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1.
Transplant Proc ; 42(5): 1643-7, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20620492

RESUMO

BACKGROUND AND PURPOSE: The influence of African-American ethnicity on outcomes of kidney transplant recipients subjected to early steroid withdrawal remains controversial. Recent studies that suggest no higher risk among African Americans may be biased by recruitment of relatively small number of African Americans or by patient selection. We compared outcomes of African Americans to non-African Americans in a center in which early steroid withdrawal has become the standard of practice. METHODS: This was a single-center prospective study of 133 consecutive patients receiving primary kidney transplants between January 2006 and December 2008, followed for >or=3 months, and managed with a similar immunosuppression regimen that included induction antibody therapy, tacrolimus, mycophenolate mofetil, and withdrawal of steroids on postoperative day 5. Acute rejection and other outcomes were compared in African-American patients (n = 55) and compared with those of non-African-American patients (n = 78). RESULTS: During the first 12 months after early steroid withdrawal, African-American patients experienced a significantly higher cumulative incidence of acute rejection than non-African Americans (23.6% vs 7.7%; P = .020). Using multivariate logistic regression, ethnicity (odds ratio 3.33; P = .047) and HLA mismatch (odds ratio 1.44; P = .041) were significantly correlated with acute rejection independent of recipient age, gender, historical peak panel reactive antibody level (PRA) or PRA at time of transplant, time on dialysis, or donor source. CONCLUSIONS: African Americans are at increased risk of acute rejection after early steroid withdrawal, particularly when they receive kidneys from poorly matched donors.


Assuntos
Corticosteroides/uso terapêutico , Negro ou Afro-Americano/estatística & dados numéricos , Etnicidade/estatística & dados numéricos , Rejeição de Enxerto/epidemiologia , Transplante de Rim/fisiologia , Adulto , Idoso , Esquema de Medicação , Quimioterapia Combinada , Antígenos HLA/imunologia , Teste de Histocompatibilidade , Humanos , Imunossupressores/uso terapêutico , Transplante de Rim/imunologia , Doadores Vivos/estatística & dados numéricos , Metilprednisolona/administração & dosagem , Metilprednisolona/uso terapêutico , Pessoa de Meia-Idade , Prednisona/administração & dosagem , Prednisona/uso terapêutico , Síndrome de Abstinência a Substâncias/epidemiologia
2.
Am J Transplant ; 10(2): 310-4, 2010 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-20055793

RESUMO

Proteinuria is an increasingly recognized effect of sirolimus (SRL) therapy in kidney transplant recipients. Predictors of proteinuria after conversion to SRL are not well described, and in particular the risk in African-American (AA) kidney recipients is unknown. We sought to analyze risk factors for proteinuria with SRL therapy in a cohort of 39 patients (44% AA) converted from tacrolimus to SRL at a mean time of 4 months posttransplantation. Patients were maintained on therapy with mycophenolate mofetil while most patients underwent early steroid withdrawal. Urinary protein to creatinine ratio (Up/cr) at a mean of 14 months postconversion increased to > or =500 mg/g in 65% of AAs versus 14% of non-AAs (p = 0.001). Mean arterial blood pressure at the time of conversion and pretransplant proteinuric kidney disease were also predictors of proteinuria after SRL conversion. In conclusion, AAs appear to be at high risk for proteinuria and should be monitored closely after conversion to SRL in calcineurin inhibitor sparing protocols.


Assuntos
Imunossupressores/uso terapêutico , Nefropatias/fisiopatologia , Rim/fisiopatologia , Proteinúria/induzido quimicamente , Adulto , Feminino , Humanos , Imunossupressores/efeitos adversos , Imunossupressores/farmacologia , Nefropatias/induzido quimicamente , Nefropatias/tratamento farmacológico , Testes de Função Renal , Masculino , Pessoa de Meia-Idade , Ácido Micofenólico/análogos & derivados , Proteinúria/tratamento farmacológico , Proteinúria/fisiopatologia , Fatores de Risco , Sirolimo/efeitos adversos , Sirolimo/farmacologia , Sirolimo/uso terapêutico , Esteroides/farmacologia , Esteroides/uso terapêutico , Tacrolimo/farmacologia , Tacrolimo/uso terapêutico
4.
Am J Kidney Dis ; 23(4): 605-18, 1994 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8154501

RESUMO

The inherited diseases of the glomerular basement membrane include Alport's syndrome (AS), nail-patella syndrome, and thin basement membrane nephropathy. Classical AS is inherited in an X-linked manner and accounts for approximately 85% of the cases. Its manifestations include hematuria, sensorineural hearing loss, ocular defects, and a progression to renal failure. A defect(s) in the alpha 5 (IV) chain of type IV collagen is believed to be the etiology of classic AS, and alterations in its encoding gene localized to the X-chromosome have been elucidated. Although isolated cases of anti-glomerular basement membrane glomerulonephritis have been reported following renal transplantation in patients with AS, it is considered an effective form of renal replacement therapy. Less is known regarding the genetic basis of the autosomal-dominant form of AS, which apparently accounts for the remaining 15% of the cases. Nail-patella syndrome is characterized by nail dysplasia, patellar hypoplasia or aplasia, and nephropathy. It is inherited in an autosomal-dominant fashion with the gene locus assigned to the long arm of chromosome 9. Possible linkage between the COL5A1 gene and the gene for nail-patella syndrome has been suggested. Approximately 30% of the patients progress to end-stage renal failure. Renal transplantation has been successful in treating patients who progress to end-stage renal failure. Thin basement membrane nephropathy is an autosomal dominant trait that accounts for approximately 30% of the cases presenting as persistent, asymptomatic hematuria. The cause of thin basement membrane nephropathy is unknown at present. No decline in renal function is associated with thin basement membrane nephropathy.


Assuntos
Colágeno Tipo IV , Glomérulos Renais/patologia , Nefrite Hereditária/patologia , Adolescente , Adulto , Autoantígenos/imunologia , Membrana Basal/imunologia , Membrana Basal/patologia , Membrana Basal/ultraestrutura , Colágeno/imunologia , Feminino , Humanos , Glomérulos Renais/imunologia , Glomérulos Renais/ultraestrutura , Masculino , Síndrome da Unha-Patela/genética , Síndrome da Unha-Patela/patologia , Nefrite Hereditária/genética , Nefrite Hereditária/imunologia
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