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The Journal of Clinical Hypertension logoLink to The Journal of Clinical Hypertension
. 2020 Aug 6;22(8):1425–1433. doi: 10.1111/jch.13956

Optimal blood pressure for the prevention of hypertensive nephropathy in nondiabetic hypertensive patients in Taiwan

Ting‐Wei Kao 1, Chin‐Chou Huang 2,3,4,5,, Jaw‐Wen Chen 3,4,5,6
PMCID: PMC8029863  PMID: 32762119

Abstract

Hypertension is a global health burden. However, clinical reference for the adequate management of blood pressure (BP) to prevent renal injury has yet to be established. Thus, this study aimed to investigate whether optimal control and maintenance of BP at < 140/90, < 130/80, or < 120/70 mmHg could prevent hypertensive nephropathy in nondiabetic hypertensive patients. A single‐center observational study of 351 nondiabetic hypertensive patients was conducted in Taiwan. The average age of the participants was 64.0 years, and approximately 57.8% of the participants were men. Kidney function was assessed using estimated glomerular filtration rate (eGFR). The baseline eGFR was 83.8 ± 19.8 mL/min/1.73 m2. All patients were followed up every 3 months and underwent office BP measurement and blood sampling. Renal events were defined as> 25% and> 50% decline in eGFR. During an average follow‐up period of 4.2 ± 2.3 years, a> 25% and> 50% decline in eGFR was noted in 49 and 11 patients, respectively. The Cox regression analysis revealed that a baseline BP ≥ 140/90 mmHg (hazard ratio [HR]: 1.965; 95% confidence interval [CI]: 1.099–3.514, P = 0.023) and ≥ 130/80 mmHg (HR: 2.799; 95% CI: 1.286–6.004, P = 0.009) increased the risk of> 25% decline in eGFR. Moreover, a baseline BP ≥ 140/90 mmHg (HR: 8.120; 95% CI: 1.650–39.956, P = 0.010) and follow‐up BP ≥ 140/90 mmHg (HR: 6.402; 95% CI: 1.338–30.637, P = 0.020) increased the risk of> 50% decline in eGFR. In conclusion, a stringent baseline BP < 130/80 mmHg and a follow‐up BP < 140/90 mmHg can be considered optimal cutoff values for clinical practice to prevent hypertensive nephropathy.

Keywords: blood pressure, Chinese, chronic kidney disease, hypertension, nephropathy

1. INTRODUCTION

Hypertension is an issue of concern for global public health. Approximately 1.13 billion individuals worldwide sustained hypertension, and the incidence is constantly rising. 1 Recognized as a major cause of global premature morbidity and mortality, hypertension is a well‐known risk factor in coronary heart disease, cerebrovascular disease, peripheral artery disease, and diabetes mellitus, among others. 2 However, despite a plethora of currently available antihypertensive medications, sufficient control of hypertension is only achieved in 20% of cases, 3 thereby marking it as a substantial unmet clinical need.

Not only hypertension itself but also secondary complications are intertwined with the development of unfavorable prognosis. Hypertension burdens pressure loading either centrally or peripherally and brings about target‐organ damage. Previous study showed downstream comorbidities were exhibited in nearly half of the hypertensive patients at primary care survey 4 . Specifically, cardiovascular sequelae secondary to elevated blood pressure (BP) have been extensively studied. Various guidelines established by the European Society of Cardiology/European Society of Hypertension (ESC/ESH), 5 American College of Cardiology/American Heart Association (ACC/AHA), 6 and Taiwan Society of Cardiology/Taiwan Hypertension Society (TSOC/THS) 7 all recommend standard values for hypertensive management primarily based on preventing further cardiovascular complications. The possible tissue damage to other organs, such as the renal system, was minimally addressed.

Although the impact of hypertension on renal function is well established, target for BP management is still debatable. Hypertension remains the second leading cause of end‐stage renal disease (ESRD) after diabetes mellitus (DM) even though the relative risk ratio of serious renal damage in patients with nonmalignant hypertension is low and not necessarily present as the premier complication. 8 Previous literature has suggested that hypertension is a strong independent risk factor for ESRD, 9 which is considered to be connected with adverse prognosis. 10 Adequate but not stringent BP control could effectively delay or prevent the onset of further microalbuminuria. 11 , 12 , 13 , 14 Nevertheless, such influence may be erased in the presence of preexisting renal injury. Pinpointing the ideal intensity of BP control in populations of Chinese origin is lacking and of clinical relevance.

This study aimed to investigate the efficacy of BP levels at 140/90, 130/80, and 120/70 mmHg when used as cutoff values for the intensive control and maintenance of BP to prevent hypertensive nephropathy. We hypothesized that an intensive control of office BP, which has a prognostic significance, is effective in preventing adverse renal events in nondiabetic hypertensive patients in Taiwan.

2. METHODS

2.1. Participants

Han Chinese patients with hypertension were included in our study from February 2012 to April 2019. The inclusion criteria were as follows: patients aged ≥ 20 years; those willing and capable of providing informed consent; those of Han Chinese descent; those who are official residents in Taiwan; those meeting one of the following hypertension criteria: (a) systolic BP (SBP) ≥140 mmHg or diastolic BP (DBP) ≥90 mmHg in at least two consecutive visits within 2 months and (b) taking one or more antihypertensive medications; those had no medical history of severe diseases, including liver, renal, cardiac, and pulmonary failure and carcinoma; those without acute disease within 2 weeks; and those without secondary hypertension. Only patients with nondiabetic hypertension were selected in this study.

The exclusion criteria were as follows: Subject was identified as a secondary hypertension patient; unable to understand or give informed consent; had one or more foreign parents. The study protocol was approved by the ethics committee of the Taipei Veterans General Hospital. This study was conducted in accordance with the principles of the Declaration of Helsinki and Title 45, U.S. Code of Federal Regulations, Part 46, Protection of Human Subjects, Revised November 13, 2001, effective December 13, 2001.

2.2. Study design

The study included a comprehensive examination of each participant’s patient history and a physical examination by a cardiologist (2nd author, Huang) at the hypertension clinic of the hospital. The patients’ office BP, including SBP and DBP, was measured, and their body mass indexes were determined. Antihypertensive drug prescriptions were recorded once present. All patients, who were followed every 3 months, received office BP measurement and blood sampling.

2.3. Office BP measurement

According to a standardized protocol, a well‐trained nurse assessed the morning office BP using an electronic BP monitor after the patients were instructed to sit for 10 min in a quiet room. During each measurement, both SBP and DBP were recorded. Three consecutive BP measurements were performed on the same upper arm. Each measurement was separated by an interval of 30 s. The average value of the last two measurements was considered the BP reading.

All patients were divided into different groups according to the baseline and follow‐up office BP (≥140/90, 130/80, or 120/70 mmHg) in the follow‐up period. Follow‐up office BP was classified according to the office BP during every visit after recruitment. Achieving the target BP in more than half of the visits was considered goal attainment.

2.4. Laboratory measurements

Fasting whole blood samples of the patients were obtained by venipuncture after 10‐minute rest in a supine position in the morning, typically between 0730 hours and 0900 hours. The participants were instructed to take all routine medications as they normally would. The blood samples were centrifuged, and the serum was thawed for analysis. Estimated glomerular filtration rate (eGFR) was calculated using the four‐variable equation proposed by the Modification of Diet in Renal Disease Study. 15

2.5. Renal outcomes

Renal events during the follow‐up period were defined as minor nephropathy, defined as> 25% decline in eGFR and major nephropathy, and defined as> 50% decline in eGFR. The latter had been previously used to indicate renal dysfunction. 16

2.6. Statistical Analysis

Statistical analysis was performed using the Statistical Package for Social Sciences software (version 18.0, SPSS Inc., Chicago, IL, USA). All data were expressed as mean ± standard deviation or frequency (percentage). Survival analysis was assessed using the Kaplan‐Meier curve, with significance based on the log‐rank test. To assess the independent effects of BP targets (baseline and follow‐up office BP ≥ 140/90, 130/80, or 120/70 mmHg) and renal outcomes, Cox proportional hazard regression analysis was performed. The adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated after adjusting for potential confounding factors. The HRs of BP targets for renal outcomes were adjusted for age, sex, body mass index, use of antihypertensive drugs, and baseline eGFR. A two‐sided P‐value < 0.05 was considered statistically significant.

3. RESULTS

A total of 419 Han Chinese hypertensive patients in Taiwan were eligible for enrollment. Among them, 351 were nondiabetic. The mean age of the participants was 64.0 ± 14.3 years, and approximately 57.8% were men. The average body mass index was 25.9 kg/m2. The heart rate at initial presentation was 70.4 ± 10.6 beats per min, and the average baseline BP measured during the office visit was 132.4/81.5 mmHg. All participants were taking at least one antihypertensive agent (average: 1.9 ± 0.9). The most common class of antihypertensive medications used in the study was calcium channel blockers (71.5%), followed by angiotensin‐converting enzyme inhibitor/angiotensin receptor blocker (65.2%), thiazide diuretics (22.5%), and beta‐blockers (21.9%). The renal function of the participants upon enrollment was generally not impaired (serum creatinine level of 0.9 ± 0.2 mg/dL and eGFR of 83.8 ± 19.8 mL/min/1.73 m2; Table 1).

Table 1.

Baseline characteristics of the subjects

All (n = 351)
Age, years 64.0 ± 14.3
Sex, n (%) men 203 (57.8%)
Body mass index, kg/m2 25.9 ± 3.9
Smoking, n (%) 18 (5.1%)
Office systolic BP, mmHg 132.4 ± 17.2
Office diastolic BP, mmHg 81.5 ± 10.5
Office heart rate, bpm 70.4 ± 10.6
ACEI/ARB, n (%) 229 (65.2%)
B‐blocker, n (%) 77 (21.9%)
CCB, n (%) 251 (71.5%)
Thiazide, n (%) 79 (22.5%)
Total antihypertensive medications, n 1.9 ± 0.9
Creatinine, mg/dL 0.9 ± 0.2
eGFR, mL/min/1.73 m2 83.8 ± 19.8
Mean follow‐up duration, years 4.2 ± 2.3

ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; bpm, beat per minute; CCB, calcium channel blocker; eGFR, estimated glomerular filtration rate.

To determine the cutoff value indicating possible kidney damage, the effect of office BP at either 140/90, 130/80, or 120/70 mmHg was examined according to the guidelines of the ESC/ESH, 5 ACC/AHA, 6 and TSOC/THS. 7 Differences were observed between the patients according to baseline or follow‐up office BP, mainly in the use of antihypertensive drugs, baseline eGFR, and mean follow‐up duration (Tables S1‐S4).

During an average follow‐up period of 4.2 ± 2.3 years, a> 25% and> 50% decline in eGFR was noted in 49 and 11 patients, respectively. In the three groups, the participants with a lower baseline office BP had less renal events than their hypertensive counterparts. A statistically significant reduction in the incidence of> 50% decline in eGFR was observed if the baseline office BP was < 140/90 mmHg (P = 0.010) or < 130/80 mmHg (P = 0.039). Moreover, a well‐controlled hypertension, as indicated by> 50% of office BP < 140/90 mmHg during the follow‐up periods, significantly reduced the incidence of> 50% decline in eGFR (P = 0.026). Furthermore, an> 50% declined in eGFR was not observed if the office BP was maintained at < 130/80 or < 120/70 mmHg (Table 2).

Table 2.

Office blood pressure and renal events

Patient number, n >25% decline in eGFR, n (%) >50% decline in eGFR, n (%)
Baseline office BP
<140/90 mmHg 205 23 (11.2%) 2 (1.0%)
≥140/90 mmHg 146 26 (17.8%) 9 (6.2%)
<130/80 mmHg 97 8 (8.2%) 0 (0.0%)
≥130/80 mmHg 254 41 (16.1%) 11 (4.3%)
<120/70 mmHg 26 1 (3.8%) 0 (0.0%)
≥120/70 mmHg 325 48 (14.8%) 11 (3.4%)
Follow‐up office BP
<140/90 mmHg 193 22 (11.4%) 2 (1.0%)
≥140/90 mmHg 158 27 (17.1%) 9 (5.7%)
<130/80 mmHg 76 9 (11.8%) 0 (0.0%)
≥130/80 mmHg 275 40 (14.5%) 11 (4.0%)
<120/70 mmHg 11 0 (0.0%) 0 (0.0%)
≥120/70 mmHg 340 49 (14.4%) 11 (3.2%)

BP, blood pressure; eGFR, estimated glomerular filtration rate.

The Kaplan‐Meier survival curves and log‐rank test were used to identify the number of participants who did not develop nephropathy in the follow‐up period. The incidence of renal events (>25% and> 50% decline in eGFR) was significantly lower in patients with a baseline BP < 140/90 mmHg (P = 0.023 and 0.002, respectively) (Figure 1). Similarly, the participants who presented with BP < 130/80 mmHg during the initial visit had less renal events (>25% and> 50% decline in eGFR) (P = 0.019 and 0.025, respectively) (Figure 2). Furthermore, a follow‐up office BP < 140/90 mmHg curtailed the presence of 50% decline in eGFR (P = 0.008) (Figure 3).

Figure 1.

Figure 1

Kaplan‐Meier survival curves showing the absence of renal events according to the baseline office blood pressure (BP) in patients with hypertension. All participants were divided into two groups according to baseline office BP levels. The blue line represents the patient group with BP < 140/90 mmHg. The green line represents the group with BP ≥ 140/90 mmHg. Renal events were defined as> 25% decline and> 50% decline in eGFR. Differences were compared using the log‐rank test. (A) Baseline office BP (<140/90 vs ≥140/90 mmHg) and> 25% decline in eGFR (P = 0.023). (B) Baseline office BP (<140/90 vs ≥140/90 mmHg) and> 50% decline in eGFR (P = 0.002)

Figure 2.

Figure 2

Kaplan‐Meier survival curves showing the absence of renal events according to baseline office blood pressure (BP) in patients with hypertension. All participants were divided into two groups according to baseline office BP levels. The blue line represents the patient group with a BP < 130/80 mmHg. The green line represents the group with a BP ≥ 130/80 mmHg. Renal events were defined as> 25% and> 50% decline in eGFR. Differences were compared using the log‐rank test. (A) Baseline office BP (<130/80 vs ≥130/80 mmHg) and> 25% decline in eGFR (P = 0.019). (B) Baseline office BP (<130/80 vs ≥130/80 mmHg) and> 50% decline in eGFR (P = 0.025)

Figure 3.

Figure 3

Kaplan‐Meier survival curves showing the absence of renal events according to follow‐up office blood pressure (BP) in patients with hypertension. All participants were divided into two groups according to the follow‐up office BP levels. Follow‐up office BP was defined according to the office BP during every visit after recruitment. Achieving the BP targets in more than half of the visits was considered goal attainment. The blue line represents the patient group with a BP < 140/90 mmHg. The green line represents the group with a BP ≥ 140/90 mmHg. Renal events were defined as> 25% and> 50% decline in eGFR. The differences were compared using the log‐rank test. (A) Follow‐up office BP (<140/90 vs ≥140/90 mmHg) and> 25% decline in eGFR (P = 0.063). (B) Follow‐up office BP (<140/90 vs ≥140/90 mmHg) and> 50% decline in eGFR (P = 0.008)

The Cox regression analysis revealed that in addition to age and initial eGFR level, the baseline office BP was significantly correlated to the development of renal events. A baseline BP ≥ 140/90 mmHg (HR: 1.965; 95% CI: 1.099–3.514, P = 0.023) and baseline BP ≥ 130/80 mmHg (HR: 2.799; 95% CI: 1.286–6.004, P = 0.009) significantly increased the risk of> 25% decline in eGFR (Table 3). Moreover, a baseline BP ≥ 140/90 mmHg remarkably increased the risk of> 50% decline in eGFR (HR: 8.120; 95% CI: 1.650–39.956, P = 0.010) after adjusting for other clinical characteristics (Table 4), and a follow‐up BP ≥ 140/90 mmHg in more than half of the visits during the follow‐up period was also a predictor of> 50% decline in eGFR (HR: 6.402; 95% CI: 1.338–30.637, P = 0.020) (Table 5).

Table 3.

Predictors of significant decline of estimated glomerular filtration rate (eGFR) (>25%)

HR 95% CI P‐value
Baseline office BP 140/90 mmHg
Age, years 1.034 (1.008‐1.061) 0.009
Sex (male vs female) 0.666 (0.365‐1.214) 0.184
Body mass index, kg/m2 1.014 (0.942‐1.093) 0.706
ACEI/ARB (yes vs no) 0.850 (0.451‐1.600) 0.614
B‐blocker (yes vs no) 1.302 (0.691‐2.452) 0.414
CCB (yes vs no) 1.304 (0.642‐2.651) 0.463
Thiazide (yes vs no) 1.178 (0.599‐2.316) 0.634
eGFR, mL/min/1.73 m2 1.036 (1.020‐1.053) <0.001
Office BP ≥ 140/90 mmHg (yes vs no) 1.965 (1.099‐3.514) 0.023
Baseline office BP 130/80 mmHg
Age, years 1.040 (1.014‐1.068) 0.003
Sex (male vs female) 0.642 (0.352‐1.172) 0.149
Body mass index, kg/m2 1.016 (0.942‐1.095) 0.685
ACEI/ARB (yes vs no) 0.837 (0.436‐1.606) 0.593
B‐blocker (yes vs no) 1.338 (0.713‐2.512) 0.364
CCB (yes vs no) 1.353 (0.659‐2.778) 0.410
Thiazide (yes vs no) 1.243 (0.620‐2.491) 0.541
eGFR, mL/min/1.73 m2 1.037 (1.021‐1.054) <0.001
Office BP ≥ 130/80 mmHg (yes vs no) 2.779 (1.286‐6.004) 0.009
Baseline office BP 120/70 mmHg
Age, years 1.038 (1.011‐1.065) 0.005
Sex (male vs female) 0.690 (0.379‐1.257) 0.226
Body mass index, kg/m2 1.006 (0.930‐1.087) 0.887
ACEI/ARB (yes vs no) 0.880 (0.467‐1.656) 0.692
B‐blocker (yes vs no) 1.261 (0.673‐2.362) 0.469
CCB (yes vs no) 1.354 (0.671‐2.734) 0.398
Thiazide (yes vs no) 1.219 (0.617‐2.406) 0.569
eGFR, mL/min/1.73 m2 1.035 (1.020‐1.051) <0.001
Office BP ≥ 120/70 mmHg (yes vs no) 4.776 (0.650‐35.070) 0.124

ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio.

Table 4.

Predictors of significant decline of estimated glomerular filtration rate (eGFR) (>50%)

Baseline Office BP 140/90 mmHg HR 95% CI P‐value
Age, years 1.081 (0.997‐1.171) 0.059
Sex (male vs female) 0.323 (0.078‐1.329) 0.117
Body mass index, kg/m2 0.995 (0.840‐1.179) 0.954
ACEI/ARB (yes vs no) 0.944 (0.231‐3.866) 0.936
B‐blocker (yes vs no) 1.485 (0.415‐5.307) 0.543
CCB (yes vs no) 0.543 (0.125‐2.363) 0.416
Thiazide (yes vs no) 2.151 (0.579‐7.993) 0.253
eGFR, mL/min/1.73 m2 1.000 (0.969‐1.031) 0.986
Office BP ≥ 140/90 mmHg (yes vs no) 8.120 (1.650‐39.956) 0.010

ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio.

Table 5.

Predictors of significant decline of estimated glomerular filtration rate (eGFR) (>50%)

Follow‐up Office BP 140/90 mmHg HR 95% CI P‐value
Age, years 1.087 (1.000‐1.180) 0.049
Sex (male vs female) 0.337 (0.080‐1.414) 0.137
Body mass index, kg/m2 0.996 (0.841‐1.180) 0.962
ACEI/ARB (yes vs no) 0.992 (0.237‐4.151) 0.991
B‐blocker (yes vs no) 1.400 (0.391‐5.009) 0.605
CCB (yes vs no) 0.635 (0.142‐2.848) 0.553
Thiazide (yes vs no) 1.849 (0.486‐7.031) 0.367
eGFR, mL/min/1.73 m2 1.000 (0.970‐1.031) 0.991
Office BP ≥ 140/90 mmHg (yes vs no) 6.402 (1.338‐30.637) 0.020

ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio.

4. DISCUSSION

This observational cohort study revealed that an adequate management of hypertension has a protective effect against subsequent nephropathy in Han Chinese hypertensive patients in Taiwan. Office BP was considered a modifiable risk factor of kidney injury, and active monitoring was found to have a clinical benefit. In addition, intensive control of baseline office BP < 130/80 mmHg and follow‐up office BP < 140/90 mmHg further decreased the occurrence of renal events in nondiabetic patients with hypertension.

The impact of hypertension on renal outcomes has been extensively assessed. In the last century, the Multiple Risk Factor Intervention Trial proposed that elevated BP was a strong independent risk factor for ESRD based on a study of 332 544 men during an average follow‐up of 16 years. 11 A subsequent 20‐year prospective observational study conducted in Washington County, Maryland, which included 23 534 Caucasian men and women, revalidated that hypertension is an important risk factor for chronic kidney disease (CKD). 12 By comparison, another study proposed that SBP was a significant predictor of ESRD in 107 192 participants (51 122 men and 56 070 women) during a 10‐year follow‐up. 9 Moreover, hypertensive nephropathy increases the risk of poor cardiovascular prognosis if the condition progresses to CKD. 10 These studies underscored the clinical need to identify individuals at risk at an earlier time to prevent renal injury secondary to poorly controlled hypertension.

To date, there is no consensus on the optimized control target for office BP to prevent hypertensive nephropathy. Data on the prognostic benefit of intensively controlling office BP are conflicting. A recent meta‐analysis of 19 randomized controlled trials showed that intensive BP control can better protect the vasculature, thereby reducing the risk of not only cardiovascular events but also albuminuria, particularly in high‐risk populations. 17 In another meta‐analysis of nine randomized clinical trials of nondiabetic CKD adults, nonblack patients or those with high protein levels might still benefit from intensive control. 16 On the contrary, the Systolic Blood Pressure Intervention Trial revealed that a high number of patients whose BP was intensively controlled presented with acute renal injury. 18 Coincidentally, the Action to Control Cardiovascular Risk in Diabetes 19 and the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial 20 showed that patients with a low follow‐up BP had a higher incidence of acute kidney injury, regardless of the presence of diabetes, which might be secondary to hypoperfusion of the renal parenchyma. In our study, we focused on nondiabetic patients with hypertension. Of the 351 nondiabetic hypertensive patients, 242 had stable renal function, and 109 presented with greater than stage 1 CKD. However, the overall renal outcomes were still superior to those of individuals with baseline BP < 130/80 mmHg.

Nonetheless, there is a lack of consensus regarding the most recent guidelines in terms of BP definition and treatment target. Hypertension is defined as BP> 140/90 mmHg, which requires lifestyle modification in addition to administration of antihypertensive agents, according to the ESC/ESH guideline. An intensive BP management at 130/80 mmHg was only recommended for patients with a high cardiovascular risk. 5 In contrast, the ACC/AHA guidelines universally set the restriction of BP at 130/80 mmHg for all individuals. 6 As for the TSOC/THS guidelines, a BP at < 140/90 mmHg was recommended for all populations except patients with DM, coronary artery disease, or CKD with proteinuria as a target BP of 130/80 mmHg may be suitable. 7 However, to date, these guidelines have focused more on consequent cardiovascular sequelae rather than renal outcomes. In our study, kidney function was better protected by intensive BP control at 130/80 mmHg compared with 140/90 mmHg. Thus, renal prognosis must be incorporated into future guidelines, and stratified BP targets for patients with different risks of nephropathy should be established.

In addition to baseline BP, we reclassified the patients according to BP reading during each visit and identified the prognostic significance of follow‐up BP. Individuals who failed to maintain an office BP < 140/90 mmHg in more than half of the visits were considered at risk of a major decrease in renal function. Daimee et al 21 and Einstadter et al 22 showed that repeated documentation of office BP improved SBP by 8–11 mmHg, probably due to the optimization of antihypertensive agents. However, there are no studies on the relationship between repetitive measurements of hypertension and downstream end‐organ complications. Our study proposed that both elevated BP at baseline and poor control of BP resulted in hypertensive nephropathy.

Diabetes nephropathy and hypertensive nephrosclerosis are still the leading causes of CKD worldwide, even though racial and sociodemographic differences can be observed in terms of the incidence and subsequent decrease in the rate of eGFR. 23 According to the 2019 statistics by the U.S. Centers for Disease Control and Prevention, the primary causes of ESRD were DM and hypertension in 38% and 26% of the US population, respectively. 24 However, studies conducted on Asian and Caucasian populations have shown comparable odds ratios for eGFR < 45 mL/min/1.73 m2 at 3.19 (1.99–5.1) for DM and 3.31 (2–5.48) for hypertension. Both variables were also significant risk factors for the decrease in eGFR to < 60 mL/min/1.73 m2. 25 Since we only assessed the effects of BP targets on nondiabetic hypertensive patients, further large‐scale studies of both diabetic and nondiabetic hypertensive patients with different ethnic backgrounds must be conducted to validate these findings.

4.1. Limitations

The current study had several limitations that must be addressed. First, this was an observational study. Thus, bias in patient enrollment and in the critical assessment of outcomes could not be completely excluded. Second, only hypertensive patients with Han Chinese heritage in Taiwan were enrolled in the current study. Hence, further studies of patients with different ethnic backgrounds should be conducted. Third, only a small number of patients were included. Thus, the correlation between hypertension management and nephropathy cannot be generalized. Randomized control trials with a larger number of participants and longer follow‐up period should be conducted to identify possible effects and causal relationships. Fourth, defining hypertensive nephropathy according to decline in eGFR was a relatively arbitrary metric. However, it is a commonly used definition in clinical practice. 16 Finally, a recent report has shown that administration of hora somni medication further decreases the cardiovascular risk. 26 However, the timing of antihypertensive drug administration was not considered in the current study. Therefore, whether the renal protective effects will be similar remains unknown.

5. CONCLUSIONS

A high office BP is a significant risk factor for the development of hypertensive nephropathy in Han Chinese hypertensive patients in Taiwan. Proper control of BP both at baseline and during follow‐up can have protective effects against consequent kidney injury. Although our study supports the standards of care recommended by the mainstream guidelines for renal dysfunction, we found that more rigorous targeting of BP at 130/80 mmHg at baseline and 140/90 mmHg at follow‐up further reduced renal events. Moreover, routine office BP measurement and adequate BP management can prevent hypertensive nephropathy.

CONFLICT OF INTERESTS

The authors declared no conflict of interests.

Supporting information

Table S1

Table S2

Table S3

Table S4

ACKNOWLEDGEMENTS

None.

Kao T‐W, Huang C‐C, Chen J‐W. Optimal blood pressure for the prevention of hypertensive nephropathy in nondiabetic hypertensive patients in Taiwan. J Clin Hypertens. 2020;22:1425–1433. 10.1111/jch.13956

FUNDING

This work was supported by research grants V108C‐151, VGHUST108‐G1‐3‐2, and VTA108‐V1‐7‐2 from Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C., and research grant MOST 108‐2314‐B‐075‐062‐MY3 from the Ministry of Science and Technology, Taiwan, R.O.C. The funders had no role in data collection or preparation of the manuscript.

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Associated Data

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Supplementary Materials

Table S1

Table S2

Table S3

Table S4


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