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D Fliser

Publications and source records attributed to D Fliser.

At least 73 records · Page 4Linked to original sources
PubMed1993

Hypertension and the kidney--an overview.

The kidney plays a major role in the genesis of any type of hypertension, as demonstrated by experiments which show that hypertension can be "transplanted" when the kidney itself is transplanted. Hypertension is common in patients with renal disease, and may occur even at normal glomerular filtration rates. The mechanisms that promote hypertension and are involved in renal disease comprise both activation of pressor mechanisms and failure of depressor mechanisms, the latter having been considerably less well studied. The major pressor mechanisms are an abnormal pressure-natriuresis relationship and inappropriate activity of the renin-angiotensin system.

Blood Pressure↗
PubMed1993

Pathophysiology of hypertensive renal damage.

The kidney may contribute to and be damaged by hypertension. Evidence from studies of renal transplant recipients and familial studies suggests a genetic component for the occurrence of hypertension and nephrosclerosis. Glomerular injury may result from glomerular hypertension caused by loss of autoregulation and afferent renal vasodilatation. Glomerular injury may be mediated by injury to endothelial cells, which, having lost their thromboresistance, may initiate intravascular coagulation and alter the balance between endothelin and endothelium-derived relaxing factor. Increased transit of protein-laden fluid into the mesangial space also may mediate hypertensive nephrosclerosis. Several studies have provided encouraging evidence that antihypertensive therapy, particularly with angiotensin-converting enzyme inhibitors or calcium antagonists, can slow the progression of renal damage.

Animals↗
PubMed1993

Angiotensin II enhances insulin sensitivity in healthy volunteers under euglycemic conditions.

OBJECTIVE: It has been postulated that vasoconstrictors cause insulin resistance. This effect has been documented for epinephrine but not for angiotensin II (Ang II). The aim of this study was to investigate the effect of the latter on insulin sensitivity. DESIGN: In order to study the influence of subpressor doses of Ang II on insulin-mediated glucose uptake under euglycemic conditions, eight healthy volunteers were allocated in random order to sham infusion or infusion of Ang II (first 0.75 ng/kg per min and subsequently 1.5 ng/kg per min). In addition, in seven of the subjects Ang II was infused after 3 days of indomethacin pretreatment (150 mg/day). METHODS: Insulin-mediated glucose uptake (expressed as M value) was measured with the euglycemic clamp technique. Insulin levels were measured enzymatically, plasma renin activity, Ang II, aldosterone and C-peptide levels by radioimmunoassay, blood pressure by Dinamap and muscle blood flow by plethysmography. RESULTS: The M value after sham infusion was 7.81 +/- 1.52 mg/kg per min and after 1.5 ng/kg Ang II per min was 9.76 +/- 1.26 mg/kg per min (P < 0.001). Indomethacin pretreatment did not abolish the Ang II-induced rise in the M value. Mean arterial blood pressure during the euglycemic clamp was unchanged with sham infusion and the low dose of Ang II. It increased slightly with the higher dose of Ang II. Inferior limb muscle perfusion was higher after infusion of Ang II than after sham infusion; this effect was not obliterated by indomethacin pretreatment. CONCLUSIONS: Ang II increases insulin-mediated glucose uptake: that is, it enhances insulin sensitivity by mechanisms independent of prostaglandins. The observations are of potential relevance to the changes in insulin sensitivity in some forms of hypertension.

Adult↗
PubMed1993

Renal functional reserve in healthy elderly subjects.

The increase in GFR after an amino acid (AA) load, the so-called renal functional reserve, is impaired in the aged rat. Whether the renal functional reserve predicts the progression of renal disease in humans is controversial, but it is possible that age-related alterations of renal hemodynamics are relevant for the evolution of renal disease in the elderly. We compared renal hemodynamics before and after an AA infusion in 15 healthy normotensive subjects of young age (seven women, eight men; median age, 26 yr; range, 23 to 32) and in 10 subjects of old age (six women, four men; median age, 70 yr; range, 61 to 82) on normal dietary protein intake. Baseline GFR and effective RPF were measured after 12 h of fasting by the inulin (Cin) and para-aminohippurate (Cpah) steady-state infusion techniques. The renal functional reserve was examined after an overnight AA infusion (7% solution; 83 mL/h). Median basal Cin and Cpah were significantly lower (P < 0.01) in the elderly (102 and 339 mL/min per 1.73 m2) than in the young subjects (122 and 647 mL/min per 1.73 m2), but virtually all GFR values of the elderly were still within the normal range. Median Cin upon infusion of AA was 118 mL/min per 1.73 m2 (range, 98 to 137) in the elderly and 146 (range, 120 to 171) in the young, respectively. Corresponding values of Cpah were 349 mL/min per 1.73 m2 in the elderly versus 689 mL/min per 1.73 m2 in the young. Cin increased significantly (P < 0.01) after the AA load in both young and elderly subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Differential effects of ACE inhibitors and vasodilators on renal function curve in patients with primary hypertension.

OBJECTIVE: In experimental studies differential effects of antihypertensive agents on the renal function curve have been observed: in SHR captopril lowered the slope of the renal function curve, i.e. blood pressure (BP) became salt sensitive, whereas hydralazine shifted the curve without changing its slope. To evaluate whether ACE inhibitors and vasodilators have different effects on salt sensitivity of BP in humans, we compared the effect of the ACE inhibitor cilazapril and the vasodilator dihydralazine on the renal function curve in a randomized prospective single blind cross-over study. DESIGN: Nine patients (1 f, 8 m, mean age 41 +/- 4 y) with mild to moderate primary hypertension were put on low (20 mmol/d) and on high salt diet (200 mmol/d). Drugs were given in random low salt+cilazapril, high salt+cilazapril; low salt+dihydralazine, high salt+dihydralazine; or in reverse order. RESULTS: All antihypertensive interventions lowered BP, but the averaged posttreatment MAP was significantly (p < 0.02) lower with cilazapril on low salt intake (83.6 +/- 2.8 mmHg) than with all of the following: cilazapril on high salt intake (86.4 +/- 2.9 mmHg), dihydralazine on low (91.6 +/- 3.2 mmHg) and high salt (90.1 +/- 3.3 mmHg) intake. Probably as a result of sympathetic activation, average daily heart rate was higher after dihydralazine on low (72.9 +/- 2.9 b/min) and high salt intake (72.4 +/- 2.8 b/min) than after cilazapril on either salt intake (68.7 +/- 3.1 and 62.7 +/- 3.2 b/min). CONCLUSIONS: The results document that BP reduction after acute ACE inhibition is a function of salt intake, i.e. with ACE inhibitor therapy, BP is "salt sensitive". In contrast, vasodilators of the dihydralazine type have similar antihypertensive effects on low and high salt intake. To the extent that the findings of this short-term study can be extrapolated to long-term effects they suggest that intrarenal mechanisms, i.e. resetting of the pressure-natriuresis relationship, are involved in the long-term antihypertensive action of ACE inhibitors.

Adult↗
PubMed1993

Serum lipid changes on low salt diet. Effects of alpha 1-adrenergic blockade.

An increase of some serum lipid fractions has been documented in normotensive healthy volunteers and patients with essential hypertension during acute drastic restriction of salt intake. To clarify the potential role of vasopressor systems, particularly the sympathetic system, in the lipid changes induced by salt restriction, we compared fasting serum lipids, glucose, insulin, and C-peptide levels in 16 normotensive healthy volunteers during 7 days of high (200 mmol/day) and 7 days of low (20 mmol/day) salt intake. The individuals were examined on either placebo or on the alpha 1-adrenergic blocker doxazosin (2 mg/day). The study was carried out using a single blind parallel group random order design with two arms of treatment. In the volunteers on placebo, total cholesterol (corrected for hemoconcentration) was significantly higher (P < .01) during low salt intake. The same was true for LDL-cholesterol, whereas HDL-cholesterol and triglycerides did not change with salt intake. The lipid changes, and, in parallel, the changes of hemoconcentration indicators, were more pronounced after 2 days than after 7 days of low salt intake. The rise of total and LDL-cholesterol on low salt was blunted after alpha 1-adrenergic blockade with doxazosin. Fasting glycemia was similar on low salt and high salt, respectively, but in placebo treated volunteers, C-peptide levels were significantly (P < .01) higher on low, rather than high, salt intake. alpha 1-Adrenergic blockade with doxazosin attenuated the rise of C-peptide levels on low salt. The results confirm previous findings that levels of total cholesterol and LDL-cholesterol change inversely with salt intake in normotensive healthy volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1993

[Dyslipoproteinemia: its importance in nephrology].

Dyslipidemia is a common feature of renal failure. It is primarily caused by delayed catabolism of lipoprotein particles. This is due to decreased activity of the key enzymes of delipidation of lipoprotein particles (LPL, HTGL) and of HDL remodeling (LCAT). In epidemiological studies no correlation has been found in dialysis patients between total lipids and atherosclerotic endpoints and a modest relation, at best, between more sophisticated apolipoprotein indices and vascular disease. Such lack of correlations are presumably explained by malnutrition as a confounding factor. Fascinating new observations in animal studies document that in various models of renal damage, development of glomerulosclerosis is accelerated by hyperlipoproteinemia, either endogenous hyperlipoproteinemia or hyperlipoproteinemia induced by feeding of fat. Conversely, correction of hyperlipoproteinemia mitigates development of glomerulosclerosis. Currently there is no firm evidence that the same is true in humans.

Animals↗
PubMed1992

Albuminuria of hypertensive patients.

Renal dysfunction as a consequence of malignant hypertension has been recognized for decades in patients with essential hypertension. It has been shown only recently, however, that albuminuria (including underlying albuminuria not detectable by conventional tests, i.e. microalbuminuria) has emerged as a frequent sequela of essential hypertension. Furthermore, renal dysfunction of the elderly as a result of ischemic nephropathy, in the absence of malignant hypertension, has turned out to be an important long-term outcome in the patient with essential hypertension. The presence of albuminuria is a strong predictor of cardiovascular events. Albuminuria is associated with more severe hypertension and with evidence of more advanced target organ damage (e.g. LVH). It is more prevalent in the elderly. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and end-organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis.

Adult↗
PubMed1992

Clinical relevance of albuminuria in hypertensive patients.

Albuminuria (including the form not detectable by conventional tests, i.e., microalbuminuria) as well as renal dysfunction have recently been recognized as important complications in the patient with essential hypertension. The presence of albuminuria predicts cardiovascular events. Albuminuria is associated with more severe hypertension, with evidence of more advanced target organ damage (e.g., left ventricular hypertrophy), and is more prevalent in high-risk groups (e.g., the elderly). On the other hand, albuminuria may also be associated with generalized endothelial barrier dysfunction and thus predispose to accelerated atherogenesis. Ischemic nephropathy from nonmalignant nephrosclerosis has emerged as an important cause of terminal renal failure in the elderly patient with essential hypertension.

Albuminuria↗
PubMed1991

The kidney in congestive heart failure.

Congestive heart failure (CHF) is characterized by activation of (i) vasopressor and antinatriuretic influences (ii) and by counter-activation of vasodilator natriuretic systems. The former comprise the sympathoadrenal, renin-angiotensin-aldosterone and arginine vasopressin systems, and possibly endothelin and withdrawal of endothelium dependent relaxing factor respectively. The latter include the prostaglandins (PGE-2, PGI-2), dopamine and atrial natriuretic factor. The response of the kidney to chronic heart failure, i.e. vasoconstriction and antinatriuresis, resembles the renal reaction to volume depletion. The adverse renal effects of ACE inhibitors in some patients with advanced congestive heart failure may be explained by lowering of renal perfusion pressure and dependence of glomerular filtration rate on angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Inhibition of complement activation with EDTA in vivo during sham hemodialysis.

To check whether in vivo EDTA prevents complement activation resulting from blood contact with the dialyzer membrane, sham hemodialysis (HD) was performed in seven healthy volunteers using Cuprophan hollow-fiber dialyzers. Blood samples were drawn from the arterial and venous blood lines of the dialyzer before and after EDTA was infused into the arterial line. Venous line plasma C3a concentrations before EDTA infusion were significantly higher than after EDTA. Also, venous line plasma C3a concentrations before and after EDTA infusion were significantly higher than in the arterial line. These results indicate that complement activation can be attenuated by EDTA during sham HD. Technical improvements in the procedure may permit complete inhibition of complement activation.

Adult↗