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Biomedical subjects

T Hannedouche

Publications and source records attributed to T Hannedouche.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Value of the analysis of pulmonary venous flow in the evaluation of hemodynamics in dialysed patients].

The aim of this study was to assess the value of analysis of pulmonary venous flow in the evaluation of the haemodynamic status of patients with chronic renal failure with normal left ventricular function, treated by haemodialysis. Pulmonary venous flow was recorded immediately before and after haemodialysis in 27 patients with chronic renal failure and a mean age of 44 years. Three groups of patients were defined according to the change in mitral E/A ratio: Group I (E/A < 1 before and after dialysis), Group II (E/A > 1 before and < 1 after dialysis) and Group III (E/A > 1 before and after dialysis). There was a significant difference between these subgroups before dialysis with respect to age, S, D, VTI S, Total VTI, VTI S/Total (p < 0.05). However, because the values overlapped, only a VTI S/Total ratio greater than 59% differentiated patients in Group II from those in group III (p < 0.05). After dialysis, the change in S/D and VTI S/Total ratios increased in Groups I and II and decreased in Group III. The authors concluded that 63% of patients without LV dysfunction on haemodialysis have abnormalities of relaxation which are latent in 47% of cases due to increased filling pressures diagnosed by a VTI S/Total ratio > 59% or simply because the patients are over 50 year old.

Female↗
PubMed1999

[Tubular hypokalemia of genetic origin].

Recent progress in molecular genetics have improved our understanding of the pathophysiology of several inherited diseases characterized by a renal hypokalemia. Some of these diseases result from inactivating mutations on the main cotransports involved in the reabsorption of sodium, namely the Gitelman and Bartter syndromes, that clinically mimics diuretic abuse with mild hypovolemia and low or normal blood pressure. Conversely some affections eventually lead to an increase in sodium reabsorption with hypervolemia and arterial hypertension: Liddle syndrome, apparent mineralocorticoid excess and dexamethasone suppressible hyperaldosteronism.

Animals↗
PubMed1998

[The "absolute" cardiovascular risk].

Diagnosis of hypertension and the thresholds for therapeutic intervention are usually defined by arbitrary values, changed along time by the Societies of Hypertension. Absolute cardio-vascular risk takes into account the full spectrum of independent cardio-vascular risk factors that have been identified by large observational epidemiological studies including Framingham Study. The advantages and the limits of the "absolute" cardiovascular risk concept and its applicability to medical practice are extensively discussed in this paper.

Alcoholism↗
PubMed1998

[Absolute cardiovascular risk among nephrology patients].

Patients with renal diseases (defined by proteinuria or pre-dialysis chronic renal failure) usually exhibit high cardiovascular morbidity and mortality. The true excess of risk associated with proteinuria or high creatinine level in this population is however poorly acknowledged. This paper aims to review the epidemiological evidence pointing at high cardio-vascular burden in these patients. This paper further analyzes whether the high cardio-vascular risk is related to a high prevalence of established risk factors or results from other factors more specific of renal diseases. Applicability to renal populations of "absolute" cardiovascular risk equations derived from Framingham Study is discussed.

Adult↗
PubMed1997

[Renal effects of AT1 angiotensin receptor antagonists (AT1ra)].

RENIN-ANGIOTENSIN ANTAGONISTS: The renal effects of angiotensin II receptor antagonists (AT1 blockers) can be compared with another class of drugs inhibiting the renin-angiotensin-aldosterone system, i.e. the angiotensin I converting enzyme inhibitors (ACE1). SIMILAR BUT SPECIFIC EFFECTS: The renal effects of these two classes of drugs are similar but each class has specific effects explained by several mechanisms. i) The system includes a large number of active peptides (angiotensin II, angiotensin III, angiotensin 1-7) which exert various effects according to their specific receptor(s): ii) several types of angiotensin II receptors have been identified (AT1, AT2, AT4 ...). Only AT1 blockers are available in clinical practice. iii) Receptor or enzyme blockade can produce varying effects; ACE inhibition is not specific since increased bradykinin activity is associated with the suppression of angiotensin peptide generation. EXPERIMENTAL AND CLINICAL TRIALS: Experimental and recent clinical studies have shown that AT1 blockers can induce, like ACE1, hypotension, renal vasodilation and natriuresis. The definite effects on discrete renal structures (vessels, glomeruli, tubules) differ however in magnitude which may suggest specific indications according to the pathophysiological background (renal disease, congestive heart failure, etc.).

Angiotensin II↗
PubMed1997

[Kidney and nitric oxide].

Nitric oxide (NO) pathway is involved in various physiological and pathophysiological processes. NO is synthesised by NO synthase. Three isoforms, ecNOS, nNOS, iNOS have been identified to date, that are encoded by 3 distinct genes on chromosome 7, 12 and 17 respectively. L-arginine is likely involved in the control of NO synthesis. In the kidney, NO regulates glomerular hemodynamics by modulating the ultrafiltration coefficient and afferent and efferent renal arteriolar resistance. NO is further involved in the pressure-natriuresis mechanism and in the tubuloglomerular feedback. Several physiopathological models have underlined the importance of the NO in arterial hypertension and in glomerular inflammation.

Animals↗
PubMed1997

[Doppler echocardiography of left ventricular filling in chronic renal insufficiency: before and after dialysis].

Hemodialysis can achieve loss of body water, variable in the different water compartments, and that depends on the dry weight and the composition of the dialysate. We have studied echocardio-Doppler findings in 26 end stage renal disease patients (from 26 to 84 years), in whom 25 have hypertension, in sinusal rythm and ejection fraction above 55%. When they achieved a 3.52% decrease in body weight, without modification of heart rate and decrease in median arterial pression, these patients exhibited decrease in auricular (p = 0.001) and ventricular diameter both in systole and diastole (p = 0.001), in maximum velocity of E wave (p = 0.001) and E/A ratio. There was no significant reduction of maximum velocity of A wave, but 4 differents patterns of E/A ratio were demonstrated. The main determinant factor of these patterns was found to be the age of the patient.

Adult↗
PubMed1996

[Selective permeability of the glomerular filtration barrier in man].

Glomerular ultrafiltration of macromolecules is a biophysical process sharing both a diffusive and a convective component, governed by glomerular hemodynamics, through a composite structure, the glomerular filtration barrier. Studies of the fractional clearance of macromolecules have showed that transcapillary filtration of macromolecules is hindered by size, electrostatic charge and to a lesser degree by spatial conformation. Several modelizations of ultrafiltration have been developped to quantify the respective role of glomerular hemodynamic and/or membrane structural alternations as found in glomerular diseases.

Capillary Permeability↗
PubMed1996

[Economic evaluation of the contribution of captopril in the treatment of diabetic nephropathy:a cost-benefit approach].

A controlled, double-blind trial, carried out by Lewis and al., has shown that in 409 patients presenting with insulin-dependent diabetes, proteinuria in excess of 500 mg/day and plasma creatinine of less than 221 mumol/l, captopril treatment was able to reduce the risk of combined events (mortality, renal dialysis and transplantation) by 50% (p = 0.006) and that of doubling plasma creatinine by 48% (p = 0.007). We evaluated the cost/benefit ratio of this treatment on the basis of the medical outcome of this study and economic data for the French health-care system. The cost of the treatment by captopril is totally offset by the reduction in costs obtained by postponing dialysis and kidney transplantation, concomitant antihypertensive treatment and hospitalisation. In this study, the health expenditure savings in the captopril group amounted to 6 million French Francs. Spending 100.-Francs on captopril to treat diabetic nephropathy yielded savings of 575.-Francs. This economic advantage, plus a reduction of 6 in the number of deaths, corresponding to 131 life-years saved, demonstrates the favorable cost-benefit ratio of this treatment strategy.

Adolescent↗
PubMed1996

[Diastolic dysfunction in chronic renal failure patients under hemodialysis].

Myocardial hypertrophy due to volume and pressure overload is common in hemodialysis patients because renal failure is usually responsible for arterial hypertension. The left ventricular filling pattern often exhibits abnormalities denoting a relaxation disorder. These abnormalities increase after hemodialysis sessions, which are sometimes followed by severe hypotension. This sequence of left ventricular hypertrophy, altered relaxation, and severe postdialysis hypotension sometimes associated with severe ventricular rhythm disorders deserves to be studied in detail. The data gathered would help to determine the prognosis in this situation, which often depends on cardiac function.

Diastole↗
PubMed1995

Progression rate to end-stage renal failure in non-diabetic kidney diseases: a multivariate analysis of determinant factors.

BACKGROUND: The respective contribution of the type of nephropathy, gender, and proteinuria, and of the potentially alterable factors blood pressure level and daily protein intake on the rate of progression in non-diabetic renal diseases is debated. METHODS: We retrospectively analysed the influence of primary renal disease, gender, urinary protein excretion, mean arterial pressure (MAP), and dietary protein intake on the rate of decline in creatinine clearance (delta Ccr) in 159 adult patients with well-defined nondiabetic kidney diseases. All patients had been followed from a baseline Crr of 40-50 ml/min/1.73 m2 until endstage renal disease and need for dialysis. RESULTS: Mean (+/- SD) delta Ccr (ml/min/1.73 m2/year) was 9.9 +/- 6.5 in 51 patients (45 males) with chronic glomerulonephritis, 6 +/- 2.5 in 50 patients (26 males) with polycystic kidney disease, 5.5 +/- 2.4 in 17 patients (16 males) with hypertensive angionephrosclerosis, and 3.9 +/- 2 in 41 patients (21 males) with chronic tubulointerstitial nephritis. delta Ccr was higher in males than in females (7.5 +/- 5.2 versus 4.8 +/- 2.5; P < 0.001). Linear regression analysis of the whole population disclosed a strong relationship between delta Ccr and proteinuria (r2 = 0.23; P < 0.001), and a weak relationship between delta Ccr and protein intake (r2 = 0.03; P = 0.02), but no relationship between delta Ccr and MAP (r2 = 0.01; P = 0.23). Stepwise multiple regression analysis identified the type of nephropathy, gender, and proteinuria as independent predictive factors of progression; however, these factors together accounted for only 36% of the variation in delta Ccr, suggesting the contribution of other yet unidentified factors. CONCLUSIONS: Primary kidney disease and urinary protein excretion (reflecting the severity of renal disease in individual cases) appear as the major determinants of the rate of progression, with faster progression in males in all types of nephropathy, whereas potentially alterable factors such as blood pressure and protein intake had only a modest influence in the range of values observed in our patients.

Adult↗
PubMed1994

Randomised controlled trial of enalapril and beta blockers in non-diabetic chronic renal failure.

OBJECTIVE: To compare the ability of angiotensin converting enzyme inhibitors and beta blockers to slow the development of end stage renal failure in non-diabetic patients with chronic renal failure. DESIGN: Open randomised multicentre trial with three year follow up. SETTING: Outpatient departments of six French hospitals. PATIENTS: 100 hypertensive patients with chronic renal failure (initial serum creatinine 200-400 mumol/l. 52 randomised to enalapril and 48 to beta blockers (conventional treatment). INTERVENTIONS: Enalapril or beta blocker was combined with frusemide and, if necessary, a calcium blocker or centrally acting drug in patients whose diastolic pressure remained above 90 mm Hg. RESULTS: 17 patients receiving conventional treatment and 10 receiving enalapril developed end stage renal failure. The cumulative renal survival rate was significantly better in the enalapril group than in the conventional group (P < 0.05). The slope of the reciprocal serum creatinine concentration was steeper in the conventionally treated patients (-6.89 x 10(-5)l/mumol/month) than in the enalapril group (-4.17 x 10(-5)l/mumol/month; P < 0.05). No difference in blood pressure was found between groups. CONCLUSION: In hypertensive patients with chronic renal failure enalapril slows progression towards end stage renal failure compared with beta blockers. This effect was probably not mediated through controlling blood pressure.

Acebutolol↗
PubMed1994

Acute renal effects of neutral endopeptidase inhibition in humans.

The acute renal effects of neutral endopeptidase 24.11 (E-24.11) inhibition induced by a single oral dose of sinorphan (100 mg) were investigated in 10 healthy normotensive subjects on normal sodium diet. Sinorphan inhibited 90% of E-24.11 activity and increased plasma atrial natriuretic peptide (ANP) and urinary guanosine 3',5'-cyclic monophosphate (cGMP) by 70 and 100%, respectively. Sinorphan increased urinary sodium output by 50% (P < 0.001) and decreased fractional distal reabsorption by 4% (P < 0.01). Sinorphan increased glomerular filtration rate (GFR) and filtration fraction by 10% 1 h after administration and decreased renal plasma flow by 10%. Mean arterial pressure, renal vascular resistance, plasma aldosterone concentration, and renin activity were unmodified. Sinorphan decreased fractional clearance of neutral dextrans over the 34- to 52-A radius range. Applying the changes along with a hydrodynamic isopore with shunt model, sinorphan significantly increased capillary pressure gradient (delta P; 39 +/- 1 vs. 34 +/- 1 mmHg; P < 0.01), whereas ultrafiltration coefficient was unchanged. In conclusion, endopeptidase inhibition increased endogenous plasma ANP and cGMP generation and induced natriuresis through both an increase in filtered load and a decrease in distal tubular reabsorption of sodium. Sinorphan increases GFR, filtration fraction, and delta P, probably through an increase in efferent over afferent arteriolar resistance ratio.

Blood Pressure↗