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Biomedical subjects

G Maschio

Publications and source records attributed to G Maschio.

At least 19 recordsLinked to original sources
PubMed1998

Angiotensin converting enzyme inhibitors in nondiabetic renal disease.

The class of antihypertensive agents that act by blocking angiotensin II has been shown in several experimental models to have the interesting ability to protect the kidney. In patients with nondiabetic renal disease, a number of controlled clinical trials have shown angiotensin converting enzyme inhibitors to achieve a better control of blood pressure and significantly reduce the rate of progression of renal failure in comparison with conventional agents. In addition, treatment with angiotensin converting enzyme inhibitors has helped to achieve new information on the optimal blood pressure target to be reached in order to protect the residual renal function maximally.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

A prospective, randomized trial of two antibiotic regimens in the treatment of peritonitis in CAPD patients: teicoplanin plus tobramycin versus cephalothin plus tobramycin.

A multicentre, comparative, randomized study was performed to compare the efficacy and tolerability of two antibiotic regimens in the treatment of peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients: teicoplanin plus tobramycin versus cephalothin plus tobramycin. After informed consent had been obtained, 68 patients were randomized prospectively to receive either teicoplanin plus tobramycin or cephalothin plus tobramycin. Patients were followed throughout the study and for up to 4 weeks after the end of treatment, when clinical and microbiological parameters were assessed again. The incidence of clinical failure was 4.6 times higher in the cephalothin plus tobramycin group than in the teicoplanin plus tobramycin group (7/28 versus 2/37; P < 0.05). There was no significant difference in bacterial eradication between the two groups. Local and systemic tolerability were good for both regimens. The study shows that teicoplanin plus tobramycin is more effective than cephalothin plus tobramycin and might become a 'first-line' treatment for peritonitis in CAPD patients.

Aged↗
PubMed1997

Diuretics in hypertension.

Despite the consistent reduction in the incidence of stroke and coronary events demonstrated in numerous clinical trials in young and elderly hypertensive subjects, the use of diuretics has declined as a first-line therapy in hypertension. The metabolic dose-dependent side effects and the increasing availability of new drugs appear the two main reasons for the decline. Although the neutral metabolic effects and the perception of a more physiological approach to hypertension has been advocated with the newer agents, no definite proof has been reported on the long-term effects on cardiovascular end-points. Many of adverse effects of diuretics can be limited by the use of low doses. For this reason, as well as their efficacy, safety, and cost-effectiveness, diuretics should remain a first-line therapy for hypertensive patients.

Diuretics↗
PubMed1997

Long-term progression of chronic renal insufficiency in the AIPRI Extension Study. The Angiotensin-Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group.

The Angiotensin-converting-enzyme Inhibition on Progressive Renal Insufficiency (AIPRI) Study showed that the ACE inhibitor benazepril provides protection against loss of renal function in patients with chronic renal insufficiency (CRI) caused by various renal diseases. As a result of unexpectedly low mortality in the placebo group, there was a substantial imbalance in mortality during the course of this study (8 patients on benazepril vs. 1 on placebo). The aim of the extension study was to follow-up the patients from the AIPRI core study until autumn 1996, focusing on CRI progression and mortality. Data collection was post hoc. Patients were treated according to investigators' usual practices, without knowledge of the core study trial medication or (initially) the core trial results. A new primary efficacy parameter was defined as the time from the start of core study treatment to the occurrence of the first event in the combined composite end-point of dialysis, renal transplantation or death related to renal disease. Serial serum creatinine levels and all-cause mortality were also recorded. The median total follow-up for core + extension periods was 6.6 years. Many patients from both treatment groups (64% on benazepril and 61% on placebo) received ACE inhibitors during follow-up. In the intention-to-treat analysis of the core + extension data, only 79 of 300 patients from the benazepril group, compared to 102 of the 283 patients from the placebo group needed dialysis or renal transplantation, or died related to renal disease (P < 0.013, log-rank test). The mortality imbalance seen in the core trial was not evident with the longer follow-up (25 deaths in the benazepril and 23 in the placebo group, before dialysis). These data clearly demonstrate a long-term beneficial effect in patients randomized to take benazepril during the core study, but because treatment during the extension period was not randomized, the results of this intention-to-treat analysis need to be interpreted with care.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. The Angiotensin-Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group.

BACKGROUND: Drugs that inhibit angiotensin-converting enzyme slow the progression of renal insufficiency in patients with diabetic neuropathy. Whether these drugs have a similar action in patients with other renal diseases is not known. We conducted a study to determine the effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of renal insufficiency in patients with various underlying renal diseases. METHODS: In a three-year trial involving 583 patients with renal insufficiency caused by various disorders, 300 patients received benazepril and 283 received placebo. The underlying diseases included glomerulopathies (in 192 patients), interstitial nephritis (in 105), nephrosclerosis (in 97), polycystic kidney disease (in 64), diabetic nephropathy (in 21), and miscellaneous or unknown disorders (in 104). The severity of renal insufficiency was classified according to the base-line creatinine clearance: 227 patients had mild insufficiency (creatinine clearance, 46 TO 60 ml per minute), and 356 had moderate insufficiency (creatinine clearance, 30 to 45 ml per minute). The primary end point was a doubling of the base-line serum creatine concentration or the need for dialysis. RESULTS: At three years. 31 patients in the benazepril group and 57 in the placebo group had reached the primary end point (P<0.001). In the benazepril group, the reduction in the risk of reaching the end point was 53 percent overall (95 percent confidence interval, 27 to 70 percent), 71 percent (95 percent confidence interval, 21 to 90 percent) among the patients with mild renal insufficiency, and 46 percent (95 percent confidence interval, 12 to 67 percent) among those with moderate renal insufficiency. The reduction in risk was greatest among the male patients; those with glomerular diseases, diabetic nephropathy, or miscellaneous or unknown causes of renal disease; and those with base-line urinary protein excretion above 1 g per 24 hours. Benazepril was not effective in patients with polycystic disease. Diastolic pressure decreased by 3.5 to 5.0 mm Hg in the benazepril group and increased by 0.2 to 1.5 mm Hg in the placebo group. CONCLUSIONS: Benazepril provides protection against the progression of renal insufficiency in patients with various renal diseases.

Adult↗
PubMed1996

Detection of two different nonsense mutations in exon 44 of the PKD1 gene in two unrelated Italian families with severe autosomal dominant polycystic kidney disease.

Sixty-seven Italian patients with autosomal dominant polycystic kidney disease (ADPKD) were screened for mutations in the PKD1 gene. We used PCR, heteroduplex and single-strand conformation polymorphism DNA analysis, and automated DNA sequencing for exons 35, 36, 38, 44 and 45. We detected abnormal heteroduplexes in affected individuals from two unrelated families with clinically severe ADPKD phenotype. These changes were absent in other, unaffected members, as well as in the probands of the other families studied. DNA sequencing revealed in both cases different C to T transitions in exon 44, which created premature stop codons. Both mutations altered restriction sites, and the abnormal patterns were observed in all the affected family members. RT-PCR performed on lymphocyte mRNA showed that both the mutant and the normal transcript are represented. To our knowledge these are the first nonsense mutations described in the PKD1 gene.

Exons↗
PubMed1995

A novel nonsense mutation in the PKD1 gene (C3817T) is associated with autosomal dominant polycystic kidney disease (ADPKD) in a large three-generation Italian family.

We have looked for disease-causing mutations in the PKD1 gene in 20 unrelated ADPKD probands from northern Italy, all members of families in which our previous studies had indicated linkage to PKD1. Using PCR with primer pairs located in the 3' unique region of the gene and heteroduplex DNA analysis, we have detected novel aberrant bands in five affected individuals from the same family, which were absent in 13 other unaffected family members. Cloning and automated DNA sequencing revealed a C to T transition at nucleotide position 3817 of the published cDNA sequence, which created a premature stop codon. The mutation destroyed a MspA1I restriction site, and the abnormal restriction pattern was observed on genomic DNA from all the affected family members. RT-PCR and restriction analysis performed on peripheral white blood cell mRNA showed that in the affected members, both the mutant and the normal transcript are represented. This mutation was not found in the probands of the other families studied. To our knowledge, this is the first nonsense mutation described in the PKD1 gene.

Adult↗
PubMed1995

Erythropoietin and systemic hypertension.

Systemic hypertension has been reported to develop, or to worsen, in 20-30% of patients treated with recombinant human erythropoietin (r-HuEPO) worldwide. The greatest increases in blood pressure affect day-time systolic and night-time diastolic blood pressure. Hypertension may develop in some patients as early as 2 weeks and in others as late as 4 months after the start of r-HuEPO treatment. In haemodialysis patients with systemic hypotension, r-HuEPO usually induces a 10% increase in blood pressure, with no significant change in the frequency of hypotensive episodes. Several risk factors for the development, or worsening, of hypertension after r-HuEPO therapy have been identified. They include the presence of pre-existing hypertension, rapid increase in haematocrit, a low baseline haematocrit before r-HuEPO administration, high doses and i.v. route of administration, the presence of native kidneys, a genetic predisposition to hypertension, and possibly a younger age. There are several potential mechanisms by which r-HuEPO therapy may increase blood pressure in haemodialysis patients. They include increased blood viscosity; the loss of hypoxic vasodilation; the activation of neurohumoral systems (catecholamines, the renin-angiotensin system); and especially a direct vascular effect. This last mechanism is supported by several data, and many factors may be involved in its pathogenesis (an increased cell calcium uptake; an imbalance in local vasoactive agents, with increased synthesis of ET-1; a mitogenic effect; and a platelet-dependent mechanism).

Blood Viscosity↗
PubMed1995

Gene linkage analysis and DNA based detection of autosomal dominant polycystic kidney disease (ADPKD) in a newborn infant. Case report.

Bilateral polycystic kidneys were detected by ultrasound at 23 weeks gestation in a male fetus. Bilateral renal cysts were subsequently also found in the asymptomatic propositus' mother and grandmother, suggesting the diagnosis of autosomal dominant polycystic kidney disease (ADPKD). The renal ultrasonograms showed cortical cysts with normal or decreased-sized kidneys. Renal function was normal. Seven available members of the family were genotyped for flanking DNA markers tightly linked to the PKD1 gene on chromosome 16p, and for a polymorphism close to a second putative disease gene (PKD2) on chromosome 2. The genetic linkage approach allowed us to detect with a high degree of accuracy the ADPKD1 at risk chromosome in the three patients, as well as in a 28-year-old unaffected female. This report illustrates the feasibility and the usefulness of recent molecular genetic strategies for diagnostic purposes in ADPKD, especially when clinical and radiological data are atypical. Furthermore, it also confirms that early or very early onset forms of the disease are not uncommon, and should be considered in the differential diagnosis of childhood cystic disease.

Blotting, Southern↗
PubMed1995

Renal reserve in patients with solitary kidneys.

The first part of this article focuses on the risk of functional deterioration in subjects with solitary kidneys; the long-term clinical outcome of various subgroups of patients is reviewed. Thereafter, the pathophysiology of the renal functional reserve in subjects with a 50% reduction in renal parenchyma and the results coming from studies eliciting the renal reserve in these subjects are summarized. Finally, the clinical significance of the renal functional reserve and its usefulness in clinical practice are critically discussed.

Glomerular Filtration Rate↗