This case describes a middle-aged male with long-standing resistant hypertension and progressively worsening renal function, ultimately diagnosed with significant atherosclerotic renal artery stenosis. Despite multidrug antihypertensive therapy, blood pressure remained uncontrolled, and renal function continued to decline. Comprehensive evaluation, including imaging of renal vasculature, revealed hemodynamically significant renal artery stenosis. Timely diagnosis and a combination of optimized medical therapy and endovascular intervention were essential in stabilizing blood pressure control and preserving renal function. The case highlights the importance of considering renovascular causes in patients with refractory hypertension and unexplained renal deterioration.
Resistant hypertension, defined as uncontrolled blood pressure despite the use of three or more antihypertensive agents of different classes (including a diuretic), is a significant clinical challenge. One important and potentially reversible cause is renal artery stenosis, most commonly due to atherosclerosis in older adults. Reduced renal perfusion activates the renin–angiotensin–aldosterone system, leading to persistent hypertension and progressive ischemic nephropathy. Early identification of renal artery stenosis is critical, as delayed diagnosis may result in irreversible kidney damage and increased cardiovascular risk.
Age / Gender: 58-year-old male
Occupation: Not specified
Medical History: Long-standing hypertension (12 years), type 2 diabetes mellitus, dyslipidemia
Surgical History: None reported
Family History: Positive for cardiovascular disease (hypertension)
Social History: Former smoker with a 25-pack-year history; no illicit drug use; alcohol use not specified
Medications: Calcium channel blocker, beta-blocker, thiazide diuretic, angiotensin receptor blocker
Chief Complaints: Poorly controlled blood pressure, progressive renal dysfunction, persistent headaches, exertional dyspnea, and intermittent lower limb edema.
On examination, the patient’s blood pressure was 176/104 mmHg in both arms. Heart rate was 86 beats per minute. A systolic abdominal bruit was audible in the periumbilical region. Mild bilateral pedal edema was noted. Fundoscopic examination revealed hypertensive retinopathy changes. Cardiovascular and respiratory examinations were otherwise unremarkable.
12 years prior: Diagnosis of hypertension
1 year prior: Gradual rise in serum creatinine and increasing antihypertensive requirements
6 months prior: Addition of fourth antihypertensive agent with minimal blood pressure response
Current presentation: Referral to nephrology for resistant hypertension and progressive renal impairment
Laboratory investigations showed elevated serum creatinine (2.1 mg/dL from a baseline of 1.3 mg/dL one year earlier), reduced estimated glomerular filtration rate, and mild proteinuria. Serum potassium was within normal limits. Urinalysis was bland, without active sediment.
Renal ultrasound demonstrated asymmetric kidney size, with the right kidney measuring smaller than the left. Doppler ultrasound revealed elevated peak systolic velocities in the right renal artery, suggestive of significant stenosis. Subsequent CT angiography confirmed severe (>70%) atherosclerotic stenosis of the right renal artery and moderate stenosis of the left renal artery.
Essential hypertension with hypertensive nephrosclerosis
Diabetic kidney disease
Primary aldosteronism
Chronic glomerulonephritis
Renal artery stenosis causing ischemic nephropathy
Initial management focused on optimizing medical therapy, including careful adjustment of antihypertensive agents and close monitoring of renal function. Given ongoing resistant hypertension, progressive renal decline, and imaging-confirmed significant renal artery stenosis, a multidisciplinary decision was made to proceed with endovascular intervention.
The patient underwent percutaneous transluminal renal angioplasty with stent placement in the right renal artery. The procedure was uncomplicated. Antiplatelet therapy was initiated post-intervention, and antihypertensive medications were gradually adjusted based on blood pressure response.
The major challenge was balancing blood pressure control with preservation of renal function, particularly while using renin–angiotensin system blockers. There was also a need to carefully select patients for revascularization, as not all individuals with renal artery stenosis benefit from intervention. The patient’s multiple cardiovascular risk factors increased procedural and long-term risks.
Within weeks of the procedure, the patient demonstrated improved blood pressure control, with readings averaging 138/86 mmHg on a reduced antihypertensive regimen. Renal function stabilized, with serum creatinine improving to 1.7 mg/dL over three months. At six-month follow-up, kidney function remained stable, and no further hypertensive crises were reported. The patient was counseled extensively on smoking cessation, dietary sodium restriction, and cardiovascular risk reduction.
This case underscores the importance of considering renal artery stenosis in patients with resistant hypertension and progressive renal dysfunction. Atherosclerotic renal artery stenosis leads to chronic renal hypoperfusion, triggering sustained activation of the renin–angiotensin–aldosterone system and contributing to both hypertension and ischemic nephropathy. Clinical clues such as refractory hypertension, abdominal bruits, asymmetric kidney size, and unexplained deterioration in renal function should prompt further evaluation. Additional warning signs may include sudden worsening of blood pressure control, rise in serum creatinine after initiation of renin–angiotensin system inhibitors, and coexisting peripheral or coronary artery disease, all of which point toward an underlying renovascular etiology.
While large trials have questioned the routine use of revascularization in renal artery stenosis, selected patients, particularly those with resistant hypertension, recurrent flash pulmonary edema, or progressive renal failure—may derive meaningful benefit. In such cases, careful patient selection, based on clinical presentation and imaging findings, is essential. Timely intervention can stabilize kidney function, reduce antihypertensive requirements, and improve blood pressure control, thereby lowering long-term cardiovascular morbidity and slowing the progression to end-stage kidney disease.
Effective management required close collaboration between nephrology, cardiology, interventional radiology, and primary care. Nephrology guided diagnostic evaluation and renal protection strategies, while interventional radiology performed revascularization. Ongoing cardiovascular risk management was coordinated across specialties.
Resistant hypertension warrants evaluation for secondary causes
Renal artery stenosis can lead to progressive renal failure if untreated
Imaging is essential for diagnosis and risk stratification
Selected patients benefit from revascularization
Multidisciplinary care improves outcomes
The patient expressed frustration with years of uncontrolled blood pressure despite multiple medications. After diagnosis and treatment, he reported improved symptoms and relief in understanding the cause of his condition. He expressed motivation to adhere to lifestyle changes and follow-up care.
Resistant hypertension accompanied by declining renal function should raise strong suspicion for renovascular disease. Renal artery stenosis remains a clinically significant and potentially modifiable cause of secondary hypertension and ischemic nephropathy. Failure to recognize this condition in a timely manner can lead to irreversible renal damage, persistent cardiovascular stress, and an increased risk of adverse outcomes such as heart failure, stroke, and progression to end-stage kidney disease. Because symptoms are often nonspecific and may overlap with other causes of chronic kidney disease, a high index of clinical suspicion is essential, particularly in patients with long-standing hypertension, widespread atherosclerotic disease, or sudden worsening of renal function.
Early recognition through targeted clinical assessment and appropriate imaging modalities such as Doppler ultrasonography, CT angiography, or MR angiography—allows for accurate diagnosis and risk stratification. Individualized management is crucial, as not all patients benefit equally from invasive interventions. Optimized medical therapy, including careful blood pressure control, lipid management, glycemic control, and antiplatelet therapy, remains the foundation of treatment. However, in selected high-risk patients with resistant hypertension, recurrent pulmonary edema, or progressive renal dysfunction, selective revascularization can offer meaningful clinical benefit.
Equally important is the role of coordinated multidisciplinary care involving nephrologists, cardiologists, interventional radiologists, and primary care physicians. Such collaboration ensures balanced decision-making, minimizes procedural risks, and supports long-term follow-up. This case highlights how timely diagnosis, appropriate patient selection, and integrated care pathways can significantly improve blood pressure control, preserve renal function, and enhance overall patient outcomes.
Safian, R. D., & Textor, S. C. (2001). Renal-artery stenosis. New England Journal of Medicine, 344(6), 431–442.
Taler, S. J. (2013). Resistant hypertension and renal artery stenosis. Current Hypertension Reports, 15(6), 540–546.
Textor, S. C., & Lerman, L. O. (2015). Renovascular hypertension and ischemic nephropathy. American Journal of Hypertension, 28(7), 915–923.
Cooper, C. J., et al. (2014). Stenting and medical therapy for atherosclerotic renal-artery stenosis. New England Journal of Medicine, 370(1), 13–22.
Rimoldi, S. F., et al. (2014). Secondary causes of hypertension. European Heart Journal, 35(19), 1245–1254.
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