Hypertension is associated with increased post‐exercise albuminuria, which may be attenuated by an active lifestyle

Abstract

Albuminuria is a known marker for endothelial dysfunction and cardiovascular events, even below the threshold of moderately increased albuminuria (MIA). Post‐exercise increased albuminuria may precede the appearance of rest MIA, enabling detection of early injury. Modifying lifestyle for a population at risk for MIA is therefore of interest. Our aim was to evaluate post‐exercise albuminuria in hypertensive compared with normotensive individuals and to analyze the effect of an active lifestyle on rest and post‐exercise albumin excretion. The study cohort consisted of 3931 adults who participated in a health‐screening program. Albuminuria was measured as urine albumin‐to‐creatinine ratio (ACR). Lifestyle was divided into three groups: non‐active, less‐active, and active according to regular sport activity, categorized as follows: none, <2.5 and ≥2.5 hours per week. Mean age was 47.7 years, and 31.2% (n = 1228) were diagnosed with hypertension. Both rest and post‐exercise ACR were higher in hypertensive compared to normotensive participants. Rest ACR was higher in non‐active compared to less‐active and active hypertensive participants. Hypertensive participants with an active lifestyle had significantly lower post‐exercise and delta ACR compared to less‐active and non‐active hypertensive participants. Parameters related to delta ACR in hypertensive participants were increased age, BMI, and diabetes, while active lifestyle and fitness (measured as METS achieved by a stress test) were protective. In conclusion, there is an association between hypertension and increased albumin excretion post‐exercise, which can be attenuated with an active lifestyle.

1. INTRODUCTION

In the general population, albuminuria is an established and strong prognostic factor for various adverse clinical outcomes, including mortality, end‐stage renal disease, and cardiovascular events.1, 2 Cardiovascular mortality in high‐risk patients is evident even when urinary albumin levels are below the clinically defined threshold for moderately increased albuminuria (MIA), formerly known as microalbuminuria,1, 3, 4, 5 and is independent of GFR (glomerular filtration rate) levels.3, 4, 6

Moderately increased albuminuria is not only a predictor of development and progression of diabetic7 and non‐diabetic8 renal diseases, but is also a marker of endothelial dysfunction.5 Furthermore, it is related to cardiovascular events in patients with diabetes mellitus, as well as in patients with metabolic syndrome, hypertension, and in the general population.9, 10, 11 Possible mechanisms may be reduced vasodilatation or elevated plasma levels of the pro‐thrombotic von Willebrand factor antigen.12, 13

Elevated blood pressure (BP) is associated with increased albuminuria, even within normal BP range.14

Exercise‐induced increased albuminuria may precede the appearance of rest MIA, enabling detection of early injury, and is associated with the metabolic syndrome and diabetes mellitus. Several studies have shown that exercise unmasks albuminuria in normo‐albuminuric diabetic individuals, suggesting that this may be an early sign of diabetic nephropathy.15, 16 Exercise leads to albuminuria by modulating both the glomerular passage and tubular re‐uptake of albumin.17 Our group recently published studies showing that increased albuminuria post‐exercise is independently correlated with a higher prevalence of metabolic syndrome in non‐diabetic individuals,18 as well as in women with abnormal exercise ECG test findings and possibly increased cardiovascular risk.19

However, to the best of our knowledge, change in albumin excretion following exercise in hypertensive individuals is unknown; the aim of this study, therefore, was to investigate albumin excretion at rest and post‐exercise in hypertensive compared to normotensive individuals and to explore a possible association related to increased albuminuria in hypertensive individuals, including parameters of an active lifestyle.

2. METHODS

2.1. Study population

The study population consisted of individuals who participated in a comprehensive health‐screening program at the Tel‐Aviv Medical Center Inflammation Survey (TAMCIS) between January 2012 and April 2017. TAMCIS is a registered databank of the Israeli Ministry of Justice19 and encompasses a large cohort of participants who attend the Tel‐Aviv Medical Center for routine annual outpatient checkups (including an interview and examination by a physician, and blood and urine tests). This databank serves multiple studies that explore epidemiological risk factors for cardiovascular diseases and inflammatory mechanisms in apparently healthy individuals.

Following a 12‐hour fast, blood and urine samples, analyzed in the same core clinical laboratory, were taken from participants upon their arrival at the Medical Center.

2.2. Albuminuria measurements

Urine tests were analyzed by an ADVIA chemistry analyzer (Siemens Healthcare Diagnostics), which is an improved albumin detection method with an extended analytic range of 3‐420 mg/L and coefficient of variation of 2%.20

Urine albumin excretion was assessed by a single‐void urine sample and expressed as the ratio of concentrations of urine albumin‐to‐creatinine ratio (ACR), as advised by the National Kidney Foundation, Kidney Disease Outcomes Quality Initiative guidelines.21

Urine samples for albumin and creatinine measurements were collected from participants before and after an ECG exercise stress test on a treadmill (Quinton, TM55 series) that was performed according to the Bruce protocol. The test was operated by a trained technician, and the results were analyzed on the spot by a cardiologist.

Delta ACR was defined as post‐exercise ACR minus ACR at rest.

Moderately increased albuminuria was defined according to the recommendations of the American Diabetes Association and the National Kidney Foundation, as ACR between 30 and 300 mg/g. Albuminuria was defined as ACR >300 mg/g.22

Estimated glomerular filtration rate (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration (CKD‐EPI) creatinine equation, a 4‐variable formula23 adjusted for body surface area (Mosteller calculation).

Stages of CKD were defined based on eGFR and albuminuria according to the KDIGO summary of recommendation statements.24

2.3. Blood pressure measurements

Blood pressure was measured using a standard automatic brachial sphygmomanometer (Welch Allyn, Vital Signs Monitor 300 series) which had passed validation. Three consecutive BP measurements were taken at 2‐minute intervals, after the participants had been seated and had rested quietly for >5 minutes with their feet on the ground and their back supported. The mean of the second and third measurements was recorded as the BP result. Hypertension was defined as a condition when participants were either on current antihypertensive medication and had systolic BP ≥ 140 or diastolic BP ≥ 90 mm Hg.25

2.4. Active lifestyle

All participants self‐reported regarding regular sport activity (defined as regular weekly sport activity causing increased heart rate). A non‐active lifestyle was defined as having no regular sport activity. A less‐active lifestyle was defined as doing regular sport activity of less than 2.5 hours per week, as recommended by the American Heart Association.26 An active lifestyle was defined as equal to or more than 2.5 hours of sport activity per week, as reported by the participants.

Maximal METS (metabolic equivalents of task) achieved during an exercise stress test was recorded by using the Bruce protocol.

The study was approved by the local ethics committee, and informed consent was obtained from all participants.

2.5. Statistical analysis

All continuous variables are displayed as means (standard deviation, SD) for normally distributed variables or median (interquartile range—IQR) for variables with abnormal distribution. Categorical variables are displayed as numbers (%) of patients within each group. The different biomarkers were compared by Student's t test for normally distributed variables and by the Mann‐Whitney U test for abnormally distributed variables. To assess associations among categorical variables, we used a chi‐square test. The values before and after the exercise test were compared using the Wilcoxon signed ranks test. ANOVA test was used to evaluate the difference in rest and post‐exercise ACR in normotensive and hypertensive participants, with an active vs non‐active lifestyle. Post hoc analysis was done using the Bonferroni correction. A general linear model was used to evaluate the estimated effect of specified covariates: age, sex, body mass index (BMI), METS achieved during the exercise stress test, treatment with angiotensin‐converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) using parameter estimates; B (with 95% confidence intervals) for rest, post‐exercise ACR and for delta ACR. P‐values of <0.05 were considered statistically significant. The IBM SPSS Statistics 24.0 statistical package was used to perform all statistical analyses (IBM SPSS Statistics for Windows, version 24.0: IBM Corp.).

3. RESULTS

Our study population included 3931 participants. Baseline participant characteristics are shown in Table 1. We lacked data for 86 participants: Of them, 44 had no ACR results, either before or after the exercise test, and 69 did not respond to the sport questionnaire.

Table 1.

Population characteristics

	All N = 3931	Normotensive N = 2703	Hypertensive N = 1228	P value
Age, y (SD)	47.7 (10.5)	45.3 (9.8)	53.0 (10.1)	<0.001
Male sex, %	75.5	70.4	86.6	<0.001
BMI, kg/m2 (SD)	26.0 (4.2)	25.2 (3.9)	27.6 (4.6)	<0.001
Current smokers, %	9.7	10.6	7.8	0.007
Total cholesterol, mg/dL (SD)	186.0 (32.5)	186.9 (32.2)	184.1 (33.1)	0.011
HDL‐c, mg/dL (SD)	52.6 (14.4)	53.9 (14.5)	49.9 (13.7)	<0.001
LDL‐c, mg/dL (SD)	111.0 (27.8)	112.0 (27.5)	109.0 (28.3)	0.002
Triglycerides, mg/dL (SD)	112.8 (66.4)	106.1 (60.1)	127.5 (76.7)	<0.001
Fasting glucose, mg/dL (SD)	87.5 (13.7)	85.4 (11.2)	92.0 (17.2)	<0.001
Systolic BP, mm Hg (SD)	125.5 (15.2)	119.2 (10.7)	139.6 (14.3)	<0.001
Hypertensive (medical treatment)a			135 (14.7)
Hypertensive (no treatment)b			143.1 (12.9)
Diastolic BP, mm Hg (SD)	77.8 (10.2)	74.3 (7.7)	85.5 (10.8)	<0.001
Hypertensive (medical treatment)a			81.1 (9.7)
Hypertensive (no treatment)b			89.3 (10.2)
METS, units (SD)	11.8 (3.8)	12.1 (3.3)	11.4 (4.7)	<0.001
Serum creatinine, mg/dL (SD)	1.01 (0.19)	1.0 (0.17)	1.03 (0.22)	<0.001
eGFRc, mL/min/1.73 m2	93.6 (18)	94.4 (19)	91.6 (15)	<0.001
CKD stages based on eGFRd, %
G1 (≥90 mL/min/1.73 m2)	72.2	73.6	68.9	0.002
G2 (60‐89 mL/min/1.73 m2)	24.2	22.9	26.8
G3a (45‐59 mL/min/1.73 m2)	2.9	2.7	3.3
G3b (30‐44 mL/min/1.73 m2)	0.8	0.7	0.9
G4 (15‐29 mL/min/1.73 m2)	0.02	0	0.08
G5 (<15 mL/min/1.73 m2)	0	0	0
Median rest ACR, mg/g (IQR)	1.37 (3.03‐7.08)	2.82 (1.29‐6.3)	3.59 (1.6‐9.23)	<0.001
Albuminuria stagesd, %
A1 (<30 mg/g)	94.5	94.8	93.6	0.113
A2 (30‐300 mg/g)	4.9	4.6	5.6
A3 (>300 mg/g)	0.56	0.5	0.7
Antihypertensive medications, %
ACEIs/ARBs	9.1	0	29.1	<0.001
Diuretics	4.4	0	14.1
Calcium channel blockers (non‐dihydropyridines)	0.5	0	1.8
Calcium channel blockers (dihydropyridines)	9.5	0	30.4
Beta‐blockers	4.0	0.07	12.7
Other	0.6	0	1.9
Regular sport activitye, %	73.9	73.6	74.8	0.439
Sport regularity, h/wk median (IQR)f	2.5 (0.83‐3.67)	2.5 (0.75‐3.33)	2.25 (1.0‐4.0)	0.005

Abbreviations: ACR, urinary albumin‐to‐creatinine ratio; ACEIs/ARBs, angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers; BMI, body mass index; BP, blood pressure; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; HDL‐c, high‐density lipoprotein cholesterol; LDL‐c, low‐density lipoprotein cholesterol; METS, metabolic equivalents of task; SD, standard deviation.

^aParticipants defined as hypertensive based on medical history including medical treatment for hypertension.

^bParticipants defined as hypertensive participants based on blood pressure measurements, who are not on antihypertensive medications.

^cGFR was estimated (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration (CKD‐EPI) creatinine equation, a 4‐variable formula23 adjusted for body surface area (Mosteller calculation).

^dCKD stages were defined based on eGFR and albuminuria according to KDIGO summary of recommendation statements.24

^eSelf‐reported any regular weekly sport activity involving increased cardiac pulse.

^fAmount of time spent in sport activity (only to those who reported "yes" to routine sport activity), in hours per week.

The mean age of participants was 47.7 years. Overall, 31.2% (n = 1228) had a diagnosis of hypertension: Of them, 60.3% (n = 741) were on chronic antihypertensive medical treatment, and 39.6% were defined as hypertensive participants according to their BP measurements. Mean BP for hypertensive patients was higher for participants diagnosed as hypertensive, based on BP measurements, compared to participants who were on antihypertensive medical treatment.

Patients with hypertension were older, had higher BMI, serum triglycerides, fasting glucose (and diabetes), and lower HDL (high‐density lipoprotein cholesterol) levels. In addition, hypertensive participants had a lower GFR and a higher level of rest albumin excretion measured as ACR. However, there was a similar prevalence of eGFR >60 mL/min/1.73 m² in both cohorts (96.6% vs 95.8%, normotensive vs hypertensive participants, respectively, P = 0.19) and ACR <30 mg/g (94.8% vs 93.6%, P = 0.113). There was a similar rate of participation in regular sport activity in both groups.

The hypertensive participants had a lower frequency of regular sport activity (defined as sport activity in hours per week) and were less fit according to a lower METS achieved during an exercise test. Among those who reported routine sport activity, the median of sport regularity was 2.5 hours, and this cutoff point was used for further analysis.

The median (IQR) of a post‐exercise urine sample collection was 20 (7‐39) minutes. (These data were available for only 710 participants.) For all participants, ACR was significantly increased following exercise (9.08 ± 37.7 vs 26.6 ± 62.3 mg/g, P < 0.001 for rest vs post‐exercise ACR, respectively). Mean change (delta) of ACR following exercise was 16.4 ± 63.8 mg/g (P < 0.001). At rest, 5.6% of participants reached the threshold of MIA, while at post‐exercise, the percentage was three times more (19.4%, P < 0.001).

Albumin‐to‐creatinine ratio was higher in hypertensive participants both before and after exercise, compared with normotensive participants (7.8 ± 24.3, 14.9 ± 56.7, 19.5 ± 51.0, 41.2 ± 105.2 mg/g, for participants at rest, normotensive, and hypertensive, and post‐exercise normotensive, and hypertensive, respectively, P‐value <0.001; Figure 1). This increase in ACR was higher in arbitrary units but not on a multiplicative scale.

Figure 1.

Rest albumin‐to‐creatinine ratio (ACR) and post‐exercise ACR differed significantly between normotensive and hypertensive patients (P < 0.0001 for both and for comparison between the four bars). P < 0.001 for all. Whiskers indicate SD

At rest, 4.3% of normotensive participants reached MIA compared to 7.7% of hypertensive participants, P < 0.001. Post‐exercise, 15.6% of normotensive compared to 26.9% of hypertensive participants reached MIA (P < 0.001).

To explore the effect of an active lifestyle, we divided each group into non‐active participants (no regular sport activity), less‐active (sport regularity <2.5 h/wk), and active lifestyle (≥2.5 h/wk).

Figure 2 demonstrates rest and post‐exercise ACR for normotensive and hypertensive participants, divided into activity levels. At both rest and post‐exercise ACR, there was a significant difference between hypertensive and normotensive participants (P < 0.001). Rest ACR was similar in normotensive participants irrespective of activity levels (7.6 ± 19.1, 7.7 ± 20.1, 8.2 ± 29.1 mg/g for non‐active, less‐active, and active, respectively, P = 0.58). However, rest ACR was significantly higher in non‐active hypertensive compared to less or active hypertensive participants (20.4 ± 43.7, 15.2 ± 63, 15.1 ± 51.2 mg/g, respectively, P = 0.02 for non‐active hypertensive participants compared to less‐active, and P = 0.017 for non‐active compared to active hypertensive participants; Figure 2A).

Figure 2.

Rest (A) and post‐exercise (B) albumin‐to‐creatinine ratio (ACR) in normotensive and hypertensive individuals with non‐active, less‐active, and active lifestyle. P < 0.001 for hypertensive vs normotensive participants for rest and post‐exercise ACR. * indicates P = 0.02 for non‐active hypertensive participants compared to less‐active and active hypertensive participants. ** indicates P = 0.01 for active hypertensive participants vs non‐active and less‐active hypertensive participants. Whiskers indicate SD

Post‐exercise ACR was also similar in normotensive participants in all levels of activity (23.7 ± 37.1, 17.7 ± 38.3, 24.2 ± 67.1 mg/g, P = 0.27). However, in hypertensive participants, those who reported on an active lifestyle had lower post‐exercise ACR compared to less‐active and non‐active hypertensive participants (35.3 ± 81.4, 44.7 ± 83.6, 42.4 ± 63.7 mg/g, respectively, P = 0.01 for active vs non‐active and less‐active hypertensive participants; Figure 2B). The results remain valid following adjustments for age, BMI, METS, diabetes, and use of ACEIs or ARBs.

Figure 3 demonstrates the change of ACR post‐exercise (delta ACR) in men and women, normotensive and hypertensive participants, with different levels of activity, analyzed as estimated marginal means, and following adjustment for age, BMI, METS, and use of ACEIs/ARBs. An active lifestyle significantly correlated to reduced delta ACR in hypertensive participants in both sexes, compared to a non‐active and less‐active lifestyle. In normotensive participants, however, an active lifestyle was not related to delta ACR following adjustment for the above covariates.

Figure 3.

The change of albumin‐to‐creatinine ratio (ACR) post‐exercise (delta ACR) in normotensive and hypertensive participants with non‐active, less‐active, and active lifestyle, in males and females. Shown are estimated marginal means adjusted for age, BMI, METS, use of ACEIs/ARBs. * indicates P value <0.05 in each cohort. Whiskers indicate SD

Next, we performed a multivariate regression analysis to estimate the effect of the tested covariates on delta ACR in normotensive and hypertensive participants (Table 2). While in normotensive participants, delta ACR was related to increased BMI and diabetes mellitus (Table 2a), in hypertensive participants, in addition to BMI and diabetes, increased age was also related to increased delta ACR, while an active lifestyle and fitness (measured as increased METS in a stress test) were protective (Table 2b).

Table 2.

Multivariate analysis for parameters related to delta ACR in normotensive (a) and hypertensive participants (b)

(a) Parameter	Delta ACR
	B	Sig	95% confidence interval
Age	0.39	0.109	−0.32 to 1.99
Sex (male)	0.71	0.175	−0.96 to 1.74
DM	1.56	<0.001	0.47 to 16.8
BMI	0.388	<0.001	0.156 to 1.738
METS	−0.231	0.058	−0.69 to 1.95
ACEi/ARBs	−0.78	0.109	−0.22 to 8.67
Sport regularity >2.5 h/wk	0.34	0.169	−0.86 to 4.15

(b) Parameter	Delta ACR
	B	Sig	95% confidence interval
Age	0.83	0.031	1.05 to 6.17
Sex (male)	−2.9	0.111	−8.3 to 1.65
DM	5.13	<0.001	1.7 to 16.0
BMI	2.9	0.015	1.5 to 3.6
METS	−0.28	0.044	1.2 to 6.4
ACEi/ARBs	−0.98	0.547	−6.1 to 14.7
Sport regularity >2.5 h/wk	3.27	0.026	1.7 to 5.81

Abbreviations: ACR, urinary albumin‐to‐creatinine ratio; ACEIs/ARBs, angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers; BMI, body mass index; DM, diabetes mellitus; METS, metabolic equivalents of task.

4. DISCUSSION

The association between urinary albumin excretion and increased cardiovascular mortality in high‐risk patients is evident even at urinary albumin levels below the clinically defined threshold for microalbuminuria1, 3, 4, 5 and is independent of eGFR levels.6 An accelerated change in ACR over time also correlates with hypertension in individuals with normal kidney function and normoalbuminuria.27 Furthermore, borderline hypertension is correlated with an excessive increase in albuminuria.28

To the best of our knowledge, our study shows, for the first time, that an active lifestyle could serve as a possible protective factor to reduce post‐exercise ACR.

Several studies have recently suggested that post‐exercise elevated albuminuria is a sensitive and early biomarker for cardiovascular risk stratification in diabetic and pre‐diabetic women.18, 19 However, post‐exercise albuminuria in hypertensive patients has not been studied extensively.

Our study, in accord with others, shows that hypertension is strongly related to increased rest albumin excretion.6, 29 One of the novel findings in our current study was that hypertensive individuals also had increased albumin excretion post‐exercise, compared to normotensive participants. Endothelial dysfunction and hypertension are related. Increased albuminuria post‐exercise may express earlier impairment than increased rest albuminuria.18 During stress, there is increased glomerular hydrostatic pressure, which may lead to increased glomerular permeability, and increased albumin excretion.30 We assumed that hypertensive patients demonstrate chronic increased glomerular pressure, which may be exacerbated during physical stress, and lead to increased albuminuria post‐exercise.

Another interesting finding in our study was that in hypertensive patients, any regular sport activity can ameliorate rest ACR, and an active lifestyle may significantly decrease ACR post‐exercise. Increased METS achieved by a routine Bruce‐protocol stress test, which is related to fitness, was also related to decreased delta ACR, which provided further evidence to strengthen our findings. It is well established that regular physical activity can attenuate oxidative stress and inflammation.31, 32

Previous studies have shown that exercise training improves endothelium‐dependent vasodilation in coronary vessels in patients with coronary disease and congestive heart failure and improves both endothelial nitric oxide formation and endothelium‐dependent vasodilation of skeletal muscle vasculature.33, 34, 35, 36 Physical activity could have similar effects on the renal vascular endothelium, which contributes to a reduction in albumin excretion.

Interestingly, the cutoff point of 2.5 weekly hours of physical activity (median value in our cohort), complies with exercise guidelines for hypertensive patients (150 minutes),26 thus raising the possibility that there is a cutoff point for overall endothelial health, renal, as well as cardiovascular.37, 38

Essential hypertension has been shown to be characterized by an impaired parasympathetic tone and marked sympathetic overdrive.39 Indeed, a recent publication from our group found that sympathetic/parasympathetic balance measured by cholinesterase activity is elevated in hypertensive and metabolic syndrome patients.40 Sympathetic overactivity effects include glomerular podocyte injury,41 increased arterial stiffness,42 and endothelial dysfunction.43 There is also an association between albuminuria and sympathetic overactivity in individuals with normal kidney function,44 and reducing sympathetic activity, even without lowering BP, has been shown to be protective to the kidney45 and has as an anti‐albuminuric effect in diabetic patients.46 Most of the participants in our study had normal kidney function, including normal range albumin excretion. Further research regarding the association and mechanism in this field is warranted.

Our study has some limitations: First, our results suggest only an association and do not prove causality. Second, our cohort consists of participants in a health‐screening program and is not a population‐based sample. However, we systematically checked for non‐response bias and found that non‐participants did not differ from participants on any of the socio‐demographic or biomedical variables. In addition, our cohort comprised mainly male participants (75.5%) and may not have accurately represented the female population. Despite the male majority, our female population did comprise almost 1000 participants, and we addressed this issue by adjusting for sex.

Another limitation in our study was that ACR values were available from a single measurement before and after exercise, and since ACR can vary from day to day, this could have resulted in inaccuracies.47 However, there is a considerable amount of evidence showing that a simple single‐void test is reliable and useful in screening, and this methodology avoids the problems associated with a 24‐hour urine collection.48, 49 Moreover, the large number of participants in this study balances out any possible imprecision regarding the ACR measurements.

The clinical implications of our study may lie in determining which antihypertensive medication is appropriate for therapy, that is, giving preference to an antiproteinuric drug in a hypertensive patient with a sedentary lifestyle. In addition, it might present another incentive through which we, as health care providers, could encourage hypertensive patients to adopt a more active lifestyle.

In conclusion, this study offers strong evidence of association between increased urine albumin in hypertensive individuals post‐exercise, and the role of regular physical activity in attenuating this complication. The cohort size is relatively large, increasing the validity of this study. However, association is not causation, and further research into the nature of these associations is warranted in order to generate a more complete understanding of their roles.

CONFLICT OF INTEREST

The authors have no conflicts of interest to disclose.

AUTHOR CONTRIBUTIONS

M. Ehrenwald and S. Shenhar‐Tsarfaty conceived the study; A. Grupper and O. Rogowski made a substantial contribution to conception and design of the study, and were critically involved in acquisition of data; M. Ehrenwald, S. Shenhar‐Tsarfaty, and A. Grupper analyzed the data; D. Schwartz, IF Schwartz, S. Berliner, M. Shashar, and R. Baruch contributed to interpretation of data; O. Rogowski, D. Zeltser, I. Shapira, S. Berliner, and S. Shenhar‐Tsarfaty performed the data collection; A. Grupper, M. Ehrenwald, D. Schwartz, S. Berliner, M. Shashar, and S. Shenhar‐Tsarfaty contributed to drafting of the manuscript; all authors critically reviewed the manuscript and approved it. conception and design. M. Ehrenwald, S. Shenhar‐Tsarfaty, S. Berliner, O. Rogowski and A. Grupper involved in analysis and interpretation of data. T. Fujiwara, S. Hoshide, T. Tsuchihashi, and K. Kario drafted the manuscript or critically revised for important intellectual content. K. Kario approved the final version of the submitted manuscript.

Grupper A, Ehrenwald M, Schwartz D, et al. Hypertension is associated with increased post‐exercise albuminuria, which may be attenuated by an active lifestyle. J Clin Hypertens. 2019;21:1171–1179. 10.1111/jch.13624