Actitud clínica frente a la disfunción renal en receptores de un trasplante renal en España

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Abstract

Antecedentes y objetivos: El presente estudio ha evaluado el criterio clínico que utilizan los nefrólogos españoles frente a la disfunción renal crónica (DRC) en receptores de trasplante renal (TR), y el grado de mantenimiento y control de la disfunción renal. Métodos: Estudio observacional, epidemiológico, multicéntrico, nacional y prospectivo, con un período de seguimiento de 6 meses. Se incluyeron 368 pacientes adultos con disfunción renal de grado 3 con un período mínimo de evolución posterior al trasplante de 24 meses. La programación de las visitas incluyó una visita retrospectiva, una visita inicial, una visita intermedia opcional y una visita final al sexto mes. Resultados: El tiempo medio desde el TR fue de 8,2 ± 5,4 años. La hipertensión (80,2%), seguida por la hipercolesterolemia (61,7%), fueron los factores de riesgo cardiovascular previos al trasplante más frecuentes. Las concentraciones de creatinina sérica entre la visita inicial y la visita de los 6 meses mostraron una diferencia estadísticamente significativa de 0,06 ± 0,22 (p < 0,0001), y la diferencia del filtrado glomerular (FG) fue de -1,03 ± 6,14 (p = 0,0014). Los factores pronósticos independientes significativos del empeoramiento del FG fueron: proteinuria a 24 h más alta (OR = 1,001 por cada mg; p = 0,020), más tiempo desde el trasplante (OR = 1,009 por cada mes; p = 0,017) y concentraciones bajas de hemoglobina (OR = 1,261 por cada g/dl; p = 0,038). También se observó cierta influencia negativa de la edad del donante (OR = 1,021 por cada año; p = 0,106). Solo se realizó biopsia en el 8% de los casos de receptores de TR con DRC de grado 3, suponiendo alguna intervención en el 25,4% de los casos. Conclusiones: Con frecuencia los marcadores secundarios y los factores de progresión de la DRC siguen sin estar controlados después del TR, principalmente la anemia. Solo aproximadamente el 2% de pacientes se benefician de una intervención terapéutica basada en una biopsia. Existe una disparidad entre la percepción clínica y los parámetros objetivos, que conduce a una clara inercia clínica del control de los factores de riesgo de estos pacientes.

Translated abstract

Background and objectives: In the present study, clinical criteria used by Spanish nephrologists when approaching chronic kidney disease (CKD) in kidney recipients, as well as their level of maintenance and control of renal function, were evaluated. Methods: An epidemiological, observational, multicenter, nation-wide, prospective study was carried out, with a 6-month follow-up period. Three hundred and sixty-eight adult patients with stage 3 kidney disease after a 24-month or longer post-transplantation follow-up period were included. Visits schedule included a retrospective visit, a baseline visit, an optional mid-term visit, and a final visit at month 6. Results: Mean time since kidney transplantation was 8.2 ± 5.4 years. Most common pre-transplant cardiovascular risk factors were high blood pressure (80.2%), followed by high cholesterol levels (61.7%). Serum creatinine levels showed a statistically significant decrease from baseline visit to 6-month visit (0.06 ± 0.22; P < .0001), and glomerular filtration rate (GFR) reduction was -1.03 ± 6.14 (P = 0.0014). Significant independent prognostic factors for GFR worsening were: higher 24-hour proteinuria (OR = 1.001 per mg; P = .020), longer time since transplantation (OR = 1.009 per month; P = .017), and lower hemoglobin levels (OR = 1.261 per g/dl; P = .038). Donor age also had some negative influence (OR = 1.021 per year; P = .106). Biopsies were obtained in only 8% of kidney transplant recipients with stage 3 CKD with an intervention being carried out in 25.4% of cases. Conclusions: Secondary markers and factors resulting in CKD progression, particularly anemia, are still frequently uncontrolled after kidney transplantation. Only about 2% of patients benefit from a therapeutic intervention based on a biopsy. Clinical perception differs from objective measures, which results in an obvious clinical inertia regarding risk factor control in such patients.

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Most cited references 53

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The natural history of chronic allograft nephropathy.

Brian Nankivell, Richard J Borrows, Caroline L S Fung … (2003)

With improved immunosuppression and early allograft survival, chronic allograft nephropathy has become the dominant cause of kidney-transplant failure. We evaluated the natural history of chronic allograft nephropathy in a prospective study of 120 recipients with type 1 diabetes, all but 1 of whom had received kidney-pancreas transplants. We obtained 961 kidney-transplant-biopsy specimens taken regularly from the time of transplantation to 10 years thereafter. Two distinctive phases of injury were evident as chronic allograft nephropathy evolved. An initial phase of early tubulointerstitial damage from ischemic injury (P<0.05), prior severe rejection (P<0.01), and subclinical rejection (P<0.01) predicted mild disease by one year, which was present in 94.2 percent of patients. Early subclinical rejection was common (affecting 45.7 percent of biopsy specimens at three months), and the risk was increased by the occurrence of a prior episode of severe rejection and reduced by tacrolimus and mycophenolate therapy (both P<0.05) and gradually abated after one year. Both subclinical rejection and chronic rejection were associated with increased tubulointerstitial damage (P<0.01). Beyond one year, a later phase of chronic allograft nephropathy was characterized by microvascular and glomerular injury. Chronic rejection (defined as persistent subclinical rejection for two years or longer) was uncommon (5.8 percent). Progressive high-grade arteriolar hyalinosis with luminal narrowing, increasing glomerulosclerosis, and additional tubulointerstitial damage was accompanied by the use of calcineurin inhibitors. Nephrotoxicity, implicated in late ongoing injury, was almost universal at 10 years, even in grafts with excellent early histologic findings. By 10 years, severe chronic allograft nephropathy was present in 58.4 percent of patients, with sclerosis in 37.3 percent of glomeruli. Tubulointerstitial and glomerular damage, once established, was irreversible, resulting in declining renal function and graft failure. Chronic allograft nephropathy represents cumulative and incremental damage to nephrons from time-dependent immunologic and nonimmunologic causes. Copyright 2003 Massachusetts Medical Society

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Chronic renal allograft dysfunction.

Alec R. Chapman, Brian Nankivell, James O'Connell (2005)

The major causes of renal transplant loss are death from vascular, malignant or infectious disease, and loss of the allograft from chronic renal dysfunction associated with the development of graft fibrosis and glomerulosclerosis. Chronic allograft nephropathy (CAN) is the histologic description of the fibrosis, vascular and glomerular damage occurring in renal allografts. Clinical programs rely on monitoring change in serum creatinine for identification of patients at risk of CAN, but this change occurs late in the course of the disease, and underestimates the severity of pathologic change. CAN has several causes: ischemia-reperfusion injury, ineffectively or untreated clinical and subclinical rejection, and superimposed calcineurin inhibitor nephrotoxicity, exacerbating pre-existing donor disease. Once established, interstitial fibrosis and arteriolar hyalinosis lead to progressive glomerulosclerosis over the subsequent years. There have been a number of approaches to treatment aimed at reducing the impact of CAN, mostly centered around avoidance of calcineurin inhibitors through their elimination in all, or just selected, patients. These immunosuppression strategies combine corticosteroids with azathioprine or mycophenolate mofetil, and/or sirolimus and everolimus. Late identification of CAN in individual patients has meant that strategies for intervening to prevent chronic renal allograft dysfunction and subsequent graft loss tend to be "too little and far too late."