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Editorial Comment from D r N ishikawa et al. to Preoperative masked renal damage in J apanese patients with primary aldosteronism: Identification of predictors for chronic kidney disease manifested after adrenalectomy

Year: 2012

Type: editorial

Abstract: There is significant accumulating clinical evidence showing that aldosterone can directly induce cardiovascular and renal tissue damage leading to a variety of manifestations in addition to that induced by hypertension. Primary aldosteronism (PA) is one of the common forms of curable hypertension.1, 2 It is also widely accepted that PA associated with inappropriately elevated aldosterone is far from being “benign”, as it was previously thought. Unilateral adrenalectomy and treatment with mineralocorticoid receptor (MR) antagonists are respectively current therapeutic options for aldosterone-producing adenoma (APA) and idiopathic adrenal hyperplasia (IHA). Aldosterone after high-salt intake is well known to activate MR, resulting in increased oxidative stress and changes in the intracellular redox potential. In this issue, Utsumi et al. investigated postoperative changes in renal function in PA and proposed potential clinical indicators for postoperative development of chronic kidney disease.3 In contrast, there were already several studies that examined renal function in PA, especially those comparing clinical covariation before and after the surgical or medicinal treatment, as the authors introduced in the article.3 It is well known that unilateral adrenalectomy can lead to a decrease in glomerular filtration rate (GFR), as a consequence of correcting the hyperfiltration state caused by hyperaldosteronism. Thus, we should always consider the possibility of decline in the renal function after unilateral adrenalectomy in PA patients. The authors found that the previous presence of dyslipidemia is an independent predictor for the postoperative development of chronic kidney disease. They also found that additional factors, such as older age, lower diastolic blood pressure and lower estimated GFR, also influence the development of this treatment-associated complication.3 It had been reported that PA patients had higher creatinine clearance and albuminuria than the patients with essential hypertension and normotensive individuals,4 showing that the escape of renin from suppression by excess aldosterone is associated with severe renal damage in PA patients, and thus, with unexpectedly unfavorable prognosis by the treatment.4 Furthermore, it was reported that patients whose renal function worsened after adrenalectomy had significantly higher preoperative levels of plasma renin activity.5 Although Utsumi's data, including those of plasma renin activity and plasma aldosterone concentration, are not consistent with the previous findings,4 their finding on dyslipidemia as the most important predictor for the development of chronic kidney disease after unilateral adrenalectomy is interesting.3 We should evaluate the presence or absence of dyslipidemia before treatment in PA patients. Indeed, we previously reported that atorvastatin, a strong statin, could reduce aldosterone production in human mesangial cells.6 It is important to clarify in future whether or not statin treatment before unilateral adrenalectomy is beneficial for maintaining renal function in PA patients after unilateral adrenalectomy. In addition to dyalipidemia, we need to consider the possibility of hyporeninemic hypoaldosteronism after unilateral adrenalectomy as a potential factor for postoperative development of chronic kidney disease, because low aldosterone with improving hypertension might decrease GFR and lead to renal impairment. We showed that the aldosterone biosynthesis in the unaffected and remaining adrenal gland was markedly suppressed as a result of autonomous production of adosterone by aldosterone-producing adenomas. It is possible that persistent hyporeninemic hypoaldosteronism, inducing renal tubular acidosis type IV, after unilateral adrenalectomy might keep GFR at low levels in some cases. Taken together, we need to carefully examine real pathogenesis inducing renal impairment in PA patients before and after treatment, and we should prevent postsurgical development of renal damages. None declared.

Source: International Journal of Urology

DOI: 10.1111/iju.12052

Authors: Tetsuo Nishikawa, Masao Omura, Jun Saito, Yoko Matsuzawa, Tomoshige Kino

Institutions: Yokohama Rosai Hospital, National Institutes of Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development

Language: English

Topic: Hormonal Regulation and Hypertension

Subfield: Endocrinology, Diabetes and Metabolism

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: bronze

Funders: National Institutes of Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development