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Epidemiology of hypertensive kidney disease

Abstract

The prevalence of hypertension, chronic kidney disease (CKD) and end-stage renal disease (ESRD) attributable to hypertension continues to rise worldwide. Identifying the precise prevalence of CKD attributable to hypertension is difficult owing to the absence of uniform criteria to establish a diagnosis of hypertensive nephropathy. Despite the increasing prevalence of CKD-associated hypertension, awareness of hypertension among individuals with CKD remains suboptimal and rates of blood-pressure control remain poor. Targeted subgroups involved in studies of CKD seem to reach better rates of blood-pressure control, suggesting that this therapeutic goal can be achieved in patients with CKD. Elevated blood-pressure levels are associated with CKD progression. However, the optimal blood-pressure level and pharmacological agent remains unclear. Physicians treating patients with CKD must recognize the importance of maintaining optimal salt and volume balance to achieve blood-pressure goals. Furthermore, agents that modify the renin–angiotensin–aldosterone axis can be an important adjunct to therapy and physicians must monitor expected changes in serum creatinine and electrolyte levels after their administration. Hypertension remains a common factor complicating CKD. Future investigations identifying early signs of hypertension-related CKD, increasing awareness of the effects of hypertension in CKD and determining optimal therapeutic interventions might help reduce the incidence of hypertensive nephropathy.

Key Points

  • The incidence of end-stage renal disease (ESRD) has increased by 18% between 2000 and 2007, but current data show a plateau in this rise

  • Rates of blood-pressure control have improved dramatically over the past decade, which might explain the plateau in ESRD rates

  • Elevated blood pressure is clearly associated with chronic kidney disease (CKD) progression; however, existing data have demonstrated that the current recommended blood-pressure goal (<130/80 mmHg) slows, but does not stop, CKD progression

  • Sustained increases in serum creatinine level reflect renal parenchymal damage and, potentially, irreversible kidney injury

  • Identifying markers of early hypertension-associated kidney injury are necessary; serum cystatin C might serve as such a marker

  • Volume removal leads to a consistent lowering of blood pressure, suggesting that maintaining euvolemia is an important strategy in achieving target blood-pressure levels in patients with CKD

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Figure 1: The relationship between pretreatment systolic blood pressure level and the subsequent occurrence of ESRD.
Figure 2: Mechanisms that contribute to salt sensitivity and hypertensive kidney injury.

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Acknowledgements

Charles P. Vega, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the MedscapeCME-accredited continuing medical education activity associated with this article.

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S. Udani and I. Luzich contributed equally to researching data for the article. S. Udani, I. Luzich and G. L. Bakris contributed equally to discussion of content, writing, and reviewing/editing the manuscript before submission.

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Correspondence to George L. Bakris.

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Competing interests

G. L. Bakris has acted as a consultant for Abbott, Boehringer–Ingelheim, CVRx, Daiichi–Sankyo, FibroGen, Forest Laboratories, Gilead, Johnson & Johnson, Merck, National Kidney Foundation, National Institute of Diabetes and Digestive and Kidney Diseases, Mitsubishi Tanabe Pharma. Novartis, Spherix, Takeda Pharmaceutical and Walgreens, and has received grant/research support from CVRx, Forest Laboratories, GlaxoSmithKline, Juvenile Diabetes Research Foundation and Novartis. The other authors declare no competing interests.

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Udani, S., Lazich, I. & Bakris, G. Epidemiology of hypertensive kidney disease. Nat Rev Nephrol 7, 11–21 (2011). https://doi.org/10.1038/nrneph.2010.154

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