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Biomedical subjects

G Mioni

Publications and source records attributed to G Mioni.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

Effects of successful renal transplantation on left ventricular mass.

Left ventricular hypertrophy is an independent cardiovascular risk factor in the general population and in patients with chronic renal failure. Relatively little is known about the effects of renal transplantation on left ventricular hypertrophy. The aim of this study was to determine the changes in left ventricular mass after successful renal transplantation and to evaluate the importance of some clinical, laboratory, and echocardiographic variables on the trend to left ventricular hypertrophy. Twenty-three patients with end-stage renal disease were studied by ambulatory blood pressure monitoring and echocardiography before and 2 years following renal transplantation. After 24 months of follow-up, all transplant recipients had adequate renal function (serum creatinine <2 mg/dL). At the end of the study, we observed a significant decrease in left ventricular mass and left ventricular mass index compared to the pretransplantation period. In renal transplant recipients, the prevalence of left ventricular hypertrophy significantly decreased (78% versus 44%, P < .03) after 2 years of follow-up. Systolic 24-hour blood pressure was the only predictor of left ventricular mass and of left ventricular mass index at 2 years after transplantation. In conclusion, successful renal transplantation produces a regression of left ventricular hypertrophy. This beneficial effect depends on a decrease in systolic pressure levels.

Adult↗
PubMedDate not supplied

Derangement of acid-base balance in uremia and under hemodialysis.

Uremic acidosis is due to impaired excretion of ammonium ions in the presence of unchanged acid production. However, the degree of acidosis is quite variable among uremic patients and pre-dialytic bicarbonate levels are mainly independent of dialytic base supply. These observations strengthen the suggestion that extra-renal mechanisms may play a significant role in controlling acid-base balance in uremic patients. The possible effects of diet, intestine, bone, intermediate metabolism, and the global acid-base balance are discussed. The metabolic and clinical effects of mild uremic acidosis are not well defined. In fact, no long-term clinical study have produced clear evidence for increased protein catabolism in humans. Some data provide evidence for reduced bone mineral content and osteomalacic lesions in uremic patients with severe acidosis. Overall, the impact of the present dialytic techniques on acid-base control is quite small, since no major difference is observed in uremic patients treated with different dialytic schedules. Furthermore, the base supply by dialysis does not seem to represent the main mechanism for acid-base correction by dialysis. In conclusion, at present time, metabolic acidosis of uremic patients is often mild and not accompanied by major symptoms. Probably, more attention needs to be paid to the possible noxious effect of over-correction of acidosis.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Surgical complications after kidney transplantation].

Chronic renal failure needs substitutive treatment such as haemodialysis and peritoneal dialysis for the patient to survive. Kidney transplantation (KTx) improves survival of the patient with chronic renal failure. Since the first KTx, performed by Merrill in Boston in 1959, advances in medical therapy, immunosuppressive therapy and refinements in surgical technique have improved the quality of life of the transplant patient. We present a review of the incidence, diagnosis and therapy of surgical complications after KTx reported in the literature and a retrospective analysis of 297 consecutive cadaveric donor kidney transplants done in our institution from September 1993 to September 2002. Vascular complications represent 5-10% of postoperative complications. Our experience showed an incidence of 1.7% renal artery thrombosis, 1.4% renal vein thrombosis, 1.7% renal artery stenosis, 1.4% arterial rupture due to fungal arteritis, 0.7% spontaneous graft ruptures and 12% lymphoceles. Urological complications account for 10-15% of postoperative complications. In our series we found an incidence of 7.4% urinary leakage, 2.7% urinary obstruction and 3% urinary reflux. Gastrointestinal complications represent 16% of postoperative complications. Our series showed 1% pancreatitis with an overall mortality of 33% and an incidence of 1.7% intestinal perforations. Surgical complications still represent a challenge that increments morbidity and mortality among kidney transplant recipients. Data shown may offer some guidance on how to deal with early and late post-transplant surgical complications.

Arteritis↗
PubMedDate not supplied

[Cardiovascular disease after renal transplantation].

Cardiovascular disease is the leading cause of morbidity and mortality following renal transplantation. Because many renal transplant recipients die with functioning grafts, deaths resulting from cardiovascular disease have became an increasingly important cause of graft loss, particularly after the first post-transplantation year. Moreover, a contribution of some cardiovascular risk factors to renal allograft dysfunction has been demonstrated. A number of observational studies suggest that cardiovascular disease is more common in renal transplant patients than in the general population. The excessive risk for cardiovascular disease is related to a high prevalence and accumulation of atherogenic risk factors before and after transplantation. Hypertension, post-transplantation diabetes and hyperlipidemia are well-recognized risk factors for the development of cardiovascular events after renal transplantation and are strongly associated with immunosuppressive therapy. Progressive renal dysfunction may also influence the risk of cardiovascular complications after renal transplantation. The elevated risk may also be caused by non- traditional risk factors such as anaemia, adhesion molecules, hyperhomocysteinemia, microinflammatory state, abnormal coagulation and oxidative stress. To prevent post-transplantation cardiovascular disease it is crucial to define the etiological risk factors. Some risk factors can be modified, and for some of these, there is strong evidence from studies in the general population that intervention improves survival. Given the significant morbidity and mortality of cardiovascular disease in renal transplant recipients, aggressive treatment intervention for potentially modifiable factors are strongly advocated after transplantation. In addition to treatment intervention, risk management should also involve tailoring the immunosuppressive regimen to minimize both direct and indirect cardiovascular risks. In this article we attempted to review and quantify the post-transplant risk factors for cardiovascular disease as well as offer suggestions on optimizing the therapy or treatment strategies to minimize the risk of cardiovascular complications in renal transplant patients. Reduction of cardiovascular morbidity and mortality can improve not only the life expectancy and quality of life of the transplant recipients but also their graft function and survival.

Anemia↗