What is the optimal blood pressure level for kidney in the general population?

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Ohno ◽  
H Takase ◽  
M Machii ◽  
D Nonaka ◽  
S Takayama ◽  
...  

Abstract Background/Introduction Hypertension induces kidney dysfunction, and vice versa. Furthermore, kidney dysfunction can be a risk factor for cardiovascular diseases as well as end-stage of kidney disease. Although blood pressure (BP) control is necessary to prevent deterioration of kidney function, strict BP control may deteriorate kidney function. Purpose The present observational study investigated effects of BP levels on the incidence of chronic kidney disease (CKD) in the general population. Methods A total of 12,753 subjects with normal kidney function (estimated glomerular filtration rate [eGFR] ≥60 mL/min per 1.73 m2) (male 7,707, mean age 51.8 years) who visited our hospital for an annual physical check-up from April 2010 to March 2018 were enrolled. After baseline examination, subjects were followed up until March 2019 (median 1769 days) with the endpoint being the development of CKD (eGFR<60 mL/min per 1.73 m2). The modified MDRD formula for Japanese was used to calculate eGFR. Hypertension was defined as BP ≥140/90mmHg or the use of antihypertensive medication. Results During the follow-up period, 1,604 subjects developed CKD (26.9 per 1,000 person-years) with the incidence being more frequent in hypertensive (n=3,098) than normotensive (n=9,655) subjects at enrollment (44.2 vs. 21.5 per 1,000 person-years, respectively; hazard ratio [95% confidence interval] from multivariate Cox proportional analysis 1.205 [1.061–1.369]). Hazard ratio of systolic BP at baseline was 1.006 [1.002–1.010] in a multivariate Cox proportional hazard regression model adjusted for possible risk factors. The incidence was lower in subjects without hypertension throughout the follow-up period (normotension group, n=7,866) than those who were diagnosed as having hypertension at least once during the period (hypertension group, n=4,887) (23.1 vs. 32.3 per 1,000 person-years, p<0.001). In the normotension group, subjects with average BP <120/80mmHg had lower incidence of CKD than in those with BP ≥120/80mmHg (17.2 vs. 36.1 per 1,000 person-years, p<0.001). In contrast, in the hypertension group, the incidences of CKD in subjects with average BP <120/80, 120–139/80–89 and ≥140/90mmHg were 34.3, 25.8, and 54.4 per 1,000 person-years, respectively (p<0.001). Moreover, in hypertensive subjects under medication (n=2,002) with average BP <120/80, 120–139/80–89 and ≥140/90mmHg, the incidence of CKD was 65.5, 41.3, and 64.3 per 1,000 person-years, respectively (p<0.01). Conclusions The incidence of CKD was higher in hypertensive than in normotensive subjects. The lower BP was associated with the lower incidence of CKD in normotensive subjects, while strict BP control may increase the risk of CKD in hypertensive subjects. Funding Acknowledgement Type of funding source: None

2019 ◽  
Vol 44 (5) ◽  
pp. 973-983
Author(s):  
Daisuke Uchida ◽  
Ryo Kido ◽  
Hiroo Kawarazaki ◽  
Masaru Murasawa ◽  
Ayami Ando ◽  
...  

Background/Aims: The association of diastolic blood pressure (DBP) with incidence of chronic kidney disease (CKD) in the general population is not well examined. Methods: Using national health check-up database from 2008 to 2011 in the general Japanese population aged 39–74 years, we evaluated the association between DBP and incidence of CKD 2 years later in 127,954 participants without CKD. DBP was categorized by every 5 mm Hg from the lowest (<60 mm Hg) to the highest category (>100 mm Hg) and was further stratified into those with and without antihypertensive medications (BP meds). We calculated the OR for estimating adjusted risk of incident CKD using logistic regression model. Results: Participants were 62% female and 25.9% with BP meds, mean age of 76 years with estimated glomerular filtration rate of 78.2 ± 13.4 and DBP of 76 ± 11 mm Hg. Two years later, 12,379 (9.7%) developed CKD. Compared to DBP 60–64 mm Hg without BP meds as reference, multivariate analysis showed no difference in CKD risk at any DBP category among those without BP meds. However, in those with BP meds, risk increased according to lower DBP from 95 to 60 mm Hg (p for trend 0.05) with OR 1.51 (95% CI 1.14–1.99) in DBP <60 mm Hg. In subgroup analysis within those with or without BP meds, CKD risk was lower at higher DBP (p for trend 0.02) only in those without BP meds. Conclusion: Lower DBP was associated with higher risk of incident CKD only in the general population taking antihypertensive medication.


Author(s):  
Frédéric Fumeron ◽  
Ray El Boustany ◽  
Jean-Philippe Bastard ◽  
Soraya Fellahi ◽  
Beverley Balkau ◽  
...  

Abstract Background High adiponectin levels are associated with diabetic nephropathy. Nevertheless, it is not known whether plasma adiponectin is associated with renal function decline in the general population. We evaluated whether adiponectin concentrations were associated with changes in renal function in a community cohort, the Data from an Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study. Methods Plasma adiponectin concentrations were measured in a random sample of 3284 people from the DESIR study, a 9-year prospective cohort from the general population. Data were analysed for three endpoints during follow-up: incidence of Stage 3 chronic kidney disease (CKD); the Kidney Disease: Improving Global Outcomes (KDIGO) criterion ‘certain drop in eGFR’ and rapid kidney function decline [estimated glomerular filtration rate (eGFR) slope steeper than −3 mL/min/1.73 m2/year]. Results After exclusion of participants with an eGFR &lt;60 mL/min/1.73 m2 at baseline and those with type 2 diabetes or impaired fasting glycaemia at any time during follow-up (remaining n = 2174), there was a 113% higher risk for a rapid decline in kidney function in participants with adiponectin above the third tertile (T3) versus below the first tertile (T1) (Ptrend = 0.004) and a 53% higher risk for kidney function decline as defined by the KDIGO criterion (Ptrend = 0.04). In a cross-sectional analysis, adiponectin was positively associated with urinary albumin:creatinine ratio at baseline (P = 0.009). Conclusions In a healthy cohort from the general population, higher levels of plasma adiponectin were associated with decreased renal function at baseline and at follow-up. This result is similar to what is observed in people with diabetic nephropathy, in contrast with animal models of nephropathy.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Baback Roshanravan ◽  
Cassiane Robinson-Cohen ◽  
Kushang V Patel ◽  
Greg Levin ◽  
Ian H de Boer ◽  
...  

Objective: Skeletal muscle dysfunction (sarcopenia) is an under-recognized complication of chronic kidney disease (CKD) that may have important clinical consequences. Gait speed is associated with sarcopenia and comorbid disease burden among older adults; however, little is known about the prognostic significance of gait speed in CKD. We determined the association of gait speed with all-cause mortality in a prospective cohort of non-dialysis CKD patients. Methods: We measured usual gait speed over 4-meters in 309 participants from a prospective study of non-dialysis CKD. Included subjects had an estimated glomerular filtration rate (eGFR ckdepi ) <90mL/min/1.73m 2 , were stroke-free and did not require a wheelchair for ambulation. Study coordinators assessed mortality during follow-up by phone contacts, medical record review, and the social security death index. We evaluated gait speed continuously, and using a cut point of 0.8 m/s, consistent with previous studies. We used Cox's proportional hazards to estimate the association of gait speed with mortality after adjustment for age, sex, race, smoking, diabetes, pre-existing CAD, BMI, eGFR and hemoglobin. Results: Median follow-up time was 2.7 years; range 27 days to 4.8 years. The mean age was 58.9 ± 13 years and mean eGFR by cystatin C (eGFR cysc ) was 48.5 ± 23mL/min/1.73m 2 . There were a total of 31 deaths (10.4%) during follow-up. Unadjusted mortality rates were 23 and 80 deaths per 1,000 person-years among participants who had a gait speed of >0.8m/s versus ≤0.8m/s, respectively. After full adjustment, gait speed ≤0.8m/s was associated with a 2.8-fold greater risk of death compared to a gait speed >0.8 m/s. Gait speed was also strongly associated with mortality when analyzed as a continuous variable ( Table ) and a stronger predictor of death than age, history of CAD, or diabetes. No. Deaths (%) Model 1 + Model 2 # Hazard Ratio 95% CI Hazard Ratio 95% CI Gait speed * 32(10) 0.74 (0.64-0.86) 0.75 (0.64-0.87) >0.8m/s 13 (6) Reference Reference ≤0.8m/s 19(19) 3.49 (1.54-7.95) 2.84 (1.25-6.48) * Gait speed analyzed continuously per 10cm/s increase in speed. +Model 1: Adjusted for age, sex, race, study site #Model 2: adds smoking, BMI, eGFR cysc , diabetes, prevalent coronary disease. Conclusion: Gait speed is strongly associated with death in a cohort of middle-aged CKD patients.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ashlyn C Harmon ◽  
Ashley C Johnson ◽  
Santosh Atanur ◽  
Klio Maratou ◽  
Tim Aitman ◽  
...  

Hypertension, diabetes and obesity, along with genetic predisposition, contribute to the growing number of chronic kidney disease patients. Our novel congenic model [S.SHR(11)] was developed through genetic modification of the Dahl salt-sensitive (S) rat, a model of hypertension related renal disease. The S.SHR(11) strain exhibits accelerated kidney injury compared to the already highly susceptible S rat. On either a low or high-salt diet, the S.SHR(11) model predominately exhibited more tubulointerstitial fibrosis compared to the S rat (17.1±1.29% vs. 12.9±1.22%). Increased α-SMA and macrophage infiltration was also observed. The S and S.SHR(11) had similar blood pressure (week 12), despite an early reduction in renal function in the S.SHR(11); however at an advanced age the S.SHR(11) demonstrated significantly higher blood pressure than the S (215±6.6 mm Hg vs. 183±5.9, respectively). This suggests that increased kidney injury is driving the development of hypertension later in life. Since these two animal models are identical with exception of chromosome 11, the causative genetic variants contributing to decreased renal function must reside within this region. The Dahl S and SHR genomes have been sequenced; this data provides a catalog of all the genetic variants between the two models. The 95% confidence interval of the genomic locus contains 28 non-synonymous SNP, with 15 of these SNP occurring within only three genes: Retnlg , Trat1 and Myh15. Two of these genes, Retnlg and Trat1, are known to play a role in immune response leading to our hypothesis that genetic variants in these genes alter protein function and lead to an increased immune response. Bone marrow transplant studies have been initiated to test our hypothesis and preliminary data shows that S rats who receive S.SHR(11) bone marrow have kidney function measurements similar to the S.SHR(11). The sequencing information has also lead to the development of nine new, more refined congenic strains. Through functional analysis of these new congenic animals, identification of the causative genetic variations will be expedited. In summary, we are employing a model of accelerated kidney disease to identify genes or genetic variants responsible for reduced kidney function and hypertension.


Author(s):  
Simon Correa ◽  
Xavier E. Guerra-Torres ◽  
Sushrut S. Waikar ◽  
Finnian R. Mc Causland

Magnesium is involved in the regulation of blood pressure (BP). Abnormalities in serum magnesium are common in chronic kidney disease (CKD), yet its association with the development of hypertension and CKD progression in patients with CKD is unclear. We analyzed data from 3866 participants from the CRIC Study (Chronic Renal Insufficiency Cohort). Linear regression assessed the association of serum magnesium with baseline systolic BP (SBP) and diastolic BP (DBP). Logistic regression explored the association of serum magnesium with various definitions of hypertension. Cox proportional hazards models explored assessed the risk of incident hypertension and CKD progression. Mean serum magnesium was 2.0 mEq/L (±0.3 mEq/L). Higher magnesium was associated with lower SBP (−3.4 mm Hg [95% CI, −5.8 to −1.0 per 1 mEq/L]) and lower DBP (−2.9 mm Hg [95% CI, −4.3 to −1.5 per 1 mEq/L]). Higher magnesium was associated with a lower risk of American Heart Association–defined hypertension (SBP≥130 mm Hg or DBP≥80 mm Hg) at baseline (adjusted hazard ratio, 0.65 [95% CI, 0.49–0.86 per 1 mEq/L]), a lower risk of suboptimally controlled BP (SBP≥120 mm Hg or DBP≥80 mm Hg; adjusted odds ratio, 0.58 [95% CI, 0.43–0.78 per 1 mEq/L]). In time-to-event analyses, higher baseline serum magnesium was associated with a nominally lower risk of incident CRIC-defined hypertension (adjusted hazard ratio, 0.77 [95% CI, 0.46–1.31 per 1 mEq/L]). Higher magnesium was associated with a significantly lower risk of CKD progression (adjusted hazard ratio, 0.68 [95% CI, 0.54–0.86 per 1 mEq/L]). In patients with CKD, higher serum magnesium is associated with lower SBP and DBP, and with a lower risk of hypertension and CKD progression. In patients with CKD, whether magnesium supplementation could optimize BP control and prevent disease progression deserves further investigation.


2021 ◽  
Vol 6 (14) ◽  
pp. 80-88
Author(s):  
Huseyin Duru ◽  
Ekrem KARA

Objective: To evaluate the effect of 24 hour systolic blood pressure (SBP) and diastolic blood pressure (DBP) variability (BPV) on renal progression in hypertensive patients with chronic kidney disease (CKD) Methods: A total 59 hypertensive patients (mean age: 54.2±14.6 years, 50.8% male) with CKD who underwent 24 hours ambulatory blood pressure measurement (ABPM) were included. Data on SBP, DBP, BPV coefficients (VC) for SBP (SBP-CV) and DBP (DBP-CV) were recorded. A decrease in e-GFR of <5 ml/min/year was considered as normal renal progression and a decrease in ≥5 ml/min/year was considered as rapid renal progression. Results: Overall, 40.6% of the patients had uncontrolled HT, while 45.8% had non-dipper pattern. Mean±SD daytime and night-time SBP and SBP-VC values were 135.3±17.9 mmHg, 128.6±23.0 mmHg, 11.7±2.8 and 9.5±3.6, respectively. Mean±SD daytime and nigh-time DBP and DBP-VC values were 84.5±13.4 mmHg, 77.2±16.1 mmHg, 13.8±3.8 and 12.0±3.7, respectively. Rapid renal progression was detected in 25.4% of patients with no significant difference in daytime, night-time and total SBP, SBP-VC, DBP and DBP-VC values between patients with rapid vs. natural renal progression. The regression analysis adjusted for age, gender, presence of DM, baseline e-GFR and dipping status revealed no significant impact of SBP-VC and DBP-VC in predicting rapid progression (p> 0.05). Conclusion: In conclusion, our finding revealed no significant association between BPV and renal progression in hypertensive patients with CKD. Larger scale prospective, randomized controlled trials with longer follow-up are needed to clarify this issue.


2018 ◽  
Vol 27 (7) ◽  
pp. 758-766 ◽  
Author(s):  
Akiko Sakaue ◽  
Hisashi Adachi ◽  
Mika Enomoto ◽  
Ako Fukami ◽  
Eita Kumagai ◽  
...  

Aims It is well known that a decline in physical activity is associated with an increase of all-cause death including cardiovascular events and cancer. Few studies have examined the association between occupational sitting time and mortality. Therefore, we investigated this issue in a general population. Methods Physical activity and occupational sitting time were measured using the Baecke physical activity questionnaire in 1999. The questionnaire generated indices in three physical activity categories: work, sport and leisure-time. A total physical activity index was calculated by adding these three indices. The Baecke physical activity questionnaire was able to evaluate occupational sitting time. Hazard ratios and 95% confidence intervals (CIs) were calculated using Cox's proportional hazard regression models. Results We enrolled a total of 1680 participants, who were followed up for 15.9 ± 3.8 years. The final follow-up rate was 93%. During the follow-up period, 397 subjects died. A significant inverse association ( p < 0.0001) was found between physical activity and mortality after adjustment for age and sex. Compared with lower levels of physical activity, the adjusted hazard ratio for mortality at higher levels of physical activity was 0.85 (95% CI: 0.78–0.92). Longer occupational sitting time was also significantly associated with higher mortality ( p < 0.01). The adjusted hazard ratio for mortality at longer occupational sitting time was 1.16 (95% CI: 1.05–1.27). These findings were observed in males, but not in females. Conclusions Our data demonstrated that higher levels of physical activity are associated with a reduced risk of cancer and cardiovascular death. Further, longer occupational sitting time is associated with increased mortality.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Amanda E Paluch ◽  
Lindsay Pool ◽  
Tamara Isakova ◽  
Myles Wolf ◽  
Rupal Mehta ◽  
...  

Introduction: Racial and ethnic minorities are at higher risk for Chronic Kidney Disease (CKD). Higher levels of cardiorespiratory fitness (CRF) can reduce the risk of a rapid decline in estimated glomerular filtration rate (eGFR) and incidence of CKD. Little is known regarding how CRF contributes to racial disparities in CKD. Hypotheses: We hypothesized that: 1) baseline CRF is inversely associated with the risk of incident CKD after adjustment for covariates and 2) differences in baseline CRF account for a proportion of the disparity in incident CKD between blacks and whites. Methods: A total of 4328 young adults without CKD (age 24.8±3.6 years, 52.8% (n=2285) women, 51.9% (n=2247 black) completed a maximal graded treadmill test at baseline. We calculated eGFR using the CKD-EPI formula (baseline eGFR: 102.1±17.9 and 92.3±14.1 mL/minute/1.73 m 2 for blacks and whites, respectively). We defined CKD status as eGFR of <60 mL/minute/1.73 m 2 during 10, 15, 20, 25, and 30 year follow-up assessments. Multivariable Cox models examined hazard ratios (HR) and 95% confidence intervals (CI) for incidence of CKD. Models adjusted for baseline race, sex, age, field center, alcohol intake, smoking status, healthy eating index, eGFR, maximal educational attainment, and time-varying BMI, diabetes, and hypertension. The percent reduction in parameter estimates determined the excess risk explained according to CRF. Results: During the 30 years of follow-up, 84 blacks and 43 whites developed CKD. Every 1-minute lower treadmill duration associated with 12% higher rate of CKD (HR=1.12 (1.01-1.22)). Blacks were 1.89 times more likely to develop CKD compared to whites (HR=1.89 (1.23-2.91)). This was reduced to 1.75 (1.13-2.70) with CRF added to the model. This corresponds to a β reduction of 14.3% for race according to CRF. Conclusion: Both low fitness during young adulthood and black race are associated with higher incidence of CKD later in life. Fitness is a modifiable factor that could be targeted to address a portion of the disparity gap in CKD.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mark Behan ◽  
Leonard Browne ◽  
Stack Austin

Abstract Background and Aims Lithium is implicated as a causative factor in the development and progression of chronic kidney disease (CKD). Few studies have assessed the independent impact of plasma levels and duration of lithium therapy on CKD progression. We examined the influence of lithium on CKD progression in the Irish health system. Method We utilised data from the Irish Kidney Disease Surveillance System (IKDSS) to explore associations of lithium levels and duration of exposure with kidney function in a regional cohort. A retrospective cohort study was conducted between 1999 to 2014 from the Midwest Region. All adult patients with lithium levels were identified and followed longitudinally. Kidney function was assessed at baseline and longitudinally using serum creatinine and estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI. Patients with &lt; 2 lithium values, missing data on creatinine were excluded. The index date was the date of the first lithium blood test. Toxicity from lithium was defined as levels &gt;1.2mmol/L as per NICE guidelines while duration of treatment was calculated based on patient –years of exposure as determined by positive blood lithium levels. Relationships between baseline kidney function, lithium levels, duration of exposure and each patients most recent eGFR value on follow up were assessed using multiple linear regression Results We identified 1,978 patients exposed to lithium from 1999-2014, mean age was 47.4 (15.6), 45.1% were men, eGFR [median (IQR)] at baseline was 84.4 (32.1) ml/min1.73m and the median duration of exposure was 3.0 years (IQR=4 years). Frequency of lithium testing increased from 1.77 in 1999 to 2.66 in 2014. In multiple linear regression, the final eGFR on follow-up was significantly lower in older patients (-0.48 ml/min/1.73m per year increase in age), P&lt;0.001; in patients with elevated baseline lithium levels (-2.18 ml/min1.73m lower per unit increase), P&lt;0.05, with long duration of exposure (-1.42 ml/min/1.73m lower for each year on lithium), P&lt;0.001, and for patients with low GFR at baseline (P&lt;0.001). Together these variables explained 58% of the variation in the final model. Conclusion Both the magnitude of and the duration of lithium exposure are both independently associated with CKD progression among lithium users in the Irish health system. Higher baseline lithium values had a more deleterious impact on kidney function. Continued efforts should be expended in minimising the risks of lithium induced nephrotoxicity through switching to alternatives and dose reduction when over possible. Funding This study is funded by the Health Research Board and the Midwest Research and Education Foundation (MKid).


2019 ◽  
Vol 188 (9) ◽  
pp. 1637-1645 ◽  
Author(s):  
Jun Hata ◽  
Tomoyuki Ohara ◽  
Yoshinori Katakura ◽  
Kuniyoshi Shimizu ◽  
Shuntaro Yamashita ◽  
...  

Abstract We examined the association between serum concentrations of β-alanine, a metabolite of carnosine and anserine, and the risk of dementia in a general population of elderly Japanese persons. In 2007, 1,475 residents of Hisayama, Japan, aged 60–79 years and without dementia were divided into 4 groups according to quartiles of serum β-alanine concentrations (quartile 1, lowest; quartile 4, highest) and followed for a median of 5.3 years. During follow-up, 117 subjects developed all-cause dementia (Alzheimer in 77 cases and vascular dementia in 31). The risk of all-cause dementia decreased with increasing serum β-alanine levels after adjustment for potential confounding factors (quartile 2, hazard ratio (HR) = 0.73 (95% confidence interval (CI): 0.45, 1.18); quartile 3, HR = 0.50 (95% CI: 0.28, 0.89); quartile 4, HR = 0.50 (95% CI: 0.27, 0.92); P = 0.01 for trend). A similar inverse association was observed for Alzheimer disease (quartile 2, HR = 0.78 (95% CI: 0.44, 1.38); quartile 3, HR = 0.53 (95% CI: 0.26, 1.06); quartile 4, HR = 0.53 (95% CI: 0.25, 1.10); P = 0.04 for trend) but not for vascular dementia. We found that higher serum β-alanine levels were significantly associated with lower risks of all-cause dementia and Alzheimer disease. Because serum β-alanine levels reflect intakes of carnosine/anserine, higher intakes of carnosine/anserine might be beneficial for the prevention of dementia.


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