Extracellular fluid volume expansion, arterial stiffness and uncontrolled hypertension in patients with chronic kidney disease

2019 ◽  
Vol 35 (8) ◽  
pp. 1393-1398 ◽  
Author(s):  
Branko Braam ◽  
Chung Foon Lai ◽  
Joseph Abinader ◽  
Aminu K Bello

Abstract Background Hypertension is prevalent in patients with chronic kidney disease (CKD) and is related to extracellular fluid volume (ECFV) expansion. Arterial stiffening is another implication of CKD that can be caused by ECFV expansion. In this study, we hypothesized that CKD patients with uncontrolled hypertension are more likely to be fluid volume expanded than normotensive patients, which in turn is associated with increased arterial stiffness. Methods Adult hypertensive patients with mild–severe CKD (n = 82) were recruited. ECFV was assessed using multifrequency bioimpedance and arterial stiffness by applanation tonometry and oscillometry. Results Patients with uncontrolled hypertension had fluid volume expansion compared with controls (1.0 ± 1.5 versus 0.0 ± 1.6 L, P < 0.001), and had a higher augmentation index (AIx) and pulse wave velocity. Fluid volume expansion was more prevalent in patients with uncontrolled hypertension (58%) than patients who were at target (27%). Fluid volume expansion was correlated with age, AIx and systolic blood pressure. In a binary logistic regression analysis, AIx, age and fluid volume status were independent predictors of uncontrolled hypertension in both univariate and multivariate models. Discussion In summary, uncontrolled hypertension among hypertensive CKD patients is associated with ECFV expansion. Our data suggest a relationship between ECFV expansion, increased arterial stiffness and uncontrolled hypertension.

2019 ◽  
Vol 96 (4) ◽  
pp. 1020-1029 ◽  
Author(s):  
Anne-Laure Faucon ◽  
Martin Flamant ◽  
Marie Metzger ◽  
Jean-Jacques Boffa ◽  
Jean-Philippe Haymann ◽  
...  

1977 ◽  
Vol 74 (2) ◽  
pp. 193-204
Author(s):  
J. T. BAKER ◽  
S. SOLOMON

A comparison of the renal response to extracellular fluid volume expansion (5% body weight) was made between 25 normal and 25 chronically hypophysectomized rats. The extracellular fluid compartments averaged 25 ± 1% of body weight in both groups during control, fasted conditions. Extracellular fluid volume increased to 33 ± 1% in hypophysectomized and 34 ± 2% in normal rats during expansion, based on body weight. In addition, filtration fraction was similar in both normal and hypophysectomized rats during control (0·29 ± 0·03 and 0·26 ± 0·02 respectively) and infusion of Ringer–Locke solution (0·24 ± 0·05 and 0·27 ± 0·05 respectively). Thus our results cannot be explained by differences in the degree of expansion or failure to increase filtration in proportion to plasma flow. During infusion of isotonic Ringer–Locke solution, fractional water and sodium excretion both averaged 5·1% in normal rats and only 1·3% and 0·82% respectively in hypophysectomized rats. The ratio of single nephron to whole kidney filtration rate failed to increase as much in hypophysectomized compared with normal rats. Significant increases of fractional volume excretion occurred in both groups by the end of the accessible portion of the proximal tubule. However, fractional water reabsorption was depressed significantly more in normal (mean = 37%) than in hypophysectomized rats (mean = 19%). Fractional water reabsorption in distal tubules was similar in both groups during expansion. Arterial pressure was lower in hypophysectomized rats under control conditions, but showed similar changes during expansion compared with normal rats. Passage time decreased significantly in all groups after Ringer–Locke infusion, but remained prolonged in hypophysectomized rats in proximal and distal tubules. It is concluded that chronic hypophysectomy results in a less efficient renal excretion of volume and sodium chloride load. This inefficiency appears to be related in part to (1) failure of the proximal tubule to depress water reabsorption to a level equivalent to normal rats, and (2) failure to re-distribute flow to outer cortical glomeruli following extracellular fluid volume expansion in hypophysectomized rats.


1977 ◽  
Vol 42 (4) ◽  
pp. 624-629 ◽  
Author(s):  
P. D. Snashall ◽  
W. J. Weidner ◽  
N. C. Staub

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.


1973 ◽  
Vol 3 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Liliana Gradowska ◽  
Sali Caglar ◽  
Ernest Rutherford ◽  
Herschel Harter ◽  
Eduardo Slatopolsky

1975 ◽  
Vol 7 (5) ◽  
pp. 317-324 ◽  
Author(s):  
Edward G. Schneider ◽  
Ralph S. Goldsmith ◽  
Claud D. Arnaud ◽  
Franklin G. Knox

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