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Biomedical subjects

A Aroldi

Publications and source records attributed to A Aroldi.

At least 55 records · Page 3Linked to original sources
PubMed1979

Thiazide diuretics in renal hypercalciuria.

Forty-six renal hypercalciuric normocalcaemic patients were treated with hydrochlorothiazide (50mg/day) and amiloride (5 mg/day), both to reduce new stone formation and to suppress parathyroid hyperfunction. A reduction of hypercalciuria and suppression of parathyroid hyperactivity were observed in 41 patients, while in the other five patients no evidence of parathyroid suppression was found and hypercalcaemia developed. Four of five patients underwent parathyroidectomy which was followed by a normalisation of biochemical signs of hyperparathyroidism. These results suggest that the appearance of hypercalcaemia in renal hypercalciuric patients during hydrochlorothiazide/amiloride treatment may be of diagnostic value in unmasking pharmacologically non-suppressible normocalcaemic hyperparathyroidism.

Adult↗
PubMedDate not supplied

High prevalence, low pathogenicity of hepatitis G virus in kidney transplant recipients.

BACKGROUND: Prevalence and pathogenicity of hepatitis G virus infection in long-term renal transplant recipients, are not fully known. AIM: To evaluate long-term impact of HGV infection on liver disease of renal transplanted patients. PATIENTS AND METHODS: A total of 155 hepatitis B surface antigen negative kidney transplant recipients, followed for a mean of 11 years after renal transplantation, were studied. Of these 48 (31%) patients had persistently elevated serum aminotransferase values. Frozen serum samples were tested for HGV-RNA and HCV-RNA by nested reverse transcribed polymerase chain reaction, and for anti-hepatitis G virus and anti-hepatitis C virus by enzyme-linked immunosorbent assay Hepatitis C virus-RNA was typed by a line probe assay and quantified by a branched DNA signal amplification assay RESULTS: Hepatitis G virus-RNA was detected in 37 (24%) patients and anti-hepatitis G virus in another 26 (17%). Seventy (45%) patients had serum anti-hepatitis C virus and 63 of these (90%) had serum hepatitis C virus-RNA. Hepatitis G virus-RNA positive and negative patients were similar in terms of age, sex, duration of dialysis, rate of transfusion, chronic liver disease, rate of hepatitis C virus infection and immunosuppressive therapy. Fifteen (41%) hepatitis G virus-RNA seropositive patients were hepatitis C virus co-infected. Hepatitis C virus-RNA levels were significantly lower in the 15 hepatitis C virus/hepatitis G virus co-infected patients than in the 48 patients with hepatitis C virus infection only (2.2 vs 10.8 MEq/ml, p = 0.02). Only 3 hepatitis G virus carriers had persistently elevated alanine aminotransferase compared to 29 hepatitis C virus carriers (14% vs 60%, p < 0.001), 10 patients co-infected with both hepatitis G virus and hepatitis C virus, and in 6 patients with neither infection (67% vs 8%, p < 0.001). CONCLUSIONS: Hepatitis G virus infection is common among kidney transplant patients, it carries a low risk of chronic liver disease even in long-term follow-up. Low levels of hepatitis C virus-RNA found in hepatitis G virus carriers suggest an interaction between these two viruses in immunosuppressed patients.

Adult↗
PubMedDate not supplied

[Bone complications of renal transplantation. How to identify and prevent them].

Bone disease is a very frequent complication after renal transplantation (RTx). The main features of transplant bone disease include the osteopenic-osteoporotic syndrome, often complicated by fractures, avascular osteonecrosis of bones, bone pain syndrome and growth retardation in the children. The bone loss is greater during the first 12 months after RTx and can reach the osteoporotic range in above 40% of patients, with a fracture rate of 2-3% per year. The story of bone disease over the long pre-uremic and uremic period is one of the main causal factors. After RTx, glucocorticoid therapy seems to play the major causal role. Much more disputed is the role of the other immunosuppressive drugs, of persistent secondary hyperparathyroidism, and age. Hypophosphatemia and some genetic factors could also affect bone loss after RTx. Diabetic patients are particularly prone to develop bone disease after RTx. The main prophylactic interventions consist in the optimal control of hyperparathyroidism during the pre-transplant period, prescribing parathyroidectomy for autonomous hyperparathyroidism, not-responding to medical therapy. After RTx, both bisphosphonate and vitamin D metabolites, variably associated with calcium supplementation, have been demonstrated to have some beneficial effect on bone loss, at least in the first year after RTx. However, there are no data about the possible efficacy of these treatments on fracture rate.

Bone Diseases, Metabolic↗
PubMedDate not supplied

[Hepatitis C virus and renal transplantation].

Liver disease has emerged as an important cause of morbidity and mortality after renal transplantation (RT). Hepatitis C virus (HCV) is the leading cause of liver disease after RT. The impact of HCV infection on patient and graft survival is currently a major concern. Retrospective studies with appropriate follow-up have mainly demonstrated that HCV positive patients have greater mortality compared to HCV negative recipients after RT. Novel investigations by large databases (United States Renal Data Systems (USRDS)) have shown that recipients of donor HCV-positive kidneys are at an independently increased risk of mortality, adjusted hazard ratio 2.12 (95% confidence interval (95% CI), 1.72-2.87, p<0.001); there was no evidence that any subgroup was less affected. With appropriate informed consent, the use of a renal graft from an HCV positive donor could be offered to an HCV infected recipient. Many renal transplant candidates have satisfactory virological responses to antiviral therapy; the persistence of HCV clearance over a prolonged follow-up after RT has been recently noted. Further prospective studies are needed to define better the course of HCV infection among renal allograft recipients.

Hepacivirus↗