Kidney Week

Abstract: SA-PO385

An Unusual Case of High-Renin Hypertension

Session Information

• Hypertension, CVD, and the Kidneys: Clinical Research
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

• 1602 Hypertension and CVD: Clinical

Authors

• Leiba, Adi, Assuta Ashdod Hospital, Ashdod, South, Israel

Adi Leiba, MD

• Angel-Korman, Avital, Assuta Ashdod Hospital, Ashdod, South, Israel

Avital Angel-Korman, MD

Introduction

We present an unusual case in which negative sodium balance was the etiology of high renin hypertension

Case Description

A 75-year-old woman consulted us due to high blood pressure.
PMH: LBP, history of excessive NSAIDS use, s/p partial colectomy
Meds : amlodipine, zolpidem, bisacodyl, pregabalin, , acetaminophen tramadol, brotizolam, atorvastatin, ezetimibe, esomeprazole
BP- 150/84mmHg
Labs - 24 hour urine collection – 240 mg protein (0 albumin), intermittent leukocytuia
Renal US – echogenic diminished parenchyma
On addition of low dose ARB ( 25mg losartan) her creatinine rose from 1.28 to 1.87 mg/dL, blood pressure dropped to 101/64 mmHg, and renin was found to be elevated to >500 microunits/ml. Aldosterone was also extremely elevated to 64.7ng/dl
Renal artery doppler showed no evidence of renal artery stenosis.
She reported keeping to a low salt diet as well self-prescribing 10 tabs of bisacodyl every evening (!) We suspected sodium malabsorption, and, indeed, her 24 hour urinary sodium was below detection limit.
The patient was advised to liberalize sodium intake, to take salt tablets, and reluctantly agreed to cut down her laxative use into 3-4 tabs/day.
Within a month her plasma creatinine improved, renin and aldosterone levels trended down, and sodium reappeared in her urine (Table 1). Despite sodium "loading" Her blood pressure was stable (132/74mmHg)

Discussion

Hypovolemia due to negative sodium balance can still cause hypertension due to the effect of the resultant high renin, angiotensin II and aldosterone.
This case emphasizes the importance of the colon in sodium reabsorption and the complex interplay of the colon, the kidneys, and the adrenal gland.
Secondary hyperaldosteronism would usually cause avid sodium reabsorption through colonic eNac, but, in our case , sodium malabsorption was dominant due to short colon and laxative abuse.
Our intervention affected this colonic-renal-adrenal axis, relieving the patient from chronic hypovolemia, negative sodium balance, worsening kidney function and uncontrolled hypertension

changes related to liberalization of salt intake, addition of salt tabs and partial bisacodyl withdrawal