Insights into hypertension in children and adolescents in (South) Africa: the role of salt sensitivity
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1 Insights into hypertension in children and adolescents in (South) Africa: the role of salt sensitivity Brian Rayner, Division of Nephrology and Hypertension, University of Cape Town
2 Satellite View of Cape Town Winelands Cape Floral Kingdom Whales, great white shark 20 0 C False Bay Cape Point Table Bay 10 0 C Robben Island Table Mountain
3 Main campus Slopes of Devil s Peak
4 Prevalence of HT in SA by Age Bradshaw et al, NCDs: the race against time, MRC, 2013
5 Prevalence of overweight/obesity
6 Unpublished Young Hypertensives, Cape Town DEMOGRAPHICS 113 records located Mean age 22 years 81% had a family history of hypertension Majority have primary hypertension Body mass index: 45% normal BMI; 29% overweight; 26% obese
7 Found no cases of hypertension in 1800 natives examined No age treated rise in BP No cases of LVH at autopsy
8 Background Non-Hispanic blacks had the highest age adjusted prevalence (44.4% men and 43.9% women) Pressure-related cardiovascular-renal complications (stroke, LVH, HF, and CKD/end-stage renal disease) occur excessively in blacks compared with whites In 2005, the death rate from HTN (per population) was 15.1 in white men, 51.0 in black men, 15.1 in white women, and 40.9 in black women Blood pressure less well controlled despite 2 : More likely to be diagnosed More likely to be treated More likely to be treated more intensively 1. John M. Flack et al. Hypertension. 2010;56: Howard G et al. Stroke 2006;37:
9 TOD in selected SSA countries First Author Country Sample Size LVH CCF Overt proteinuria/ CKD Oladapo Nigeria Ayodele Nigeria Ekore Nigeria Ayodele Nigeria Addo Ghana Rayner Peer South Africa South Africa Salako Nigeria Stewart South Africa Ogah, Rayner, Heart 2013
10 SBP Responses in Blacks Class Mean (mmhg) CI P value CCB P< Diuretic P< Non-RAS drugs ACE inhibitor P< ARB P< RAS drugs blocker P=0.02 Adapted Brewster et al, Intern Emerg Med (2016) 11:
11 ALLHAT Combined CVD Subgroup Comparisons (32% Black) Total 1.04 (0.99, 1.09) Age < (0.94, 1.12) Age >= (0.99, 1.12) Men 1.04 (0.98, 1.11) Women 1.04 (0.96, 1.13) Black 1.06 (0.96, 1.16) Non-Black 1.04 (0.97, 1.10) Diabetic 1.06 (0.98, 1.15) Non-Diabetic 1.02 (0.96, 1.09) Amlodipine Better Chlorthalidone Better Total 1.10 (1.05, 1.16) Age < (0.97, 1.15) Age >= (1.06, 1.20) Men 1.08 (1.02, 1.15) Women 1.12 (1.03, 1.21) Black 1.19 (1.09, 1.30) Non-Black 1.06 (1.00, 1.13) Diabetic 1.08 (1.00, 1.17) Non-Diabetic 1.12 (1.05, 1.19) Lisinopril Better P =.04 for interaction Chlorthalidone Better 11
12 Change in 24 hour una, and SBP and DBP in hypertensive and normotensive individuals in Na by ethnic group Ethnic group Hypertensive-white Trials Participants Mean effect P value SBP (mmhg) <0.001 DBP (mmhg) <0.001 Table 2 24h UNa <0.001 Hypertensive-black SBP (mmhg) <0.001 DBP (mmhg) < h UNa <0.001 Hypertensive-Asian SBP (mmhg) DBP (mmhg) h UNa <0.001 BMJ 2013;346:f1325 doi: /bmj.f1325 (Published 5 April 2013)
13 HISTORY Almost 113 years ago, Ambard and Beaujard explored the association between salt intake and BP It seems to us that one can say that each individual who is able to retain chloride is, by that very fact, apt to develop arterial hypertension Ambard L, Beaujard E. Causes de l hypertension artérielle. Arch Gén Méd. 1904;81:
14 Salt Sensitivity Hereditary* Acquired Older age CKD Obesity* Diabetes
15 Percentage of variance explained in SBP by the top SNPs of 6 loci identified in 2 large GWA meta-analysis studies 40-50% attributable risk Approximately 1% identified Wang, X. et al. Hypertension 2010;56: Copyright 2010 American Heart Association
16 GENOTYPE/PHENOTYPE CAUSAL ORIGINS Genotype Environment PHENOTYPES (observed expressions) Close Intermediate Distant Enzymes Hormones BP Receptors Organ processes measurement Cell process Provocative tests Na transporter in kidney Na/ K intake Impaired Na excretion Na overload, renin, aldosterone Hypertension Na Impaired Na reabsorbtion Na depletion, Renin aldosterone Hypotension
17 24,000 mmol Na GRK-4 ENaC Gordon s syndrome Gitelman s syndrome Na-Cl co-transporter, WINK Thiazide Dopamine, ANP +ve Ang II, norepinephrine ve NEP inhibitor Liddle syndrome Pseudohypoaldosteronism SCNN1B, SCNN1G Na- K or H Amiloride mmols Barter s syndrome KCNJ1 CASR Uromodulin ROMK Na-K-2Cl Furosemide Torasemide In experimental models kidney transplantation from hypertensive to normotensive rat causes hypertension, and vice versa
18 Common Variants in Genes Underlying Monogenic Hypertension and Hypotension and Blood Pressure in the General Population Martin D. Tobin, Maciej Tomaszewski, Peter S. Braund, Cother Hajat, Stuart M. Raleigh, Thomas M. Palmer, Mark Caulfield, Paul R. Burton, Nilesh J. Samani (Hypertension. 2008;51: ) The findings show that common variants KCNJ1, CASR, NR3C2, SCNN1B, and SCNN1G in genes responsible for some Mendelian disorders of hypertension and hypotension affect blood pressure in the general population. Notably, variants in KCNJ1
19 Ethnic differences in proximal and distal tubular sodium reabsorption are heritable in black and white populations Murielle Bochuda, Jan A. Staessen, Marc Maillardd, Muzi J. Mazekoe,Tatiana Kuznetsova, Angela Woodiwiss, Tom Richart, Gavin Norton,Lutgarde Thijs, Robert Elston and Michel Burnier J Hypertens 27: ,2009 Conclusion Segmental sodium reabsorption along the nephron is highly heritable
20 Aldosterone and PRA in normotensive populations in SA Molecular and clinical investigations in patients with low-renin hypertension. Isla S. Mackenzie Æ. Morris J. Brown. Clin Exp Nephrol (2009) 13:1 8 Liddle-like phenotype P<0.001 P<0.001 Black White 1 0 PRA Aldosterone No difference in Na intake PRA = ng/ml/hr, aldosterone pmol/l x 10-2 Rayner et al, S Afr Med J 2002
21 24,000 mmol Na ENaC Liddle s syndrome SCNN1B, SCNN1G Na- K or H mols
22 Renal epithelial Na+ channel Na+ aldosterone + subunit membrane a g }Inactivating mutations cause psuedohypoaldosteronism N C } activating mutations cause Liddle s syndrome
23 Novel sodium channel mutation in SCNN1B normal sequence patient N.T. R563Q (p.arg563gln) Heterozygote, 3 base pairs from the original Liddle syndrome
24 RESULTS Populatio n group Diagnosis n R563Q negative R563Q positive % p vs. Controls d p vs. normalhigh renin HT e Black LRHT a normal-high renin HT b unknown renin HT c % ns Controls % Mixed Ancestry LRHT normal-high renin HT ns unknown renin HT ns Controls White LRHT normal-high renin HT unknown renin HT Rayner et al, J Hypertens, 2003
25 Prevalence of the R563Q mutation in patients with pre-eclampsia compared to normotensive controls. Normotensive pregnant Preeclampsia p value All subjects n age (y) mean ± SD 25.7 ± ± 6.8 p= a R563Q +ve (%) 5 (2.6%) 18 (7.8%) p=0.014 b a Student s unpaired t-test (2-tailed) b Fisher s Exact test (1-sided) Dhanjal et al, BJOG, 2006
26 Prevalence in Urban South Africans Analyzed R563Q +ve Hypertensives Normotensives Hypertensives Normotensives P value* Total (5.9%) 8 (1.7%) < Jones E, et al, Am J Hypertens 2013
27 RESPONSE TO AMILORIDE 22 heterozygous patients with resistant hypertension Amiloride 5-10 mg was added to their antihypertensive regimen The mean BP at initiation was 172/99 mmhg The average decrease in BP was 36/17mmHg (p<0.0001) Jones E, et al, Am J Hypertens 2013
28 Bantu Migration San.Cape Town (Xhosa, Coloured)
29 Typical San People
30 OVERALL SAN In the Namibian and Khomani San 19% of unselected subjects were R563Q positive respectively including 4 homozygotes Hardy-Weinberg frequencies borderline statistical significance, Χ 2 = (p=0.095) No association with hypertension Jones E, et al, Am J Hypertens 2013
31 SAN Data Khomani San Cape Town subjects Mean ± SD (n) Mean (n) P value Potassium, mmol l ±0.4 (46) 4.4±0.4 (86) <0.005 Aldosterone*, pmol l ; (49) 310; (86) <0.001 Urine Sodium-Creatinine* 7.3; (31) 12.2; (86) Jones E, et al, Am J Hypertens 2013
32 The mean levels of PRA, plasma aldosterone in normotensive blacks and in whites Children Adults Tu W et al. Hypertension. 2014;63: Copyright American Heart Association, Inc. All rights reserved.
33 Changes from baseline parameters in response to 2 week of treatment with 9-α fludrocortisone (ENaC) Tu W et al. Hypertension. 2014;63: Copyright American Heart Association, Inc. All rights reserved.
34 Model of aldosterone action in the principal cell of the ASDN Rossier, B. C. et al. Hypertension 2008;52: Copyright 2008 American Heart Association
35 A Functional Variant of NEDD4L Is Associated With Hypertension, Antihypertensive Response, and Orthostatic Hypotension Fang Luo, Yibo Wang, Xiaojian Wang, Kai Sun, Xianliang Zhou, Rutai Hui Hypertension. 2009;54: Genetic variation in NEDD4L, an epithelial sodium channel regulator, is associated with cardiovascular disease and cardiovascular death Jonas Dahlberg, Marketa Sjogren, Bo Hedblad, Gunnar Engstrom, and Olle Melander Journal of Hypertension 2014, 32:
36 24,000 mmol Na GRK-4 Dopamine, ANP +ve Ang II, norepinephrine -ve mols
37 Table 1. Ethnic distribution of genotypes of the p.ala142val and p.arg65leu in Black and White South Africans p.ala142val Black White P value AA 3.7% 41.7% AV 30.2% 42.7% VV 66.1% 15.6% P< p.arg65leu RR 3.3% 16.1% RL 36.7% 51.6% LL 60% 32.3 P=0.05
38 Baseline A142V (Normotensive, lean adolescents) Parameter AA (sd) AV (sd) VV (sd) P value SBP (mmhg) (12.7) (12.3) (12.4) 0.38 DBP (mmhg) 69.2 (4.8) 73.9 (5.4) 76.1 (9.2) 0.07* MAP 89.7 (6.8) 94.9 (7.1) 96.6 (8) 0.1* Pulse (beats/min) Aldosterone (pmol/l) 64.8 (15.4) 67 (12.7) 71.4 (13.2) (143.7) 242 (112.8) (112.8) * AA vs AV and VV, p=0.04 Rayner et al, Nephrol Rev 2011
39 AA AV VV AA vs AV, p=0.004, AA vs VV, p =0.001 Rayner et al, Nephrol Rev 2011
40 Study design: RCT double-blind Control diet (N = 20) Visit 1 Visit 2 Visit 3 BP (Omron) 24hr urine 24hr dietary recall 24hr ambulatory BP Anthropometry DEXA Blood analyses Randomization BP (Omron) Reduced Na, High K, Mg, Ca diet (N = 20) Week 4 Week 8 BP (Omron) 24hr urine 24hr dietary recall BP (Omron) 24hr urine 24hr dietary recall 24hr ambulatory BP 3-week Run-in 8-week Intervention
41 Systolic BP (mmhg) Diastolic BP (mmhg) Control Low salt Intervention (week) Change in BP (Pre to Post) Systolic BP Between-diet difference (mean (SE)) = (2.63) mmhg (P<0.05) 95 % CI: to mmhg Diastolic BP Between-diet difference (mean (SE)) = (1.22) mmhg (ns) 95 % CI: to 1.83 mmhg
42 CONTROL AA/AV VV RR/RL LL Figure 5.1. Changes in mean 24 systolic BP in the control group according to genotype Rayner et al, J Hum Hypertens 2011
43 mmhg Changes in mean 24 systolic BP in the intervention group according to genotype p= P= AA/AV VV RR/RL LL Pre SBP Post SBP A142V R65L Rayner et al, J Hum Hypertens 2011
44 Effects of G protein coupled receptor kinase 4 65L-142V haplotype on blood pressure (BP) response in Pharmacogenomic Evaluation of Antihypertensive Response (PEAR) trial. Vandell A G et al. Hypertension. 2012;60: Copyright American Heart Association, Inc. All rights reserved.
45 GRK Variant Parameter Comment p.arg65leu, p.ala142val, and p.val486ala p.ala142val p.arg65leu Hypertension in rats Enhanced activity of AT1 in smooth muscle Impaired stress related Na excretion in normotensive blacks p.ala142val shows greatest activity p.ala142val p.arg65leu, p.ala142val, and p.val486ala p.val486ala p.arg65leu, p.ala142val, and p.val486ala p.arg65leu, p.ala142val p.142ala genotype Impaired incremental Na excretion in healthy men, and lower aldosterone levels Impaired Na excretion and higher BNP levels in healthy Japanese with 2 or more variants Association with hypertension in Australian population 94.4% predictive of salt sensitive renin hypertension in Japanese population BP response to Na restriction in black South Africans with hypertension In AASK males less likely to respond to metoprolol p.ala142val significantly more common in blacks compared to whites p.ala142val 78.4% predictive Especially if co-inherited the p.65leu variant 65Leu/142Val haplotype In 2 major hypertension studies predicted a reduced response to atenolol and increased cardiovascular outcomes Rayner, Ramesar, IJMS, 2015
46 Low-renin HT in African-Americans David Spence, Robarts Institute, Canada ~6% of HT in blacks due to Liddle s variant 1,2 more likely to have 1 hyperaldo 3 More likely to have bilateral adrenocortical hyperplasia 4 Despite greater awareness and Rx, less control 5 Stroke belt discrepancies could likely be reduced by individualized therapy. 6 1.Baker EH et al. Hypertension 2002; 40: Rayner BL, et al. J Hypertens 2003;21: Spence JD. Am J Hypertens 1999; 12: Russell RP, Masi T. Ann Int Med 1970;73: Howard G et al. Stroke May; 37(5): Spence JD. Hypertension 2006 Mar; 47(3):e11.
47 Physiologically individualized therapy in resistant hypertension in Blacks Spence JD. Nat. Rev. Neurol. 2010;6: Spence JD Curr Cardiol Rev 2010; 6:
48 Am J Hypertens /105 participants completed the study (42 UC, 52 PhysRx) Control of both SBP and DBP was obtained in 11.1% of UC vs. 50.0% of PhysRx (P = ). SBP control was achieved in 13.9% of UC vs. 60.3% of PhysRx (P = ) DBP control in 36.1% of UC vs. 67.2% of PhysRx (P = 0.003).
49
50 Na excretion by the kidney e.g. ENaC or GRK-variants Na retention, renin, aldosterone? Na / K LOW RENIN HYPERTENSION Figure 1. Putative pathogenesis of salt sensitive hypertension in Blacks
51 Salt Intake in SA Blacks 7.8 gm/day Coloureds 8.5 gm/day Whites 9.5 gm/day All had inadequate K+ intake Charlton et al 2005
52 UN SUMMIT ON NCDs Smoke-free workplaces and public places Warnings about the dangers of tobacco Comprehensive bans on tobacco advertising, promotion and sponsorship Raising excise taxes on tobacco and alcohol Restricting access to retail alcohol Enforcing bans on alcohol advertising Reducing salt (5-6 gram/day) and sugar content in packaged and prepared foods and drinks Replacing trans-fats with unsaturated fat in food Promoting public awareness about diet and physical activity through education and consumer information, including through mass media
53 Rayner et al, Comprehensive Clinical Nephrology, 2013 South African Situation Over 75 % of total salt intake from packaged and restaurant foods Reducing the sodium content of bread, margarine, soups and gravies, would decrease salt intake by 0.85 grams per day Resulting in 7,000 fewer deaths due to CVD and 4,000 less non-fatal strokes in the country per year Save ~40 million USD each year in healthcare costs associated with non-fatal strokes alone
54 Conclusions and recommendations Africans have a predisposition to salt sensitivity and salt sensitive hypertension This probably has an underlying genetic predisposition compounded by changes in diet from rural to urban ( Na K amongst other factors) Genes that regulate Na balance in the kidney are a fertile source to understand salt sensitivity and hypertension in diverse ethnic populations of Southern Africa and Blacks in the rest of the World A population approach to regulation of dietary Na is recommended to prevent hypertension especially in children and adolescents This also suggests a differential approach to treatment
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