Abstract 12882: Renal Hemodynamics in Chronic Heart Failure With Preserved and Reduced Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Susanne Jung ◽  
Agnes Bosch ◽  
Julie Kolwelter ◽  
Kristina Striepe ◽  
Dennis Kannenkeril ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Chronic Heart Failure ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Inverse Association ◽  
Hemodynamic Parameters ◽  
Renal Hemodynamic ◽  
Renal Vascular

Introduction: Chronic heart failure (CHF) and impaired renal function are two co-existing medical conditions and known to be associated with adverse outcome. The cardiorenal interaction has not yet been analyzed thoroughly. The aim of this study was to assess renal and intraglomerular hemodynamics by constant infusion input clearance technique in subjects with CHF compared to healthy controls. Methods: This was a cross-sectional observational study including 85 subjects. The group of subjects with CHF consisted of 27 individuals with HFpEF and 27 individuals with HFrEF, who were compared to 31 controls. All subjects underwent renal clearance examination to determine measured -not estimated- glomerular filtration rate (GFR), renal blood and plasma flow (RBF, RPF) and to calculate renal hemodynamic parameters such as filtration fraction (FF), renal vascular resistance (RVR), intraglomerular pressure (P glom ) and resistances of the afferent (R A ) and efferent arterioles (R E ). Results: GFR was lower in subjects with CHF (88.6±13.1ml/min/1.73m 2 ) compared to controls (108.6±17. ml/min/1.73m 2 ) after adjustment for age and BP (p adj =0.037). There were no significant differences regarding RPF, RBF, FF, RVR, P glom , R A as well as R E after adjustment for age and BP. Similarly, there were no significant differences regarding renal hemodynamic parameters between HFpEF and HFrEF subjects. Bivariate correlation analysis in the group of subjects with CHF revealed an inverse association between NT-proBNP and RPF (R=-0.421, p=0.002), RBF (R=-0.414, p=0.002) and a positive association with FF (R=0.324, p=0.019), RVR (R=0.346, p=0.012) and R E (R=0.318, p=0.022). Conclusions: The findings of this study indicate that in CHF renal function is slightly reduced even though renal perfusion is preserved. With progressive severity of CHF as indicated by increasing NT-proBNP, renal vascular resistance in particular at the postglomerular side increases. Our data are in accordance with neuroendocrine activation in CHF since vasoconstriction at the postglomerular site points towards angiotensin II as mediator. The association between NT-proBNP and renal hemodynamics documents a close cardiorenal interaction in CHF.

scholarly journals Enhanced Responses of Blood Pressure, Renal Function, and Aldosterone to Angiotensin I in the DD Genotype Are Blunted by Low Sodium Intake

2002 ◽  
Vol 13 (4) ◽  
pp. 1025-1033
Author(s):  
Frank G. H. van der Kleij ◽  
Paul E. de Jong ◽  
Rob H. Henning ◽  
Dick de Zeeuw ◽  
Gerjan Navis
Keyword(s):  
Renal Function ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Angiotensin I ◽  
Low Sodium ◽  
Renal Hemodynamic ◽  
Intake Level ◽  
Renal Vascular

ABSTRACT. Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, renal hemodynamic parameters, and renin-angiotensin system parameters were similar for all genotypes with either sodium intake level. With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes ± 95% confidence intervals), with mean MAP increases of 22 ± 2% (DD genotype), 13 ± 5% (ID genotype), and 12 ± 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 ± 19.7% (DD genotype), 73.0 ± 16.3% (ID genotype), and 63.2 ± 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 ± 189% (DD genotype), 343 ± 71% (ID genotype), and 254 ± 99% (II genotype) (P < 0.05). Also, the decrease in GFR was more pronounced for the DD genotype, with mean decreases of 17.9 ± 4.7% (DD genotype), 8.8 ± 3.4% (ID genotype), and 6.4 ± 5.9% (II genotype) (P < 0.05). The effective renal plasma flow, plasma AngII concentration, and plasma renin activity values were similar for the genotypes. In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. The responses to AngII were also similar for all genotypes, with either sodium intake level. In conclusion, the responses of MAP, renal hemodynamic parameters, and aldosterone concentrations to AngI are enhanced for the DD genotype with liberal but not low sodium intake. These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake.

scholarly journals Association of Noise Annoyance with Measured Renal Hemodynamic Changes

2021 ◽  
pp. 1-8
Author(s):  
Dennis Kannenkeril ◽  
Susanne Jung ◽  
Christian Ott ◽  
Kristina Striepe ◽  
Julie Kolwelter ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Filtration Fraction ◽  
Noise Annoyance ◽  
Renal Hemodynamic ◽  
Renal Vascular

<b><i>Background:</i></b> Chronic mental stress is recognized as a modifiable risk factor for cardiovascular disease. The aim of this study was to demonstrate that noise annoyance-induced stress is associated with changes in renal hemodynamics. <b><i>Methods:</i></b> Renal hemodynamic parameters were measured using steady-state input clearance with infusion of para-aminohippuric acid and inulin in individuals with normal, high normal, and elevated blood pressure. All individuals ranked subjective annoyance due to noise in everyday life on a 7-grade Likert scale. The median of all rankings was used as a cutoff point to divide the group into noise-annoyed and non-noise-annoyed individuals. Different renal hemodynamic parameters were calculated based on the Gomez equation. <b><i>Results:</i></b> Noise-annoyed individuals (<i>n</i> = 58) showed lower renal plasma flow (599 ± 106 vs. 663 ± 124 mL/min, <i>p</i> = 0.009), lower renal blood flow (1,068 ± 203 vs. 1,172 ± 225 mL/min, <i>p</i> = 0.047), higher filtration fraction (22.7 ± 3.3 vs. 21.3 ± 3.0, <i>p</i> = 0.012), higher renal vascular resistance (88.9 ± 25.6 vs. 75.8 ± 22.9 mm Hg/[mL/min], <i>p</i> = 0.002), and higher resistance of afferent arteriole (2,439.5 ± 1,253.4 vs. 1,849.9 ± 1,242.0 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.001) compared to non-noise-annoyed individuals (<i>n</i> = 55). There was no difference in measured glomerular filtration rate (133 ± 11.8 vs. 138 ± 15 mL/min, <i>p</i> = 0.181), resistance of efferent arteriole (2,419.4 ± 472.2 vs. 2,245.8 ± 370.3 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.060), and intraglomerular pressure (64.0 ± 3.1 vs. 64.6 ± 3.5 mm Hg, <i>p</i> = 0.298) between the groups. After adjusting for age, renal plasma flow, renal blood flow, and renal vascular resistance remained significantly different between the groups, with a trend in increased afferent arteriolar resistance and filtration fraction. <b><i>Conclusion:</i></b> In this study, noise annoyance was associated with reduced renal perfusion attributed to increased renal vascular resistance predominantly at the afferent site. Long-term consequences of this renal hemodynamic pattern due to noise annoyance need to be investigated.

Effects of a new dihydropyridine derivative, S12968 (pranedipine), and its stereoisomer, S12967, on renal effects of endothelin-1

1994 ◽  
Vol 72 (11) ◽  
pp. 1294-1298 ◽  
Author(s):  
Immaculada Montañés ◽  
Olga Flores ◽  
Nélida Eleno ◽  
José M. López-Novoa
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Fold Increase ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Potassium Excretion ◽  
Endothelin 1 ◽  
Dihydropyridine Derivative ◽  
Renal Vascular

The purpose of the present study was to assess in rats the prevention by two enantiomers of a new dihydropyridine derivative (pranedipine) (called S12967 for the dextrogyre(+) and S12968 for the levogyre (−) molecules) of the renal and cardiovascular effects induced by endothelin-1. The injection of endothelin-1 (1 nmol/kg body weight) induced a sharp and transient decrease in urine flow, sodium and potassium excretion, glomerular filtration rate, renal plasma flow, and renal blood flow, a significant increase in renal vascular resistance, and a small but significant increase in arterial pressure. Treatment with S12968 alone (0.3 mg/kg) induced a 2.5-fold increase in urine flow and potassium excretion and a 4.5-fold increase in sodium excretion. Pretreatment with S12968 completely blocked the endothelin-1 induced increase in arterial pressure, did not affect the acute effect of endothelin-1 on urine flow, sodium and potassium excretion, filtration rate, and renal blood flow, but blunted the effect on renal vascular resistance. Administration of S12967 alone (1 mg/kg) did not induce changes in either renal function or arterial pressure. In S12967-treated animals, endothelin-1 also induced a transient increase in arterial pressure and renal vascular resistance but failed to change renal function in a significant manner. In summary, the above reported experiments show that at the higher, nonhypotensive doses, the levogyre enantiomer (S12968) of a new dihydropyridine derivative (pranedipine) completely prevented the hypertensive effect of endothelin 1, and partially prevented the effect of endothelin-1 on renal vascular resistance. The dextrogyre enantiomer (S12967) had almost no effect on either mean arterial pressure or renal vascular resistance but completely blocked the endothelin-1-induced decrease in urine flow and urinary sodium excretion.Key words: calcium antagonists, endothelin, dihydropyridines, kidney, renal function (rat).

Acetylcholine chloride and renal hemodynamics during postnatal maturation in conscious lambs

1999 ◽  
Vol 87 (4) ◽  
pp. 1296-1300 ◽  
Author(s):  
Alp Sener ◽  
Francine G. Smith
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Postnatal Maturation ◽  
Renal Vasoconstriction ◽  
Acetylcholine Chloride ◽  
Renal Vascular ◽  
Dose Dependent ◽  
Conscious Animals

To test the hypothesis that acetylcholine-induced relaxation of the renal artery decreases with postnatal age, we measured parameters of renal hemodynamics before and for 35 s after aortic suprarenal injection of acetylcholine in conscious, chronically instrumented lambs aged ∼1 wk ( n = 5) and ∼6 wk ( n = 5). Acetylcholine was administered in one of five doses ranging from 0 to 10 mg/kg body wt; doses were administered randomly, in the same volume. There were significant age- and dose-dependent changes in renal vascular resistance after acetylcholine administration, such that the response was greater in 1-wk-old lambs. After the highest dose tested, renal vascular resistance decreased by 13.6 ± 7.3 (SD) mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 1-wk-old lambs and by 9.1 ± 3.2 mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 6-wk-old lambs at 35 s. We also observed a transient renal vasoconstriction before the renal vasodilatation in 6-wk-old lambs but not in 1-wk-old animals. These data provide the first age- and dose-dependent effects of exogenous administration of acetylcholine on renal hemodynamics during maturation in conscious animals.

Effects of acute acid-base changes on renal hemodynamics in anesthetized dogs

1965 ◽  
Vol 209 (6) ◽  
pp. 1180-1186 ◽  
Author(s):  
Daniel H. Simmons ◽  
Richard P. Olver
Keyword(s):  
Vascular Resistance ◽  
Electromagnetic Flowmeter ◽  
Respiratory Acidosis ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Acid Base ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Renal Vascular

Renal hemodynamics were studied in 58 experiments during acid-base disturbances in anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter on the left renal artery. Arterial pressure was also measured and renal vascular resistance calculated. Flow and resistance were measured during respiratory acidosis and alkalosis, metabolic acidosis and alkalosis, and combined respiratory and metabolic acid-base disturbances such that arterial pH was maintained normal while pCO2 changed. pH changes were approximately 0.2 unit above and below normal and pCO2 changed to approximately double or half control. Renal vascular resistance was shown to be pCO2 dependent but not pH dependent. Doubling the control pCO2, whether pH changed or remained constant, resulted in decreased resistance (–16%) while decreasing pCO2 to approximately one-half normal resulted in increased resistance (+17%). Resistance was not influenced by the degree of renal denervation resulting from the use of the flowmeter. Changes in resistance appear likely to be related to local rather than central factors.

Diabetic nephropathy

1997 ◽  
Vol 38 (2) ◽  
pp. 296-302 ◽  
Author(s):  
D. Soldo ◽  
B. Brkljacic ◽  
V. Bozikov ◽  
I. Drinkovic ◽  
M. Hauser
Keyword(s):  
Renal Function ◽  
Diabetic Nephropathy ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Diabetic Patients ◽  
Renal Changes ◽  
Duplex Doppler ◽  
Renal Vascular ◽  
Parenchymal Thickness ◽  
Renal Length

Background: the purposes of this study were: to compare conventional and duplex Doppler ultrasonography in the detection of renal changes in diabetes mellitus; to investigate whether a correlation was found with various clinical stages; and to assess whether increased renal vascular resistance in asymptomatic patients correlated with mild renal functional impairment. Material and Methods: in 190 diabetic patients and 85 controls, conventional ultrasonography was used to assess renal length, parenchymal thickness, and cortical echo-genicity. Renal vascular resistance was estimated by duplex Doppler measurements of intrarenal arterial resistive indices. According to clinical stage, the patients were classified into 3 groups. Resistive indices were compared between controls and patient groups and correlated with age and renal function. Results: in asymptomatic diabetic nephropathy, renal length and parenchymal thickness were significantly increased compared to that of controls, reflecting hyperfiltra-tion-induced nephromegaly. Differences between controls and patients with clinically manifest nephropathy were insignificant; only in advanced renal disease were both values significantly decreased. Cortical hyperechogenicity was noted only in very advanced disease. Resistive indices correlated well with renal function, and pathologic values (i. e. ≥ 0.70) were observed in 15% in the asymptomatic group and in 87% in the group with advanced nephropathy. Conclusion: Renal changes in diabetic patients are detectable by conventional ultrasound only in very advanced stages of the disease. Pathologic resistive indices, however, may be detected in the earlier stages. Resistive indices correlate with serum cre-atinine levels and creatinine clearance rates. However, it remains unclear as to whether a diagnostic or prognostic benefit can be expected as compared to standard laboratory examinations.

scholarly journals Renal responses to sodium restriction in patients with early diabetes mellitus.

1997 ◽  
Vol 8 (5) ◽  
pp. 749-755 ◽  
Author(s):  
J A Miller
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Resistance ◽  
Insulin Dependent Diabetes Mellitus ◽  
Renal Vascular Resistance ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Sodium Restriction ◽  
Renal Hemodynamic ◽  
Insulin Dependent ◽  
Renal Vascular

Increased GFR and decreased renal vascular resistance are common renal hemodynamic changes in persons with early, uncomplicated, insulin-dependent diabetes mellitus. It has been hypothesized that excess total-body sodium in patients with diabetes contributes to the renal vasodilation, possibly by suppressing vasoconstricting neurohormonal systems. This study was undertaken to examine whether sodium restriction could normalize these renal abnormalities. Subjects were 12 male patients with uncomplicated insulin-dependent diabetes mellitus (duration, < 5 yr). Results were compared with those of an age- and gender-matched control group. All subjects received either a high-sodium diet (200 mmol/day) or a sodium-restricted diet (20 mmol/day) for 7 days, according to a randomized crossover protocol. GFR and RPF were measured using inulin and para-aminohippurate clearance techniques, respectively. Subjects with diabetes were maintained euglycemic during the clearance measurements. GFR was significantly higher in the diabetic group than in the control group with sodium repletion (124 +/- 4 versus 107 +/- 8 mL/min/1.73 m2; P = 0.03), and renal vascular resistance was significantly reduced (94 +/- 6 versus 107 +/- 17 mm Hg/L/min; P = 0.05). In response to sodium restriction, the hematocrit increased significantly in both groups, as did PRA and aldosterone, although responses in the diabetic group were somewhat blunted, indicating persisting volume expansion. Despite this humoral activation, sodium restriction had little effect on renal hemodynamic function in control subjects. In the diabetic subjects, this maneuver appeared to exacerbate the underlying renal abnormalities, with the GFR increasing to 131 +/- 4 mL/min/1.73 m2 (P = 0.05) and the renal vascular resistance declining to 73 +/- 5 mm Hg/L/min (P = 0.001). These data indicate that, rather than correcting renal hyperperfusion, sodium restriction exacerbates these characteristic abnormalities, suggesting that mechanisms other than suppression of vasoconstrictor activity are operative in the underlying renal hemodynamic abnormalities of early, uncomplicated, insulin-dependent diabetes mellitus.

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