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Riñón , Donadores Vivos , Supervivencia de Injerto , Humanos , Fallo Renal Crónico , Trasplante de RiñónRESUMEN
Chronic metabolic acidosis (CMA) is a common complication of the more advanced stages of chronic kidney diseases (CKD), and is associated with morbidity and mortality of CKD patients and possibly with the progression of renal disease. Nevertheless, there is limited evidence or information on the prevalence, the potential causal factors, the clinical impact and the effects of correction of CMA in kidney transplant recipients. In this review, we briefly look at the more relevant, though scanty, studies which have, over time, addressed the above-mentioned points, with the hope that in the future the interest of transplant nephrologists and surgeons will grow towards this unreasonably neglected issue.
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Acidosis/etiología , Enfermedades Renales/cirugía , Trasplante de Riñón/efectos adversos , HumanosRESUMEN
BACKGROUND: To assess the long-term effectiveness and safety of adefovir (ADV) plus lamivudine (LMV) in LMV-resistant (R) kidney transplants with chronic hepatitis B, 11 such patients were treated with add-on ADV. METHODS: Serum alanine aminotransferase, renal function and serum hepatitis B virus (HBV) DNA levels were assessed every 3 months; ADV mutations were searched for by INNO-LiPA HBV DR v2 assay. RESULTS: During 36 months (12-48), nine patients cleared serum HBV DNA with a 3-year cumulative virological response rate of 88%, without the emergence of ADV mutations. ADV dose was reduced in six patients (55%) showing a decline of creatinine clearance, in the absence of proximal tubulopathy. CONCLUSIONS: In LMV-R kidney graft recipients, long-term add-on therapy with ADV is efficacious and safe with timely adaptation of ADV dose.
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Adenina/análogos & derivados , Antivirales/uso terapéutico , Farmacorresistencia Viral/efectos de los fármacos , Hepatitis B Crónica/tratamiento farmacológico , Trasplante de Riñón , Lamivudine/uso terapéutico , Organofosfonatos/uso terapéutico , Adenina/uso terapéutico , Adulto , Fármacos Anti-VIH/uso terapéutico , ADN Viral/genética , Quimioterapia Combinada , Femenino , Estudios de Seguimiento , Virus de la Hepatitis B/genética , Virus de la Hepatitis B/aislamiento & purificación , Humanos , Masculino , Persona de Mediana Edad , Tasa de Supervivencia , Factores de Tiempo , Resultado del TratamientoRESUMEN
Secondary hyperparathyroidism (SHPT) is a classical feature of chronic kidney disease (CKD). Commonly, hypocalcemia, hyperphosphatemia, and vitamin D deficiency are involved into the pathogenesis of SHPT. Parathyroid (PT) glands are characterized by a low turnover and rarely undergo mitoses. However, in the presence of low calcium, high phosphorus, vitamin D deficiency, and uremia, PT cells leave quiescence. In the last decade, both new molecular and cellular mechanisms have been investigated in the pathophysiology of SHPT, between them the emerging role of the PT vitamin D receptor and calcium-sensing receptor. Furthermore, recent studies indicate that the fibroblast growth factor-23 may play a central role in the regulation of phosphate-vitamin D metabolism in CKD. Certainly, in the next future, these new insights into the pathogenesis of SHPT will give the possibility to improve the treatment of this condition in the CKD population.
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Calcio/metabolismo , Enfermedades Renales/metabolismo , Fosfatos/metabolismo , Humanos , Hiperparatiroidismo Secundario/etiología , Hiperparatiroidismo Secundario/metabolismo , Hiperparatiroidismo Secundario/terapia , Enfermedades Renales/fisiopatología , Enfermedades Renales/terapia , Deficiencia de Vitamina DRESUMEN
BACKGROUND/AIMS: HFE protein controls iron absorption and cycling, and HFE mutations influence iron status. The aim was to evaluate the effect of the HFE genotype on the need for iron and erythropoietin in Italian hemodialysis patients. METHODS: Ninety-six prevalent patients were evaluated at the time of enrolment and prospectively followed for 3 years. Patients were given r-HuEPO and Fe3+-gluconate according to guidelines. The HFE genotype was determined by restriction analysis. RESULTS: Three patients (3%) carried the C282Y mutation, 4 (4%) were homozygous and 18 (19%) heterozygous for the H63D mutation, and 71 (74%) were negative for both. At enrolment, subjects positive for HFE mutations had higher iron stores (ferritin 617 +/- 663 vs. 423 +/- 386 ng/ml, p = 0.05), were receiving less iron (82.5 +/- 66 vs. 110 +/- 154 mg/month, p = 0.05) and a lower r-HuEPO dosage (98 +/- 83 vs. 142 +/- 138 U/kg/week, p = 0.03). Consistently during the study period, patients positive for HFE mutations received a lower amount of r-HuEPO (94.5 +/- 63 vs. 186 +/- 344 U/kg/week, p = 0.01) and iron (97 +/- 63 vs. 121 +/- 68 mg/month, p = 0.07). Upon Cox regression analysis, after adjustment for confounding variables, the presence of HFE mutations was associated with a reduced risk of death (HR 0.6, 95% CI 0.34-1.03, p = 0.06). CONCLUSION: HFE mutations reduce the amount of r-HuEPO and iron necessary to support erythropoiesis in hemodialysis.
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Eritropoyesis , Eritropoyetina/uso terapéutico , Genotipo , Antígenos de Histocompatibilidad Clase I/genética , Proteínas de la Membrana/genética , Insuficiencia Renal/genética , Anciano , Femenino , Proteína de la Hemocromatosis , Humanos , Hierro/metabolismo , Italia , Masculino , Persona de Mediana Edad , Mutación , Estudios Prospectivos , Proteínas Recombinantes , Diálisis Renal , Insuficiencia Renal/terapiaRESUMEN
BACKGROUND/AIMS: Hyperferritinemia has been associated with cardiovascular mortality in hemodialysis patients. The aim of this study was to evaluate whether serum ferritin was affected by iron and oxidative status and by genetic factors (HFE mutations and the Ala9Val MnSOD polymorphism), and to assess the association between ferritin and cardiovascular damage evaluated by ecocolor-Doppler. METHODS: 63 hemodialysis patients were tested for HFE and MnSOD genotype by restriction analysis and oxidative status; vascular damage was assessed by measuring intima-media thickness, and by detecting plaques at carotid and femoral arteries. RESULTS: Ferritin was correlated with transferrin saturation (p = 0.003), decreased iron-specific serum antioxidant activity (p = 0.01), age (p = 0.03), and C282Y and H63D HFE mutations (p = 0.05), but not with the MnSOD polymorphism. Ferritin was associated with advanced vascular damage, as evaluated by the presence of plaques, both at carotid (p = 0.03) and femoral arteries (p = 0.001), the other risk factors being age and low albumin. Low iron-specific antioxidant activity was associated with carotid plaques (p = 0.03). CONCLUSION: In hemodialysis patients, hyperferritinemia reflects a relative increase in iron availability and a decrease in iron-specific antioxidant activity, is favored by HFE mutations, and represents a risk factor for advanced cardiovascular damage.