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Biomedical subjects

G C Viberti

Publications and source records attributed to G C Viberti.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effect of low protein diet on the renal response to meat ingestion in diabetic nephropathy.

We measured the renal haemodynamic and proteinuric response to a meat meal (MM) in ten persistently proteinuric insulin-dependent diabetic patients in a randomized cross-over study of 3 weeks on low protein diet (LPD) or normal protein intake (NPD). On LPD, protein intake (0.64 +/- 0.05 vs 1.15 +/- 0.09 g kg-1 body weight (BW) per day, P less than 0.001), plasma urea (6.6 +/- 1.3 vs 11.0 +/- 2.0 mmol l-1, P less than 0.01) and urea appearance (0.06 +/- 0.01 vs 0.16 +/- 0.03 gN kg-1 body weight per day, P less than 0.001) were lower. Baseline glomerular filtration rate (GFR), renal plasma flow (RPF) and renal vascular resistance (RVR) were similar on the two diets and there were no significant average changes in these variables after the meat meal on either diet (NPD, before vs after MM: GFR: 67 +/- 11 vs 71 +/- 13 ml min-1 1.73 m-2; RPF: 479 +/- 70 vs 512 +/- 81 ml min-1 1.73 m-2; RVR: 181 +/- 45 vs 179 +/- 52 mmHg min-1 l-1); (LPD, before vs after MM: GFR: 64 +/- 10 vs 67 +/- 11 ml min-1 1.73 m-2; RPF: 506 +/- 60 vs 533 + 52 ml min-1 1.73 m-2; RVR: 151 +/- 28 vs 146 +/- 32 mmHg min-1 l-1). However, all patients with baseline GFR above 60 ml min-1 1.73 m-2 showed a GFR rise in response to the meat meal on both diets, while patients with lower baseline values tended to reduce their GRF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Diabetic renal disease in type 1 diabetes: aetiology and prevention.

Diabetic renal disease affects a subset of about 35% of patients with Type 1 diabetes and is characterized by a triad comprising increased albuminuria, arterial pressure, and volume fraction of the mesangium. This leads to a decline in the glomerular filtration rate and ultimately end-stage renal failure or premature cardiovascular mortality. Individuals at risk can be detected before the development of persistent proteinuria by screening for microalbuminuria which has proved predictive of clinical nephropathy in about 80% of cases. Microalbuminuria is often accompanied by subclinical increases in arterial blood pressure and plasma lipid levels and is usually not apparent until 5 years after stabilization of newly diagnosed diabetes. This latter finding suggests that microalbuminuria is an indicator of early disease rather than a marker of susceptibility to it. Recent evidence suggests that diabetic renal disease may be linked to a familial, possibly genetically determined, predisposition to arterial hypertension or to some factor closely related to the risk of hypertension. This underlying predisposition may be one of the mechanisms leading to severe glomerular damage and may help to explain why clinical renal disease only occurs in a subset of diabetic patients. A number of therapeutic interventions, ranging from strict blood glucose control to low-protein diet and angiotensin-converting enzyme inhibition are effective in reducing or preventing further increases in microalbuminuria. If current long-term trials confirm that treatment of microalbuminuric diabetic patients prevents the onset of heavier persistent proteinuria secondary prevention of diabetic renal failure may become possible. The current criteria for diagnosis of diabetic nephropathy will then require revision.

Albuminuria↗
PubMed1991

Risk factors for renal and cardiovascular disease in diabetic patients.

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.

Albuminuria↗
PubMed1989

Restriction of dietary protein and progression of renal failure in diabetic nephropathy.

In a study of the effect of a low-protein diet on the progression of renal disease 19 insulin-dependent diabetic patients with persistent clinical proteinuria were observed for 12-39 (mean 29) months while they were on a normal-protein diet (1.13 [0.06] g/kg per day), then for 12-49 (mean 33) months on a low-protein diet (0.67 [0.03] g/kg per day). The low-protein diet had no adverse effect on nutrition or glycosylated haemoglobin concentration. Mean supine blood pressure (BP) fell slightly on the low-protein diet and was probably due to the start or modification of antihypertensive medication in 9 patients. The mean rate of decline in glomerular filtration rate fell from 0.61 (SEM 0.14) ml/min per month with the normal-protein diet to 0.14 (0.08) with the low-protein diet, and this effect remained highly significant after adjustment for blood pressure, energy intake, and glycosylated haemoglobin. The rise in the fractional clearance of albumin during a normal-protein diet stopped with the low-protein diet, and there was a significant fall in albumin excretion from 467 (95% CI 234-895) micrograms/24 h on the normal-protein to 340 (138-719) on the low-protein diet. Thus, a low-protein diet, with its reduction in protein and possibly other dietary components such as phosphate or fat, seems to retard the rate of decline of glomerular filtration rate in diabetic nephropathy independently of blood pressure changes and glycaemic control.

Adult↗
PubMed1989

Plasma lipid and coagulation factor concentrations in insulin dependent diabetics with microalbuminuria.

OBJECTIVE: To determine whether insulin dependent diabetics with microalbuminuria have significant abnormalities in concentrations of lipoproteins, apolipoproteins AI and B, fibrinogen, and clotting factor VII which could result in increased cardiovascular risk. DESIGN: Case-control study. SETTING: Outpatient department of a metabolic ward. PATIENTS: Group of 20 insulin dependent diabetics with urinary albumin excretion rates greater than 30 micrograms/min (microalbuminuria) and 20 individually matched insulin dependent diabetics with normal urinary albumin excretion rates (below 30 micrograms/min) matched for age, sex, and duration of diabetes. INTERVENTIONS: Fasting venous blood samples were taken for determination of concentrations of glucose, glycated haemoglobin, lipoproteins, apolipoproteins AI and B, fibrinogen, and factor VII. Height, weight, arterial pressure, and usual insulin dose were recorded, and each patient was given a dietary questionnaire to be completed at home. END POINT: Comparison of blood pressure and concentrations of lipoproteins, apolipoproteins AI and B, and fibrinogen in the diabetics with microalbuminuria and the controls. MEASUREMENTS AND MAIN RESULTS: Patients with microalbuminuria had significantly higher concentrations of low density lipoprotein cholesterol (mean 3.33 (SE 0.20) v 2.84 (0.12) mmol/l) and very low density lipoprotein cholesterol (0.30 (0.05) v 0.17 (0.03) mmol/l) than controls but significantly lower concentrations of high density lipoprotein 2 subfraction cholesterol (0.32 (0.04) v 0.54 (0.04) mmol/l). Concentrations of total triglyceride (1.11 (0.14) v 0.68 (0.08) mmol/l), very low density lipoprotein triglyceride (0.56 (0.10) v 0.30 (0.05) mmol/l), apolipoprotein B (0.88 (0.06) v 0.67 (0.03) g/l) and fibrinogen (2.2 (0.1) v 1.9 (0.1) g/l), and diastolic arterial pressure (80 (2) v 74 (2) mm Hg), were also higher in patients with microalbuminuria. CONCLUSIONS: Cardiovascular risk factors--namely, disturbances in lipoprotein and apolipoprotein concentrations, increased fibrinogen concentration, and increased arterial pressure--are already present in insulin dependent diabetics with microalbuminuria. The increased risk of coronary heart disease in patients with clinical proteinuria may result from prolonged exposure to these risk factors, which are present before any impairment of renal function.

Albuminuria↗
PubMed1989

Interventions based on microalbuminuria screening and low-protein diet in the treatment of kidney disease of diabetes mellitus.

Microalbuminuria in insulin-dependent diabetics appears to indicate early renal damage rather than susceptibility to it, yet a series of relatively small, short-term intervention studies in insulin-dependent diabetes mellitus patients have already demonstrated reduction in albumin excretion rates or arrest in the increase of fractional clearance of albumin. Treatments have ranged from the use of angiotensin-converting enzyme inhibitors aimed at lowering BP to the use of diets restricted to 0.5 to 0.6 g/kg protein and strict blood glucose control by intensified insulin treatment. Large, long-term intervention studies of cohorts of insulin-dependent and non-insulin-dependent diabetic patients with microalbuminuria are now needed to assess the effects of the different modalities of care on the development of persistent proteinuria, end-stage renal disease, and cardiovascular mortality as well as associated quantitative changes in the renal structure.

Albuminuria↗
PubMed1989

Glomerular hyperfiltration and urinary prostaglandins in type 1 diabetes mellitus.

In order to determine whether glomerular hyperfiltration in diabetes is related to renal prostaglandin production we have studied the urinary excretion of PGE2, 6-keto-PGF1 alpha, and TXB2 in two sex, age and duration of diabetes matched groups of 9 and 10 Type 1 diabetic patients with either normal (mean 121, range 105-129 ml min-1 1.73 m-2) or supranormal glomerular filtration rate (154, 135-206 ml min-1 1.73 m-2). A group of 15 matched healthy volunteers served as control subjects. Urine was collected overnight for an uninterrupted period of at least 6 h. All studies in the patients were performed during insulin-induced sustained euglycaemia to prevent the confounding effect of variable degrees of blood glucose control on urinary prostaglandin excretion. Blood pressure was normal in all subjects. Urinary excretion of 6-keto-PGF1 alpha was significantly higher in the patients with glomerular hyperfiltration (median 17.1, range 4.5-33.6 ng h-1) than in those without (8.8, 1.5-13.8 ng h-1; p less than 0.05) or in normal control subjects (9.6, 5.2-15.5 ng h-1; p less than 0.05). No significant differences were found in the excretion rates of PGE2 and TXB2 between the three groups. Under conditions of controlled plasma glucose and insulin concentrations the urinary excretion of 6-keto-PGF1 alpha, the stable breakdown product of PGI2, a compound of endothelial, possibly glomerular, origin was elevated only in the diabetic patients with glomerular hyperfiltration.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Patterns of hyperinsulinaemia in type 1 diabetic patients with and without nephropathy.

The prevalence and patterns of insulinaemia in five groups of patients with Type 1 diabetes have been reinvestigated using a free insulin assay which minimizes in vitro redistribution of the free and antibody-bound insulin components. In 18 diabetic patients managed by conventional insulin injection treatment and 19 patients treated by continuous subcutaneous insulin infusion (CSII), the mean 24-h serum free insulin level exceeded a non-diabetic reference range in 78% (injections) and 68% (CSII). Twenty-four-hour profiles showed that hyperinsulinaemia occurred in the basal state before meals and at night, but not immediately post-prandially. The serum free insulin concentration at 0800 h, 1200 h, and 1600 h was significantly (p less than 0.001) correlated with mean 24-h free insulin in injection-treated and CSII patients, and samples at one of these time-points may thus provide a simple, single measure of integrated insulinaemia for population studies. There was no significant difference in 24-h mean free insulin levels in 7 patients randomly crossed-over between injection treatment and CSII, but the profiles had a more physiological pattern during CSII, with a mean post-prandial serum free insulin level which was significantly higher on CSII than injections (mean +/- SE = 37.2 +/- 3.1 vs 26.9 +/- 2.5 mU l-1, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Hypertension and microalbuminuria as predictors of diabetic nephropathy.

Renal disease affects approximately 35% of insulin-dependent diabetic patients with a maximal incidence of approximately 25 per 1 000 patient-years after a duration of about 16 years, declining thereafter to less than 7 per 1 000 patient-years after 35 years of diabetes and suggesting that only a particular subset of patients is at risk. The renal disease is characterized by a triad comprising increased albuminuria, arterial pressure and volume fraction of mesangium and leads to a decline in the glomerular filtration rate and ultimately to end stage renal failure or premature cardiovascular mortality. Individuals at risk can be detected before the development of persistent proteinuria by screening for microalbuminuria which has proven predictive of clinical nephropathy in about 80% of cases. Microalbuminuria is accompanied by subclinical increases in arterial blood pressure and plasma lipids and may be associated with increased glomerular filtration rate. It is not usually apparent within the first five years of diagnosis of diabetes. Microalbuminuria thus appears to be a marker for the presence of early renal disease rather than a predictor of susceptibility to it and its many associations indicate it to be a marker of systemic rather than merely renal disease. Recent evidence suggests that diabetic renal disease may be linked to a familial, possibly genetically determined predisposition to arterial hypertension or to some factor closely related to the risk of hypertension. Such a predisposition may help to explain why clinical renal disease occurs in only a subset of diabetic patients.

Albuminuria↗
PubMed1988

Microalbuminuria in non-insulin-dependent diabetes: its prevalence in Indian compared with Europid patients.

Non-insulin-dependent diabetes mellitus is strikingly common in British Indians, but their susceptibility to diabetic complications is unknown. The ratio of albumin to creatinine concentrations was measured in samples of the first urine voided in the morning in 154 Indian and 82 Europid patients with non-insulin-dependent diabetes and in a control group of 129 non-diabetic Indians. The ratio was significantly higher in the Indian patients than in the Europid patients and the Indian controls. There were no significant correlations between the logarithm of the albumin: creatinine ratio and age, known duration of diabetes, haemoglobin A1 concentration, or body mass index within either diabetic group. Hypertension and raised albumin:creatinine ratio were significantly associated, and significant correlations were seen between the logarithm of the albumin:creatinine ratio and systolic and diastolic blood pressures in the Indian but not the Europid diabetics. Because of the high prevalence of diabetes at a relatively early age in Indians, nephropathy may emerge as an important clinical problem.

Adult↗