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Blood pressure response to exercise in unaffected relatives of autosomal dominant polycystic kidney disease patients: an observational study

  • Nephrology - Original Paper
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Abstract

Introduction

Hypertension is an early finding of autosomal dominant polycystic kidney disease (ADPKD) and is related to different mechanisms. Cyst expansion-related renin secretion or early endothelial dysfunctions are some of these hypotheses. In addition, the underlying genetic factor is thought to play a role in the inheritance of hypertension. The differential course of hypertension in ADPKD preoccupies that relatives of ADPKD patients may also be at risk for this underlying mechanisms with a genetically determined abnormal endothelial-vascular state. In this study, we aimed to evaluate blood pressure response to exercise as an initial vascular problem in unaffected and normotensive relatives of hypertensive ADPKD patients.

Methods

This is an observational study including unaffected and normotensive relatives (siblings and children) of ADPKD patients (relative group) and healthy controls (control group) who performed an exercise stress test. A 6-lead electrocardiogram was recorded and blood pressure was measured automatically with a cuff worn on the right arm, immediately before the test and every 3 min during the exercise and the recovery phase. Participants continued the test until their age-specific target heart rate was reached or symptoms occurred that required discontinuation of the test. The highest blood pressure and pulse values during exercise were noted. In addition, as a marker for endothelial function, nitric oxide (NO) and asymmetric dimethylarginine (ADMA) levels were measured at baseline and post-exercise.

Results

There were 24 participants in the relative group (16 female, mean age 38.45 years) and 30 participants in the control group (15 female, mean age 37.96 years). Two groups were similar in terms of age, gender, body mass index (BMI), smoking status, resting systolic blood pressure (SBP)/diastolic blood pressure (DBP) and biochemical parameters. Mean SBP and DBP were similar in both groups during 1st, 3rd and 9th minutes of exercise (1st minute: 136.25 ± 19.71 mmHg vs 140.36 ± 30.79 mmHg for SBP, p = 0.607, 84.05 ± 14.75 mmHg vs 82.60 ± 21.60 mmHg for DBP, p = 0.799; 3rd minute: 150.75 ± 30.39 mmHg vs 148.54 ± 27.30 mmHg for SBP, p = 0.801, 98.95 ± 26.92 mmHg vs 85.92 ± 17.93 mmHg for DBP, p = 0.062; 9th minute: 156.35 ± 30.84 mmHg vs 166.43 ± 31.90 mmHg for SBP, p = 0.300, 96.25 ± 21.99 mmHg vs 101.78 ± 33.11 mmHg for DBP, p = 0.529 for control and relatives, respectively). During the recovery phase, SBP decreased in both groups in 6th minute (119.85 ± 14.06 mmHg vs 122.86 ± 16.76 mmHg, p = 0.538 for control and relatives respectively); however, in the relatives of ADPKD patients DBP remained high at the end of the 6th minute (78.95 ± 11.29 mmHg vs 86.67 ± 9.81 mmHg p = 0.025 for control and relatives, respectively). Baseline and post-exercise NO and ADMA levels were similar in both groups (Baseline p = 0.214 and p = 0.818, post-exercise p = 0.652 and p = 0.918 for NO and ADMA, respectively).

Conclusion

Abnormal blood pressure response to exercise was observed in unaffected normotensive relatives of ADPKD. Although its clinical significance needs to be demonstrated by additional research, it is an important finding that unaffected relatives of ADPKD may be at risk for an altered arterial vascular network. Furthermore, these data are the first to demonstrate that relatives of ADPKD patients may also be under risk with a genetically determined abnormal vascular state.

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We declare data availability upon request.

References

  1. ERA-EDTA Registry: ERA-EDTA Registry Annual Report 2019. Amsterdam UMC, location AMC, Department of Medical Informatics, Amsterdam, the Netherlands, 2021.

  2. Ecder T (2007) Diseases of the kidney and urinary tract. Lippincott Williams & Wilkins, Philadelphia

    Google Scholar 

  3. Hateboer N, Dijk MA, Bogdanova N, Coto E, Saggar-Malik AK, San Millan JL, Torra R, Breuning M, Ravine D (1999) Comparison of phenotypes of polycystic kidney disease types 1 and 2 European PKD1-PKD2 Study Group. Lancet 353(9147):103–107

    Article  CAS  PubMed  Google Scholar 

  4. Ecder T, Schrier RW (2001) Hypertension in autosomal-dominant polycystic kidney disease: early occurrence and unique aspects. J Am Soc Nephrol 12:194–200. https://doi.org/10.1681/ASN.V121194

    Article  PubMed  Google Scholar 

  5. Chapman AB, Stepniakowski K, Rahbari-Oskoui F (2010) Hypertension in autosomal dominant polycystic kidney disease. Adv Chronic Kidney Dis 17(2):153–163. https://doi.org/10.1053/j.ackd.2010.01.001

    Article  PubMed  PubMed Central  Google Scholar 

  6. Chapman AB, Johnson A, Gabow PA, Schrier RW (1990) The renin-angiotensin-aldosterone system and autosomal dominant polycystic kidney disease. N Engl J Med 323(16):1091–1096. https://doi.org/10.1056/NEJM199010183231602

    Article  CAS  PubMed  Google Scholar 

  7. Wang D, Strandgaard S (1997) The pathogenesis of hypertension in autosomal dominant polycystic kidney disease. J Hypertens 15:925–933. https://doi.org/10.1097/00004872-199715090-00002

    Article  CAS  PubMed  Google Scholar 

  8. Wang D, Iversen J, Wilcox CS, Strandgaard S (2003) Endothelial dysfunction and reduced nitric oxide in resistance arteries in autosomal-dominant polycystic kidney disease. Kidney Int 64:1381–1388. https://doi.org/10.1046/j.1523-1755.2003.00236.x

    Article  CAS  PubMed  Google Scholar 

  9. Wang D, Iversen J, Strandgaard S (1999) Contractility and endothelium-dependent relaxation of resistance vessels in polycystic kidney rats. J Vasc Res 36:502–509. https://doi.org/10.1159/000025693

    Article  CAS  PubMed  Google Scholar 

  10. Wang D, Iversen J, Strandgaard S (2000) Endothelium-dependent relaxation of small resistance vessels is impaired in patients with autosomal dominant polycystic kidney disease. J Am Soc Nephrol 11:1371–1376. https://doi.org/10.1681/ASN.V1181371

    Article  CAS  PubMed  Google Scholar 

  11. Torres VE, Harris PC (2009) Autosomal dominant polycystic kidney disease: the last 3 years. Kidney Int 76(2):149–168. https://doi.org/10.1038/ki.2009.128

    Article  PubMed  PubMed Central  Google Scholar 

  12. Martinez-Vea A, Bardaj A, Gutierrez C, Garca C, Peralta C, Marcas L, Oliver JA (2004) Exercise blood pressure, cardiac structure, and diastolic function in young normotensive patients with polycystic kidney disease: a prehypertensive state. Am J Kidney Dis 44(2):216–223. https://doi.org/10.1053/j.ajkd.2004.04.026

    Article  PubMed  Google Scholar 

  13. Kocaman O, Oflaz H, Yekeler E, Dursun M, Erdogan D, Demirel S (2004) Endothelial dysfunction and increased carotid intima-media thickness in patients with autosomal dominant polycystic kidney disease. Am J Kidney Dis 43:854–860. https://doi.org/10.1053/j.ajkd.2004.01.011

    Article  PubMed  Google Scholar 

  14. Pei Y, Obaji J, Dupuis A et al (2009) Unified criteria for ultrasonographic diagnosis of ADPKD. J Am Soc Nephrol 20(1):205–212. https://doi.org/10.1681/ASN.2008050507

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Bruce RA, Kuzumi F, Hosmer D (1973) Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J 85:546–562. https://doi.org/10.1016/0002-8703(73)90502-4

    Article  CAS  PubMed  Google Scholar 

  16. Gottdiener JS, Brown J, Zoltick J, Fletcher RD (1990) Left ventricular hypertrophy in men with normal blood pressure: relation to exaggerated blood pressure response to exercise. Ann Intern Med 112:161–166. https://doi.org/10.7326/0003-4819-112-3-161

    Article  CAS  PubMed  Google Scholar 

  17. Bruce RA, Kusumi F, Hosmer D (1973) Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J 85(4):546–562

    Article  CAS  PubMed  Google Scholar 

  18. Griffin MD, Torres VE, Grande JP, Kumar R (1997) Vascular expression of polycystin. J Am Soc Nephrol 8:616–626. https://doi.org/10.1681/ASN.V84616

    Article  CAS  PubMed  Google Scholar 

  19. Wang D, Braendstrup O, Larsen S, Horn T, Strandgaard S (2004) The expression and activity of renal nitric oxide synthase and circulating nitric oxide in polycystic kidney disease rats. APMIS 112(6):358–368. https://doi.org/10.1111/j.1600-0463.2004.apm1120606.x

    Article  CAS  PubMed  Google Scholar 

  20. Kavey REW, Kveselis DA, Gaum WE (1997) Exaggerated blood pressure response to exercise in children with increased low-density lipoprotein cholesterol. Am Heart J 133:162–168. https://doi.org/10.1016/s0002-8703(97)70204-7

    Article  CAS  PubMed  Google Scholar 

  21. Singh JP, Larson MG, Manolio TA, O’Donnell CJ, Lauer M, Evans JC, Levy D (1999) Blood pressure response during treadmill testing as a risk factor for new-onset hypertension. The Framingham heart study. Circulation 99(14):1831–1836

    Article  CAS  PubMed  Google Scholar 

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The authors declared that this study has received no financial support.

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All the authors declare that they have all participated in the design, execution, and analysis of the paper, and that they have approved the final version.

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Correspondence to Ezgi Coskun Yenigun.

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Informed consent was obtained from all the participants and the study protocol was approved by the local Medical Ethics Committee of Health Sciences University, Ankara Numune Education and Research Hospital (decision no. 1570/2017; 08.11.2017). The study was conducted in accordance with the 2013 Helsinki Declaration and its later amendments or comparable ethical standards.

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Yenigun, E.C., Turgut, D., Cevher, S.K. et al. Blood pressure response to exercise in unaffected relatives of autosomal dominant polycystic kidney disease patients: an observational study. Int Urol Nephrol 55, 2313–2319 (2023). https://doi.org/10.1007/s11255-023-03535-y

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