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Biomedical subjects

E Bognetti

Publications and source records attributed to E Bognetti.

33 records · Page 2Linked to original sources
PubMed1992

Protein intake and blood glucose as modulators of GFR in hyperfiltering diabetic patients.

Glomerular hyperfiltration has been claimed to be a risk factor for the development of diabetic nephropathy. Protein intake and hyperglycemia can both increase GFR in diabetic and normal subjects. Our study was designed to explore the relative importance of short-term changes in protein intake and glycemia on the modulation of renal hemodynamics in insulin-dependent diabetic (IDDM) patients with and without glomerular hyperfiltration. The renal hemodynamic response to a protein challenge was studied in eight hyperfiltering (HF) and eight normofiltering (NF) patients after a three week period of low or normal protein diet (LPD, NPD), each study being conducted twice, in random order, under conditions of prevailing hyperglycemia (H) and euglycemia (E). In HF patients GFR failed to increase significantly in response to protein challenge during NPD under conditions of either H or E (Baseline vs. 2 hr H: 151 +/- 4 vs. 155 +/- 6, NS; E 147 +/- 4 vs. 157 +/- 7 ml/min/1.73 m2, NS). A more normal response was restored following LPD with GFR increasing in all but one patient after challenge during H and in all patients during E (Baseline vs. 2 hr H: 130 +/- 7 vs. 145 +/- 8, P less than 0.07; E: 127 +/- 7 vs. 143 +/- 7 ml/min/1.73 m2, P less than 0.01). Changes in RPF paralleled the changes in GFR and filtration fraction remained stable under all study conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Impaired renal response to a meat meal in insulin-dependent diabetes: role of glucagon and prostaglandins.

The renal response to 100 g/1.73 m2 protein load in the form of a meat meal was studied in 19 normal subjects and 35 normoalbuminuric insulin-dependent diabetic patients (IDDs) under conditions of sustained euglycemia. The area under the glomerular filtration rate (GFR) curve rose above base line by 1,904 +/- 292 in normals and 502 +/- 237 ml/1.73 m2 in IDDs (P less than 0.01). The meat meal induced a greater increment in the area under the glucagon curve in normals (14,930 +/- 186 pg.ml-1.min-1) than in IDDs (7,227 +/- 67, P less than 0.01); similarly urinary excretion of prostaglandin E2 and 6-ketoprostaglandin F1 alpha rose by 119 and 98%, respectively, in normals but only by 2% (P less than 0.01 vs. normals) and 10% (P less than 0.01 vs. normals) in IDDs. The fractional albumin clearance rose by 102 and 251% in normals and IDDs, respectively. In five normal subjects indomethacin administration abolished the GFR, glucagon, prostaglandin, and albuminuric response to meat ingestion. Glucagon replacement under indomethacin treatment failed to restore these responses. In five diabetic patients, selected for having a flat glucagon and GFR response to a meat meal, replacement of glucagon to postprandial levels increased urinary vasodilatory prostaglandins and restored a normal GFR response. Thus in normal subjects renal vasodilatory prostaglandins appear to be the final effector of the renal hemodynamic and albuminuric response to a meat meal. The prostaglandin increase is likely to be mediated under physiological conditions by a glucagon rise, which, however, has no effect per se on renal hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Blood sugar response to administration of bran or guar added to pasta in children with type I diabetes].

Blood sugar profiles after administration of pasta with (PG) and without (P) guar have been evaluated in 30 young type I diabetic children. Maximum increase of blood sugar was observed at 30' (mean = 21 mg/dl) after P and at 90' (mean = 6 mg/dl) after PG. Maximum decrease in blood sugar levels was reached at 180' in both groups (50 mg/dl after P and 25 mg/dl after PG). Blood sugar level was significantly different only at 180'. No significant difference was observed analyzing rates of increase.

Blood Glucose↗
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

Early diagnosis of subclinical complications in insulin dependent diabetic children and adolescents.

212 insulin dependent young diabetics with mean age of 16 yr and mean diabetes duration of 9 yr, have been examined for prevalence of subclinical signs of microvascular disease. Prevalence of retinopathy is increased in subjects of older age when matched for diabetes duration. Subclinical abnormalities of peripheral nervous system, identified by neurophysiological techniques, are present in about 20% of patients. These abnormalities are mainly related to metabolic control as evaluated by HbA1c determination. Albumin excretion rate over 10 mcg/min is observed in about 40% of subjects and is related to increased blood pressure values and poor metabolic control.

Adolescent↗
PubMed1987

Changes in renal function in response to protein restricted diet in type 1 (insulin-dependent) diabetic patients.

Glomerular filtration rate, renal plasma flow and urinary albumin excretion rate were measured during insulin-induced euglycaemia in 12 male Type 1 (insulin-dependent) diabetic patients after a 3-week period of low protein diet (45 g/day) or a similar period on unchanged conventional diet (103 g/day). No changes in glycaemic control, indicated by home blood glucose profiles and serum fructosamine concentration, or in arterial pressure, were noted on either diet. On low protein diet, glomerular filtration rate was lower (p less than 0.001) in all patients, but there was no difference in renal plasma flow between low protein diet and normal protein diet; filtration fraction fell significantly on low protein diet (p less than 0.001). Fractional clearance of albumin was also lower (p less than 0.05) on low protein diet. This study suggests that reduction of dietary protein induces, independently of changes in plasma glucose and arterial pressure, modifications in glomerular filtration rate, filtration fraction and fractional clearance of albumin, which may be associated with a beneficial effect on the evolution of diabetic renal disease.

Adult↗
PubMed1987

Effect of protein-restricted diet on renal response to a meat meal in humans.

To study the influence of preceding dietary protein intake on the renal response to a protein meal we examined renal hemodynamic and excretory responses to a meat meal in six normal human subjects either taking their normal-protein diet (NPD, 75 +/- 5 g/day) or after 3 wk of a low-protein diet (LPD, 43 +/- 3 g/day; P less than 0.005). Glomerular filtration rate (GFR) was lower on LPD than on NPD (107 +/- 7 vs. 124 +/- 5 ml X min-1 X 1.73 M-2, respectively; P less than 0.01), as was renal plasma flow (RPF) (NPD, 666 +/- 44; LPD, 605 +/- 43 ml X min-1 X 1.73 M-2; P less than 0.05). Filtration fraction (FF) was not different (NPD, 0.19 +/- 0.01; LPD, 0.18 +/- 0.01). Urinary excretion of albumin was also lower after LPD than NPD (2.1 +/- 0.5 vs. 4.2 +/- 0.8 micrograms/min; P less than 0.05). After an 80-g protein meat meal, GFR rose to a ceiling significantly higher on NPD than on LPD (132 +/- 4.8 vs. 120 +/- 5.2 ml X min-1 X 1.73 M-2; P less than 0.02), even though the percent changes were greater on LPD than on NPD (12.7 +/- 3.3 vs. 6.6 +/- 1.5%, respectively; P less than 0.05). There was a rise in RPF that was entirely attributable to a fall in renal vascular resistance, and FF did not change. On both diets, oral protein loading produced a 200-300% increase in the urinary excretion and fractional clearance of albumin and IgG, but failed to alter that of beta 2-microglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Pancreatic polypeptide secretion after insulin infusion and protein meal in juvenile type 1 diabetic subjects.

An impaired pancreatic polypeptide response (PP) after hypoglycemia has been described in type I diabetic patients with overt autonomic neuropathy. Some authors have suggested that PP release might be useful as sensitive indicator of autonomic neuropathy. The meal test is safer and simpler than the insulin infusion test as PP stimulus. The aim of this study was to compare PP response to insulin infusion and protein meal test and to correlate these responses to the presence of measurable neuropathic disturbances. We thus studied 13 IDDM children and adolescents and 6 normal children. In diabetics the PP response to both tests was not different from that of the control subjects, but PP response to insulin infusion was inversely correlated to the duration of illness and was significantly lower in subjects with pathological heart rate response when compared to the control group. PP responses to the two stimuli were not correlated. We suggest that reduced PP response to hypoglycemia is an early sign of autonomic neuropathy as well as impairment of beat-to-beat variation when impaired PP response to meal test is still not evident.

Adolescent↗
PubMedDate not supplied

Cardiovascular and hormonal responses to cold pressor test in insulin-dependent diabetic adolescents with microalbuminuria.

Cardiovascular responses to cold pressor test and associated changes in blood concentrations of renin, aldosterone, and catecholamines were measured in 11 type I diabetic patients with microalbuminuria; 11 type I diabetic patients with normoalbuminuria matched for age, duration of diabetes, metabolic control; and in nine normal control subjects. Heart rate, renin, aldosterone, and catecholamines concentrations in diabetic patients and controls at baseline were similar, but higher mean blood pressure was evident in microalbuminuric than normoalbuminuric patients (p < 0.01) and controls (p < 0.05). Heart rate and mean blood pressure during cold pressor test in control subjects and type I diabetic patients increased significantly but similarly, regardless of the presence of microalbuminuria. Catecholamines, but not renin-aldosterone release, was associated to blood pressure modifications during the test. Peak values of mean blood pressure induced by cold test were positively correlated to baseline values in control subjects (r = 0.658, p < 0.05) and normoalbuminuric (r = 0.725, p < 0.01), but not microalbuminuric diabetics. These data suggest that the higher blood-pressure values at rest observed in microalbuminuric than normoalbuminuric diabetics are not associated with a higher cardiovascular response to cold hypertensive stimulus.

Adolescent↗
PubMedDate not supplied

Prevalence and correlations of early microvascular complications in young type I diabetic patients: role of puberty.

The prevalence and correlates of the early signs of renal, retinal and neurological microvascular complications were evaluated in 317 young patients with type I diabetes mellitus. Microalbuminuria was detected in 11% of patients and appeared to be strongly and positively related to HbA1c (p < 0.01) and less significantly to duration of diabetes (p < 0.02). Retinopathy was detected in 22.7% of patients and it was associated with duration of diabetes (p < 0.001). Peripheral neuropathy was detected in 18.5% of patients and there was a strong association with HbA1c (p < 0.01) and a weaker one with duration of diabetes (p < 0.05). Microalbuminuria was not detected in prepubertal patients while a similar frequency of retinopathy and neuropathy was observed in prepubertal and postpubertal patients. These results suggest that: 1) In short-term type I diabetic patients neuropathy is the most frequent microvascular complication, but after 10 years of diabetes, retinopathy exceeds the other complications; 2) Short-term metabolic control may influence the frequency of neuropathy and microalbuminuria but not retinopathy; 3) Puberty is involved in the appearance of microalbuminuria.

Adolescent↗
PubMedDate not supplied

Etiology, diagnosis, and prevention of renal involvement in insulin-dependent diabetes mellitus.

Overt diabetic nephropathy is a well-established clinical picture characterized by macroproteinuria and irreversible decline of glomerular function. The first phase of renal involvement has been widely investigated in the last decade in the hope to individuate early lesions. Five stages of glomerular damage have been identified by morphological abnormalities and clinical tests. Although renal hypertrophy, hyperfiltration, and microalbuminuria are present in all diabetics at onset, subsequent evolution shows different patterns: some patients may present no further progression, while others show a rapid and irreversible decline of kidney function. This suggests that other factors, i.e., risk factors, may play important roles in the renal involvement in diabetics. The predictive role of microalbuminuria and of hyperfiltration was investigated, and, so far, only an albumin excretion rate above 30 micrograms/min had been proved to be associated with a decline of renal function. Actually no practical hints can be given to prevent the disease apart from persistent strict glycometabolic control during the course of diabetes. Antihypertensive treatment can slow glomerular damage when overt diabetic nephropathy and hypertension are present. Aggressive treatment in the early phases of renal involvement might change the natural history of the disease.

Adolescent↗