Features of pharmacotherapy of arterial hypertension in a patient with acute renal failure against the background of a symptomatic abdominal aortic aneurysm with thrombosis of the left renal artery: a clinical case

Introduction

The prevalence of arterial hypertension (AH) in the general population of the Russian Federation is approximately 45% — a figure that is reflected in everyday clinical practice and imposes a considerable burden on both patients and physicians. The challenge of selecting an optimal antihypertensive regimen is not always resolved, as a proportion of cases present with resistant hypertension. Resistant hypertension is diagnosed when the administration of three antihypertensive agents (including a diuretic) at optimal or maximally tolerated doses fails to achieve target blood pressure (BP) in treatment-adherent patients [1]. This condition is often driven by a comorbid background, which must be taken into account when managing AH.

Below, we present a clinical case of the development of resistant hypertension in a patient who underwent surgery for a symptomatic abdominal aortic aneurysm, complicated by several concurrent conditions.

Description of the clinical case
Patient B., a 66-year-old male, was admitted to the vascular surgery department on September 20, 2024, with complaints of girdling abdominal pain. The pain syndrome first developed more than one month prior; comprehensive outpatient evaluation with computed tomography (CT) angiography revealed a fusiform aneurysm of the suprarenal and infrarenal segments of the abdominal aorta. Hospitalization was elective to decide on aneurysm resection with graft placement.
His medical history indicated that the patient had long suffered from essential hypertension (outpatient cardioprotective therapy: losartan 100 mg daily, amlodipine 10 mg, bisoprolol 2.5 mg, indapamide 2.5 mg, atorvastatin 20 mg), and chronic moderate anemia; he underwent an appendectomy in 1980.

Objective status on admission
The patient was in moderate condition, conscious and alert; normosthenic physique (body mass index – 23.2 kg/m²). Skin and visible mucous membranes were unremarkable. No peripheral edema was noted. Muscle development was satisfactory. Vesicular breathing, no wheezing, clear lung sound on percussion. Blood pressure (BP) – 125/75 mm Hg; heart rate (HR) – 60 beats/min, pulse – 60 beats/min, of moderate fullness and tension. Cardiac rhythm was regular, heart sounds were muffled, no murmurs. Borders of relative cardiac dullness: left border shifted 1.0 cm outward from the left midclavicular line. The abdomen was not enlarged, round-shaped, not distended, participating in respiratory movements; on palpation, it was tense and tender over the entire surface. Peritoneal irritation signs were negative. Urination was unimpaired and painless. The kidney region was unremarkable.
Local status: clear symmetric pulsation of the temporal arteries. No pathological bruits over the carotid arteries. Pulsation of the upper and lower extremity arteries was detected at all levels, symmetric. Over the aorta, a pulsating mass of soft-elastic consistency with a systolic bruit was palpable.

Results of the initial diagnostic evaluation

Ultrasound of the abdominal organs, kidneys, and retroperitoneal space: a trace homogeneous layer 7 mm thick under the right lobe of the liver was detected. The abdominal aorta was saccularly dilated to 54 mm. No reliable evidence of extravasation was found. At the level of the aneurysmal dilation, compression of the inferior vena cava was noted. Kidney sizes were unchanged, the parenchymal layer was sufficient. Mild prominence of the pyramids (diffuse changes) was observed. The pelvicalyceal system was not dilated. Perinephric fat was unaltered. The urinary bladder was collapsed. The large bowel was pneumatized. Small bowel loops were not dilated, peristalsis was present.
CT angiography of the chest, abdomen, and pelvis with contrast (100 mL of low-osmolar contrast agent Omnipaque): no pulmonary pathology; no evidence of aneurysm rupture (see Fig. 1).

Fig. 1. Computed tomography angiography of the abdominal organs
Description: An aneurysm measuring 56x55x70 mm is detected at the level of the renal arteries (the area is indicated by the red arrow); no penetration of contrast agent beyond the aneurysm is detected.

Fluoroscopy and radiography of the stomach and duodenum with contrast: findings of diffuse esophageal spasm, cardial incompetence. Duodenal bulb spasm, dyskinesia of the duodenum of hypomotor-hypertonic type with a spastic component.
Radiography of contrast passage through the intestine: no signs of organic pathology.
Electrocardiogram (ECG): regular sinus rhythm with HR – 65 beats/min. Normal electrical axis of the heart (EAH). Incomplete right bundle branch block. Prolonged QT interval (QTc = 490 ms).
Echocardiography (EchoCG): aorta thickened, not dilated. Aortic valve leaflets thickened, opening amplitude sufficient. Mitral valve leaflets thickened, calcified, with opposing motion. Cardiac chambers not dilated. Global systolic function of the left ventricle (LV) not reduced (ejection fraction (EF) by Simpson – 57%). No regional wall motion abnormalities. Slight asymmetric LV myocardial hypertrophy. Diastolic dysfunction type 1. No signs of pulmonary hypertension (systolic pulmonary artery pressure (sPAP) – 19 mm Hg). No pericardial effusion.

Disease course and outcomes
The patient was being prepared for elective surgery: aneurysm resection and abdominal aortic grafting.
Laboratory findings by September 23, 2024, revealed the following notable changes: hemoglobin – 109 g/L, leukocytosis – up to 28 x 10⁹/L, serum potassium – 5.7 mmol/L, urea – 29 mmol/L, creatinine – 324 µmol/L, C‑reactive protein elevation to 219 mg/L, procalcitonin (PCT) – 3.16. On September 24, 2024, progression was noted: uremia to 25 mmol/L, hyperazotemia to 507 µmol/L. Control ultrasound of the abdomen, kidneys, and retroperitoneum: at the level of the aneurysmal dilation, compression of the inferior vena cava persisted; otherwise unchanged. On September 24, 2024, renal replacement therapy (RRT) was initiated using selective hemosorption.
On September 25, 2024, surgery was performed – resection of the suprarenal aortic aneurysm with left renal artery grafting and balloon angioplasty of the superior mesenteric artery. Intraoperatively, thrombosis of the left renal artery ostium (which was found to be the cause of the developing renal failure) and atherosclerotic stenosis of the superior mesenteric artery up to 50% were diagnosed. Total blood loss was 4000 mL, aortic cross-clamp time – 40 minutes. Pathological examination of biopsy (operative) material: aortic wall fragments of uneven thickness, with areas of fibrosis, hyalinosis, and rare focal microcalcifications; adjacent adipose tissue with focal hemorrhages; in the lumen of small vessels, their walls, and perivascularly, a polymorphic cellular inflammatory infiltrate extending into adjacent adipose and fibrous tissue.
On September 25, 2024, in the early postoperative period, RRT was continued – prolonged hemodiafiltration was chosen. Laboratory findings also showed a decrease in hemoglobin to 57 g/L; serum iron – 2 µmol/L. Replacement therapy with blood components was administered (subsequently, throughout hospitalization, repeated transfusions of packed red blood cells were given until complete restoration of oxygen-carrying capacity).
On September 26, 2024, the patient developed acute left ventricular failure (ALVF) manifesting as pulmonary edema with persistent arterial hypertension (mean BP – 220/120 mm Hg). Loop diuretic, parenteral nitrates, and intravenous fractional boluses of morphine hydrochloride were initiated, and respiratory support (non-invasive ventilation sessions) was established.
Follow-up ECG: sinus bradycardia with HR – 59 beats/min, normal EAH (˂ α = 35°), incomplete right bundle branch block, preserved QRS voltage, prolonged LV electrical systole (QTc by Bazett formula = 595 ms), marked changes in the anterior LV wall (mainly anteroseptal) as deeply inverted T waves in leads avL, V1-V2, biphasic T waves in leads I, V4-V6 (Fig. 2). Elevated cardiac troponin I up to 404 ng/L (reference range: 0-29 ng/L).

Fig. 2. ECG in dynamics (see text)

Follow-up EchoCG: global LV systolic function moderately reduced (EF – 48%). Hypokinesis of the mid and apical septum, anteroseptal segment, mid and apical anterior wall of the LV. Signs of grade 1 pulmonary hypertension (sPAP – 42 mm Hg). Small pericardial effusion (separation of pericardial layers of 2-5 mm along the inferolateral LV wall, 2-3 mm over the right chambers).
Emergency coronary angiography was performed (working diagnosis – non-ST-segment elevation acute coronary syndrome): no hemodynamically significant coronary stenosis was found (right dominant coronary circulation; left main coronary artery unremarkable; coronary arteries tortuous throughout; anterior descending artery – contour irregularities at the origin of the second-order diagonal branch with initial stenosis up to 40%, stenosis of the first-order diagonal branch ostium up to 40%; circumflex artery unremarkable, tortuous). 200 mL of low-osmolar contrast agent Omnipaque was used. Type 2 myocardial infarction was suspected.
On September 27, 2024, CT of the brain, abdomen, and chest with contrast enhancement: no evidence of intracranial pathology; 65-70% stenosis at the origin of the left internal carotid artery. Compressive atelectasis of the lower lung lobes bilaterally. Trachea and main bronchi were patent. Fluid layer in the right pleural cavity up to 56 mm (~ 730 mL), left up to 37 mm (~ 450 mL). No free gas detected. Pulmonary vessels without contrast defects. Pericardial effusion 8 mm. CT signs of minimal para-aortic and aortocaval gas-containing collection (possibly hematoma). No evidence of contrast extravasation. Aortic graft and left renal artery – contrast-enhanced. Signs of left kidney ischemia. Celiac trunk and superior mesenteric artery – contrast-enhanced.
PCT level on follow-up was 59.
On September 27, 2024, to decompress the basal lung segments, puncture and drainage of the right pleural cavity were performed. Subsequently, full management (including RRT sessions) and monitoring continued, first in the intensive care unit, then in the vascular surgery department.
EchoCG dated October 5, 2024: global LV systolic function normal (EF – 58%), improvement in LV regional wall motion, mild residual hypokinesis of the apical septal and anterior segments of the LV. No signs of pulmonary hypertension (sPAP – 30 mm Hg).
A gradual decrease in troponin I levels to 191-35 ng/L was noted; follow-up ECG showed normalization of T waves in precordial leads with resolution of QTc prolongation (440 ms). Given the above – transient LV wall motion abnormalities with a tendency to resolution, absence of occlusive-stenotic coronary artery disease, rapid stabilization of myocardial necrosis biomarkers – the cardiovascular changes were interpreted as manifestations of stress-induced cardiomyopathy.
Subsequently, during the entire inpatient stay, a total of 13 additional extracorporeal hemocorrection procedures were performed, both for "renal" indications (the main reason being acute kidney injury due to persistent left kidney ischemia, likely exacerbated by contrast administration during further evaluation) and for "extrarenal" indications (multisystem inflammatory response syndrome), including selective lipopolysaccharide hemosorption, prolonged hemodiafiltration, and prolonged hemodialysis.

Final clinical diagnosis formulated
Primary disease: Symptomatic inflammatory aneurysm of the suprarenal aorta. Thrombosis of the left renal artery ostium. Status post surgical correction: resection of suprarenal aortic aneurysm with left renal artery grafting and balloon angioplasty of the superior mesenteric artery on September 25, 2024.
Background: Grade III essential hypertension, stage 3 AH, uncontrolled. Asymmetric left ventricular myocardial hypertrophy. Very high cardiovascular risk (IV). Target BP ≤120-129/70-79 mm Hg.
Complications: Acute kidney injury from September 24, 2024, progressing to acute kidney disease from October 1, 2024. Multisystem inflammatory response syndrome. Repeated sessions (15) of extracorporeal hemocorrection from September 24, 2024, to October 4, 2024 (selective hemosorption, prolonged hemodiafiltration, prolonged hemodialysis). Severe hypochromic, normocytic anemia of mixed etiology (posthemorrhagic, iron deficiency). Transfusion of leukoreduced packed red blood cells (7 units) from September 25, 2024, to October 5, 2024. Stress-induced cardiomyopathy (takotsubo). Coronary angiography on September 26, 2024 (no hemodynamically significant coronary stenosis). Acute left ventricular failure. Pulmonary edema on September 26, 2024. Bilateral hydrothorax (right ~730 mL, left ~450 mL). Puncture and drainage of the right pleural cavity on September 27, 2024. Minimal hydropericardium. Non-invasive ventilation sessions from September 26, 2024, to September 28, 2024.
Concomitant diseases: Atherosclerosis of the brachiocephalic arteries (stenosis at the origin of the left internal carotid artery up to 70%). Cardial incompetence. Duodenal dyskinesia of hypomotor-hypertonic type with a spastic component.
During the entire hospitalization, in addition to surgical treatment of the primary disease, extracorporeal hemocorrection, and puncture-drainage procedures, the patient received multicomponent therapy including: antimicrobial – combination of an oxazolidinone (linezolid) and carbapenems (doripenem, later replaced by a dehydropeptidase inhibitor-protected carbapenem – imipenem+cilastatin); anticoagulant (postoperative) at "prophylactic" doses considering severe anemia (low-molecular-weight heparin – nadroparin – switched to unfractionated heparin by discrete regimen due to persistent renal failure); transfusion of red blood cell-containing products, albumin; iron therapy (ferric carboxymaltose at calculated dose + folates); erythropoietin administration; symptomatic therapy (antisecretory, analgesic, antiemetic); combined cardioprotective therapy including management of pulmonary edema (0.1% nitroglycerin solution – 20 mg IV via infusion pump, 1% furosemide – up to 200 mg daily IV, 1% morphine hydrochloride – 10 mg fractional bolus).
Special attention should be given to the cardioprotective, particularly antihypertensive, strategy, which posed considerable difficulties. After resolution of ALVF, largely achieved by microstream infusion of nitroglycerin and furosemide, persistent hypertension persisted. Selection of a rational combination of antihypertensive agents was hampered by persistently elevated renal failure parameters. Initial therapy consisted of amlodipine 10 mg, IV furosemide bolus, and bisoprolol 10 mg. As target BP was not achieved, resistant hypertension was diagnosed, and therapy required adjustment considering pharmacokinetics, drug-drug interactions, presence of renal failure, and ongoing extracorporeal hemocorrection by various methods including hemodialysis. The following antihypertensive regimen was selected, achieving adequate BP control (with gradual attainment of BP <130/80 mm Hg): valsartan 160 mg twice daily, carvedilol 12.5 mg twice daily, torasemide 10 mg in the morning, modified-release nifedipine 30 mg four times daily; urapidil (up to 50 mg daily IV bolus or infusion via pump) or moxonidine (up to 0.6 mg daily) were used as needed.
By October 8, 2024, positive dynamics were noted both clinically (resolution of respiratory and heart failure, stable hemodynamics) and in laboratory/instrumental findings. Key laboratory parameters: potassium – 4.5 mmol/L, creatinine – 180 µmol/L, urea – 18 mmol/L, C-reactive protein – 36 mg/L, PCT – 0.477, hemoglobin – 90 g/L, leukocytes – 13 x 10⁹/L. Ultrasound of the abdomen, kidneys, retroperitoneum, and pelvis: a small amount of free homogeneous fluid in the pelvis about 20 mL; elsewhere, no significant fluid collections or layers; left kidney unchanged in size (111 x 49 mm, parenchyma 15 mm), pelvicalyceal system not dilated, perinephric fat unchanged, blood flow velocity in interlobar arteries – 47.1 cm/s, resistive index – 0.61 (normal mean 0.5-0.7); right kidney unchanged in size (110 x 40 mm, parenchyma 15 mm), prominence of pyramids noted, no reliable evidence of abscesses; at the renal hilum extending into the sinus, single loci of arterial turbulent flow (velocity – 104.6 cm/s) with resistive index – 0.44 mm. Ultrasound of pleural cavities: in semi-recumbent position, homogeneous fluid about 100 mL on each side was detected.
On October 10, 2024, the patient was discharged from the hospital with recommendations to continue follow-up with an internist, cardiologist, nephrologist, and surgeon on an outpatient basis (see Fig. 3).

Fig. 3. Timeline of disease development

Discussion
This detailed description of the present case allows us to understand and thoroughly analyze the clinical context preceding the decision to adjust antihypertensive therapy. In addition to the presence of an abdominal aortic aneurysm, pre-existing AH, the extent of the surgical procedure, and manifestations of heart failure, the situation was significantly aggravated by the development of acute kidney injury (AKI) requiring correction with extracorporeal methods. RRT (particularly hemodialysis) is often an independent predictor of resistant hypertension, which can be explained by the influence of the following possible mechanisms/contributing factors: sodium and water overload (overload syndrome), increased arterial stiffness, activation of the sympathetic nervous system (SNS), activation of the renin-angiotensin-aldosterone system (RAAS), endothelial dysfunction, erythropoietin use, in some patients – contribution of obstructive sleep apnea syndrome, underlying essential hypertension, resistance to natriuretic peptide, dialysate composition, etc. [2].
According to the 2024 European Society of Cardiology guidelines for the management of elevated blood pressure and hypertension, for the population aged ≤85 years, a general target (considering possible diverse comorbidities) is set in the range of 120-129/70-79 mm Hg, provided good tolerability, with class and level of recommendation IA [3]. The 2024 Russian Society of Cardiology guidelines "Hypertension in Adults" indicate a target BP ≤130/80 mm Hg with the same class and level IA [4]. However, the 2021 KDIGO guidelines for BP control in patients with chronic kidney disease set a target BP of <120/80 mm Hg, largely driven by the results of the SPRINT randomized clinical trial, which can only be partially extrapolated to our case, as the trial a priori excluded patients with an estimated glomerular filtration rate <20 mL/min/1.73 m² [5].
Before the RRT phase in our patient, the selection of baseline antihypertensive therapy was critically dependent on understanding the pharmacokinetics and appropriateness of using specific agents in the setting of progressive end-stage renal disease (ESRD), which significantly limited therapeutic approaches. Therefore, we chose dihydropyridine calcium channel blockers (CCBs) (amlodipine – extensive experience in ESRD patients, robust evidence base, half-life unchanged in renal failure), β1-adrenoceptor blockers (bisoprolol – hepatic metabolism, evidence base in renal failure for mortality reduction), and loop diuretics (furosemide – extensive experience and evidence base in renal failure) [6-7]. Since extracorporeal detoxification methods, including hemodialysis, were initiated rather quickly, we were guided by the existing understanding that any antihypertensive agents may be used in hemodialysis patients; however, in each case, dosing must be adjusted considering the ability of a given drug to cross dialysis membranes – this approach greatly facilitated and expanded the possibilities for selecting an optimal antihypertensive strategy [8-9]. Thus, the final combination that allowed gradual, safe, and effective reduction of BP to target included: an angiotensin II type 1 receptor blocker (ARB, valsartan), a non-selective β1,β2,α1-adrenoceptor blocker (carvedilol), a dihydropyridine CCB (modified-release nifedipine), and a loop diuretic (torasemide).
RAAS inhibitors are recommended for use in ESRD patients because they help preserve diuresis longer, providing an additional advantage during RRT. However, almost all angiotensin-converting enzyme inhibitors are eliminated during dialysis sessions, unlike ARBs, which is why the latter class was chosen [7-8]. In an open randomized trial of 366 hemodialysis patients, ARB therapy (including valsartan) compared to other antihypertensive therapy demonstrated a 49% reduction in the risk of cardiovascular events and all-cause mortality over 36 months of follow-up (hazard ratio: 0.51; 95% confidence interval: 0.33–0.79) [10].
It should be noted that the priority given to drugs not eliminated during dialysis sessions is an undoubted advantage in terms of greater efficacy and sustainability of the achieved antihypertensive effect.
It is well known that SNS hyperactivation is a significant predictor of adverse cardiovascular events and arrhythmias in the dialysis population; therefore, the use of β-adrenoceptor blockers, which are first-line agents in this patient category, was fully justified. The switch between β-blockers was largely dictated by the dialyzability of bisoprolol versus the non-dialyzability of carvedilol [11].
Dihydropyridine CCBs are known to have potent antihypertensive potential and are widely used in the dialysis population; loop diuretics are also the diuretics of choice in ESRD. Importantly, all representatives of both classes are not removed by dialysis [6-8]. The reason for switching from amlodipine to nifedipine in our case was more sustained and effective BP control with the latter.

Conclusion
The described case illustrates the challenges in managing a patient with an operated suprarenal aortic aneurysm whose course was complicated by left renal artery ostium thrombosis leading to AKI, as well as the development of stress-induced cardiomyopathy; the focus of this article is a detailed demonstration of the antihypertensive treatment strategy integrated into the overall, already complex, management approach. In the labyrinth of currently available options for hypertension therapy, it is crucial to consider the presence and nature of comorbidities, which often jeopardizes achievement of the desired outcome. For some representatives of certain antihypertensive classes, evidence base limitations still exist, for example, for the management of hypertension in the setting of renal failure. One possible combination of antihypertensive agents is reflected in this publication. Obviously, there can be a myriad of potential clinical scenarios that may require solving the difficult problem of treating hypertension; the main principle is to maintain a balance between evidence, empirical components, and understanding of clinical pharmacology of drugs.