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Abstract: PO1847

Nonsuppressed Plasma Renin Activity in Primary Aldosteronism with Hypertensive Kidney Disease

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms


  • Ayesh, Hazem, University of Toledo - Health Science Campus, Toledo, Ohio, United States

Primary aldosteronism (PA) prevalence has been estimated at 4.7–25.5% of all hypertensive patients. Renin aldosterone ratio (ARR) serves as a widely used screening test. Elevated ARR with suppressed plasma renin activity (PRA) is considered a positive screening test which should be followed by confirmatory testing. There are cases when PA is associated with non-suppressed PRA as in our case.

Case Description

A 37-year-old African American female patient with a past medical history of chronic kidney disease stage 4 presented to the hospital with a complaint of severe headache for 2 days associated with nausea and vomiting. Physical exam was remarkable for tachycardia and elevated blood pressure at 190/101 mmHg. Notable labs include low potassium at 3.4 [3.5 – 5.0 mmol/L], elevated creatinine at 4.84 [0.40 – 1.00 mg/dL] with a baseline creatinine of 2.36 mg/dL, urinalysis was positive for proteinuria. Secondary hypertension workup showed unremarkable renal duplex ultrasound, unremarkable thyroid function test, normal free plasma metanephrine, unremarkable urine drug screen. Screening for Cushing’s syndrome wasn’t performed given there were no supporting clinical manifestations. Plasma aldosterone concentration (PAC) elevated at 64.1 [3.1 – 35.4 ng/dL] with normal PRA at 1.7 ng/mL/hr. Calculated ARR was elevated at 37.7 ng/dL per ng/mL/hour, which raised the suspicion for primary aldosteronism (PA). Saline infusion test (SIT) showed elevated post-infusion PAC at 78.1 ng/dL which confirmed the diagnosis of PA.


There are reports in literature that PA is more common than initially thought and has adverse effects on cardiovascular and renal systems independent of hypertension. So early diagnosis and management are highly recommended. The initial finding of non-suppressed PRA despite elevated ARR complicated diagnostic process. Multiple case studies reported non-suppressed PRA in patients with PA, especially when associated with hypertensive kidney disease and arteriosclerosis. In our case, kidney biopsy showed glomerulosclerosis with arteriopathy consistent with hypertensive kidney disease.

We suggest focusing on ARR as a reliable screening for PA and not solely depend on the fact that PA is associated with suppressed PRA, especially in these cases. Another important point is to consider lowering ARR cutoff for diagnosis of PA since PRA isn’t completely suppressed in these cases.