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Kidney Week

Abstract: PUB048

Screening Renin-to-Aldosterone in Patients with Hypertension: How High Is Too High?

Session Information

Category: Cardiovascular-Kidney-Metabolic Health

  • 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

  • Mehmood, Tahir, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
  • Reule, Scott, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
  • Pickthorn, Sean, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
Introduction

New guidance from the American Heart Association and the Endocrine Society have expanded screening criteria for primary aldosteronism. Particularly for patients with grade 2 hypertension (>140/90mmHg). This is anticipated to increase detection of primary aldosteronism, but comes with clinical questions on how to interpret abnormal results. Significantly elevated Renin is commonly explored through evaluation of a reninoma, but secondary causes of hyperreninemia are known and should be recognized in the setting of expanded screening criteria.

Case Description

A 55-year-old male with a history of hypertension (controlled on lisinopril/hydrochlorothiazide 25mg/20mg), diet controlled diabetes mellitus, obstructive sleep apnea, and obesity presents to general surgery clinic for evaluation for elective umbilical hernia repair. Blood pressure is noted to be 136/87mmhg in clinic. Further evaluation of hypertension is evaluated with a renin and aldosterone testing showing a normal aldosterone (2ng/dL by LC/MS/MS) and a markedly elevated plasma renin activity (51ng/mL/h; ref range 0.25-5.82) prompting additional evaluation by nephrology. Initially this was felt to have some correlation to ongoing medications, as both lisinopril and hydrochlorothiazide are anticipated to increase plasma renin activity. Repeat testing was planned as well as a renal arterial duplex to further evaluate renal anatomy. Testing again showed elevated renin 64ng/mL/h; ref range 0.25-5.82). Renal ultrasound revealed normal kidney size without cysts or hydronephrosis and normal caliber renal arteries without clinically significant stenosis. The renal ultrasound also identified indeterminate liver lesions which were further characterized on MRI as multifocal hepatocellular carcinoma and probable early cirrhosis with evidence of portal hypertension. GI was consulted who pursued a liver biopsy which confirmed hepatocellular carcinoma and assumed further management.

Discussion

In retrospect, the elevated renin may be reflecting his underlying portal hypertension from his newly discovered liver disease. Many recognize renal artery stenosis and a reninoma as causes of significantly elevated renin, but as indications for testing is expanded it is important to remember that renin is a marker for how the body is attempting to compensate for circulatory dysfunction and other etiologies may need to be explored.