ failure. We must consider GVHD in renal transplant recipients without homozygous or identical HLA, who had only watery diarrhea without other typical GVHD symptoms such as skin rash and fever, although GVHD is rare in renal transplant recipients.
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PMID:Graft-versus-host disease after kidney transplantation. 2206 80

Chronic kidney disease (CKD) occurs commonly (prevalence of approximately 20% in a large series) after allogeneic hematopoietic stem cell transplantation (HSCT). There are three distinct clinical entities that occur after HSCT: thrombotic microangiopathy (TMA), nephrotic syndrome (NS), and idiopathic or graft-versus-host disease (GVHD)-related CKD. Acute renal function decline occurs in the majority of patients in the first months after transplantation. This acute kidney injury can persist and is a risk factor for the later development of CKD. However, the potentially independent role of GVHD, chronic inflammation, and chronic exposure to calcineurin inhibitors in the development and progression of CKD warrants further investigation. Careful monitoring of blood pressure, renal function, and proteinuria is mandatory in patients undergoing HSCT, especially older patients with pre-existent renal impairment. Renal function should be evaluated before HSCT and monitoring should occur at least every 6 to 12 months in these patients. Renal biopsies are indicated in patients with proteinuria and persistent or progressive rises in serum creatinine to determine etiology and prevent progression to end-stage renal disease (ESRD).
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PMID:Chronic kidney diseases in long-term survivors after allogeneic hematopoietic stem cell transplantation: monitoring and management guidelines. 2222 87

Plasmacytoid dendritic cells play important roles in inducing immune tolerance, preventing allograft rejection, and regulating immune responses in both autoimmune disease and graft-versus-host disease. In order to evaluate a possible protective effect of plasmacytoid dendritic cells against renal inflammation and injury, we purified these cells from mouse spleens and adoptively transferred lipopolysaccharide (LPS)-treated cells, modified ex vivo, into mice with adriamycin nephropathy. These LPS-treated cells localized to the kidney cortex and the lymph nodes draining the kidney, and protected the kidney from injury during adriamycin nephropathy. Glomerulosclerosis, tubular atrophy, interstitial expansion, proteinuria, and creatinine clearance were significantly reduced in mice with adriamycin nephropathy subsequently treated with LPS-activated plasmacytoid dendritic cells as compared to the kidney injury in mice given naive plasmacytoid dendritic cells. In addition, LPS-pretreated cells, but not naive plasmacytoid dendritic cells, convert CD4+CD25- T cells into Foxp3+ regulatory T cells and suppress the proinflammatory cytokine production of endogenous renal macrophages. This may explain their ability to protect against renal injury in adriamycin nephropathy.
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PMID:Lipopolysaccharide-pretreated plasmacytoid dendritic cells ameliorate experimental chronic kidney disease. 2231 23

Stem cells are undifferentiated cells with the ability of proliferation, regeneration, conversion to differentiated cells and producing various tissues. Stem cells are divided into two categories of embryonic and adult. In another categorization stem cells are divided to Totipotent, Multipotent and Unipotent cells.So far usage of stem cells in treatment of various blood diseases has been studied (such as lymphoblastic leukemia, myeloid leukemia, thalassemia, multiple myeloma and cycle cell anemia). In this paper the goal is evaluation of cell therapy in treatment of Parkinson's disease, Amyotrophic lateral sclerosis, Alzheimer, Stroke, Spinal Cord Injury, Multiple Sclerosis, Radiation Induced Intestinal Injury, Inflammatory Bowel Disease, Liver Disease, Duchenne Muscular Dystrophy, Diabetes, Heart Disease, Bone Disease, Renal Disease, Chronic Wounds, Graft-Versus-Host Disease, Sepsis and Respiratory diseases. It should be mentioned that some disease that are the target of cell therapy are discussed in this article.
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PMID:Stem cell therapy in treatment of different diseases. 2235 76

Chemokines help facilitate the recruitment of inflammatory cells into tissues in response to infection or inflammation, and help coordinate the actions of the leukocytes that underlie an immune response. Animal models are the experimental tools of choice for the validation of chemokine biology and have provided much insight into the workings of chemokine biology. This review summarizes findings from chemokine research obtained through the application of animal models of pulmonary fibrosis, graft-versus-host disease, colitis, renal disease and allograft rejection.
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PMID:Dissection of inflammatory processes using chemokine biology: Lessons from clinical models. 2269 84


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