RESUMEN
Investigations conducted in medical centers worldwide and ours indicate that patients with chronic allograft nephropathy (CAN) will have short kidney graft survival when proteinuria and/or azotemia develop early, during the first post transplantation year. The analysis of published results suggests that angiotensin-converting enzyme (ACE) DD genotype represents unfavorable marker of rapid progression of chronic renal allograft dysfunction (CRAD). Differences of response to ACEi therapy in patients with chronic nephropathy of one's one or transplanted kidney could be explained by ACE genotype variety, where ACE DD is unfavorable genotype. Related factors influencing the ACEi therapy success in patients with particular ACE genotype are highly salt diet, interactions of genotype variety of all renin-angiotensin-aldosterone system (RAS) molecules, i.e. diversity in the ACE, angiotensinogen, AT1 receptor or aldosterone genotype, as well as differences of ACEi responses in patients with glomerular and tubulointerstitial kidney diseases. Retardation of chronic renal failure in patients with ACE DD genotype who developed chronic allograft nephropathy has been obtained with long-term ACEi treatment and restricted salt intake to 50 mmol Na+ per day. We consider that genotype investigation of RAS molecule, primarily of ACE genotype in recipient and kidney donor should be done before high-risk kidney transplantation.
Asunto(s)
Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Enfermedades Renales/fisiopatología , Trasplante de Riñón/efectos adversos , Peptidil-Dipeptidasa A/genética , Enfermedad Crónica , Genotipo , Humanos , Enfermedades Renales/tratamiento farmacológico , Enfermedades Renales/etiología , Enfermedades Renales/genéticaRESUMEN
Angiotensin II plays a crucial role in pathologic processes of chronic allograft nephropathy (CAN) leading to chronic and progressive renal allograft dysfunction (CRAD). Systemic and glomerular hypertensions together with proteinuria occur in CAN under conditions of JGA hypertrophy with up-regulated RAS activity in the renal allograft, and they represent independent factors of rapid progression of chronic renal allograft failure. ACEi are safe and efficient antihypertensives with renoprotective effects in patients with CAN. Favorable response to ACEi has been reflected in diminished proteinuria, slow increase of creatininemia, regulation of arterial hypertension and better long-term survival of patients and kidney allografts. Our pilot study highlights the importance of ACEi therapy in CAN after renal transplantation from elder donors (>55 years).