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World J Diabetes. Mar 10, 2016; 7(5): 101-111
Published online Mar 10, 2016. doi: 10.4239/wjd.v7.i5.101
Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management
André Gustavo P Sousa, João Victor de Sousa Cabral, William Batah El-Feghaly, Luísa Silva de Sousa, Adriana Bezerra Nunes
André Gustavo P Sousa, Adriana Bezerra Nunes, Department of Clinical Medicine, Federal University of Rio Grande do Norte, Natal, RN 59012-300, Brazil
João Victor de Sousa Cabral, William Batah El-Feghaly, Luísa Silva de Sousa, Onofre Lopes University Hospital, Federal University of Rio Grande do Norte, Natal, RN 59012-300, Brazil
Author contributions: Sousa AGP, Cabral JVS, El-Feghaly WB, Sousa LS and Nunes AB contributed equally to this paper; all authors made substantial contributions to the conception and design of the manuscript, performed the literature review and analysis, wrote the paper, made critical revisions related to the content of the manuscript, and approved the final version of the article to be published.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: André Gustavo P Sousa, MD, PhD, Associate Professor, Department of Clinical Medicine, Federal University of Rio Grande do Norte, Av Nilo Peçanha, 620, Petrópolis, Natal, RN 59012-300, Brazil. agpsousa@ig.com.br
Telephone: +55-84-33429706 Fax: +55-84-33429706
Received: November 3, 2015
Peer-review started: November 3, 2015
First decision: December 28, 2015
Revised: January 12, 2016
Accepted: January 27, 2016
Article in press: January 29, 2016
Published online: March 10, 2016
Abstract

Patients with diabetes mellitus (DM) frequently develop electrolyte disorders, including hyperkalemia. The most important causal factor of chronic hyperkalemia in patients with diabetes is the syndrome of hyporeninemic hypoaldosteronism (HH), but other conditions may also contribute. Moreover, as hyperkalemia is related to the blockage of the renin-angiotensin-aldosterone system (RAAS) and HH is most common among patients with mild to moderate renal insufficiency due to diabetic nephropathy (DN), the proper evaluation and management of these patients is quite complex. Despite its obvious relationship with diabetic nephropathy, HH is also related to other microvascular complications, such as DN, particularly the autonomic type. To confirm the diagnosis, plasma aldosterone concentration and the levels of renin and cortisol are measured when the RAAS is activated. In addition, synthetic mineralocorticoid and/or diuretics are used for the treatment of this syndrome. However, few studies on the implications of HH in the treatment of patients with DM have been conducted in recent years, and therefore little, if any, progress has been made. This comprehensive review highlights the findings regarding the epidemiology, diagnosis, and management recommendations for HH in patients with DM to clarify the diagnosis of this clinical condition, which is often neglected, and to assist in the improvement of patient care.

Keywords: Hyporeninemic, Diabetes, Hyperkalemia, Renal tubular acidosis, Hypoaldosteronism

Core tip: Hyporeninemic hypoaldosteronism is the most significant cause of hyperkalemia in patients with diabetes mellitus. In order to help physicians, diabetologists, and endocrinologists in proper management of this condition, this review will focus on the current available evidence, highlighting the consequences of this condition for the treatment of arterial hypertension and proteinuria in these patients.