Extracellular Fluid Volume Is an Independent Determinant of Uncontrolled and Resistant Hypertension in Chronic Kidney Disease: A NephroTest Cohort Study

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.

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SP057Association between asymptomatic hyperuricemia and apparent treatment resistant hypertension in chronic kidney disease in Korea : KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD)

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfz103.sp057 ◽

2019 ◽

Vol 34 (Supplement_1) ◽

Author(s):

Young Jin Kim ◽

Hong Sang Choi ◽

Chang Seong Kim ◽

Eun Hui bae ◽

Ma Seong Kwon ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Cohort Study ◽

Kidney Disease ◽

Resistant Hypertension ◽

Treatment Resistant

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Extracellular fluid volume: A suitable indexation variable to assess impact of bariatric surgery on glomerular filtration rate in patients with chronic kidney disease

PLoS ONE ◽

10.1371/journal.pone.0256234 ◽

2021 ◽

Vol 16 (8) ◽

pp. e0256234

Author(s):

Caroline Grangeon-Chapon ◽

Audrey Laurain ◽

Vincent L. M. Esnault ◽

Coralie Cruzel ◽

Antonio Iannelli ◽

...

Keyword(s):

Bariatric Surgery ◽

Chronic Kidney Disease ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Kidney Disease ◽

Glomerular Filtration ◽

Filtration Rate ◽

Extracellular Fluid ◽

Extracellular Fluid Volume ◽

One Year

Background Bariatric surgery (BS) might be a nephroprotective treatment in obese patients with chronic kidney disease (CKD), and the non-linear relation between body surface area (BSA) and extracellular fluid volume (ECFV) in obese people raises the question of the most relevant way to scale glomerular filtration rate (GFR) for assessing renal function changes after BS. Methods We screened 1774 BS candidates and analysed 10 consecutive participants with CKD stage 3. True GFR (mGFR), measured by the renal clearance of 51Cr-ethylenediaminetetraacetic acid (EDTA), was scaled either to BSA (mGFRBSA) or to ECFV measured by 51Cr-EDTA distribution volume (mGFRECFV) before and one year after BS. Results The 10 candidates for BS had a mean body mass index of 43.3 ± 3.6 kg/m2 and a mean GFR of 48 ± 8 mL/min/1.73 m2. Six participants had a sleeve gastrectomy and four had a Roux-en-Y gastric bypass. One year after BS, ECFV decreased (23.2 ± 6.2 to 17.9 ± 4.3 L, p = 0.001), absolute mGFR was not significantly modified (74 ± 23 versus 68 ±19 mL/min), mGFRBSA did not change significantly (53 ± 18 versus 56 ± 17 mL/min/1.73 m2) whereas mGFRECFV significantly increased (42 ± 13 versus 50 ± 14 mL/min/12.9 L, p = 0.037). The relation between mGFRECFV and mGFRBSA was different from the identity line before (p = 0.014) but not after BS (p = 0.09). Conclusion There is a difference between mGFRBSA and mGFRECFV following BS and the latter might better reflect the adequacy between renal function and corpulence.

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Posterior Reversible Encephalopathy Syndrome in End-Stage Kidney Disease: Not Strictly Posterior or Reversible

American Journal of Nephrology ◽

10.1159/000381316 ◽

2015 ◽

Vol 41 (3) ◽

pp. 177-182 ◽

Cited By ~ 20

Author(s):

Mark Canney ◽

Dearbhla Kelly ◽

Michael Clarkson

Keyword(s):

Brain Injury ◽

Kidney Disease ◽

Posterior Reversible Encephalopathy Syndrome ◽

Extracellular Fluid ◽

Fluid Volume ◽

Extracellular Fluid Volume ◽

End Stage Kidney Disease ◽

Posterior Reversible Encephalopathy ◽

End Stage ◽

Reversible Encephalopathy

Posterior reversible encephalopathy syndrome (PRES) is an uncommon clinico-radiological condition that can result in severe brain injury. The pathogenesis of cerebral vasogenic edema, the hallmark of PRES, is not fully understood. Despite its name, there is substantial heterogeneity both in terms of imaging findings and outcome. Relatively little is known about PRES in kidney disease despite the clustering of risk factors including hypertension, autoimmune disease and immunosuppression. In a retrospective observational study of incident end-stage kidney disease patients in Southwest Ireland over a ten year period, we discovered five cases of PRES representing an incidence of 0.84% in this patient population. These five cases highlight the variability in clinical presentation and the potentially life-threatening nature of this condition. We provide an in-depth review of the existing literature regarding PRES in terms of its pathogenesis and heterogeneity, as well as the experience of PRES in ESKD patients. PRES appears to be rare in the ESKD population but could be under-recognized. Marked hypertension is a cardinal risk factor in this population, associated with extracellular fluid volume expansion. Neuroimaging findings can be diverse involving both anterior and posterior circulation territories. Three of the five patients described had commenced haemodialysis within four weeks of their presentation. These patients may be particularly vulnerable to microvascular brain injury, which can be devastating. This emphasises the need for clinicians to pay meticulous attention to extracellular fluid volume control during this potentially hazardous period.

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The effects of oral sodium bicarbonate on extracellular water in patients with chronic kidney disease

10.36811/cjn.2019.110002 ◽

2019 ◽

pp. 04-13

Author(s):

Colin Jones ◽

Louise Wells ◽

Graham Woodrow ◽

David Ashford

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Sodium Bicarbonate ◽

Total Body Water ◽

Extracellular Fluid ◽

Body Water ◽

Fluid Volume ◽

Extracellular Fluid Volume ◽

Total Body ◽

Oral Sodium

Background: Metabolic acidosis in chronic kidney disease (CKD) is often treated with oral sodium bicarbonate. There is limited evidence around the effects of sodium bicarbonate on extracellular fluid and blood pressure in CKD. Methods: In a double blind randomised comparison patients with stage 3-5 CKD were randomised to either oral sodium bicarbonate 1.5 g three times a day (n=18) or placebo (n=21) for 4 weeks. Assessments performed at 0 and 4 weeks included: body weight, office blood pressure and assessment for peripheral/pulmonary oedema; serum creatinine, electrolytes and venous bicarbonate; 24-hour urine for sodium excretion; extracellular fluid volume and total body water determined by sodium bromide and deuterium oxide dilution respectively; extracellular fluid volume and total body water by bioimpedance. Differences between the active and placebo groups at week 4 were analysed by ANCOVA. Results: At week 4, serum bicarbonate was higher (25.6±2.4 vs 23.3±3.1 mmol/l) and blood urea lower (14.2±5.6 vs 17.0±5.8 mmol/l) in the active treatment group. Urine sodium concentration was also higher (82.7±25.3 vs 59.0±21.9 mmol/l). Extracellular fluid volume (20.0±4.3 vs 18.0±2.9) and total body water (42.3±9.6 vs 39.0±6.8) measured by bioimpedance and total body water by deuterium dilution (41.7±8.3 vs 39.4±6.2) were significantly greater in the treatment arm at week 4. Differences in systolic and diastolic blood pressure did not reach statistical significance. Conclusions: Oral sodium bicarbonate has a biological effect and increases body water content, without evidence of a clinical consequence. This may reflect the fact that some of the ingested sodium is excreted in the urine.

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