Obstructive uropathy and acute-on-chronic kidney disease from common iliac artery aneurysm: A case report

Abstract

BACKGROUND

Extrinsic ureteral compression is an uncommon but clinically significant cause of obstructive uropathy. Iliac artery aneurysms rarely present with urinary tract obstruction and may be overlooked in the differential diagnosis of hydronephrosis, particularly in patients with underlying chronic kidney disease (CKD) in whom acute-on-chronic renal deterioration may develop rapidly.

CASE SUMMARY

A 63-year-old woman with hypertension, dyslipidemia, hypothyroidism, CKD, and coronary artery disease presented with pelvic pain, decreased oral intake, and vomiting. On admission, serum creatinine was 2.7 mg/dL, representing an acute rise of 1.1 mg/dL from a documented baseline of 1.6 mg/dL within the preceding seven days, fulfilling Kidney Disease: Improving Global Outcomes criteria for acute kidney injury superimposed on CKD. Noncontrast computed tomography (performed without intravenous contrast given the acute renal deterioration) revealed a large right common iliac artery aneurysm measuring 4.8 cm at its maximal diameter, compressing the right ureter at the pelvic brim with severe right-sided hydronephrosis and hydroureter. Percutaneous nephrostomy was performed, achieving successful decompression. Serum creatinine improved to 1.9 mg/dL by post-procedure day 4, establishing a new functional baseline. Multidisciplinary evaluation by urology, vascular surgery, nephrology, and cardiology was performed. Endovascular aneurysm repair was successfully carried out eight weeks after discharge, following cardiac optimization. The nephrostomy tube was removed twelve weeks after insertion, with serum creatinine stable at 1.8 mg/dL at three-month follow-up.

CONCLUSION

Common iliac artery aneurysm is a rare but important cause of obstructive uropathy and acute kidney injury superimposed on CKD. Early vascular imaging, prompt urinary decompression, and multidisciplinary coordination are essential to prevent irreversible renal impairment and to facilitate timely definitive aneurysm repair.

Key Words: Obstructive uropathy; Iliac artery aneurysm; Hydronephrosis; Ureteral compression; Acute kidney injury

Core Tip: Common iliac artery aneurysm is a rare but clinically significant cause of extrinsic ureteral compression leading to obstructive uropathy and acute kidney injury. In patients presenting with unexplained hydronephrosis and renal dysfunction, vascular etiologies should be considered, particularly when conventional causes are absent. Noncontrast imaging may identify obstruction in the setting of acute kidney injury, while magnetic resonance angiography can provide further vascular characterization. Early decompression and coordinated multidisciplinary management are critical to preserving renal function.

INTRODUCTION

Obstructive uropathy represents a structural or functional impediment to urinary flow that may result in progressive renal dysfunction. It accounts for approximately 5%-10% of acute kidney injury (AKI) cases and remains a potentially reversible cause of renal impairment when identified early; delayed diagnosis can lead to irreversible nephron loss[1].

Etiologies of obstructive uropathy are broadly categorized as intrinsic (urolithiasis, ureteral strictures, intraluminal malignancy) or extrinsic. Extrinsic causes are less common and may be diagnostically challenging; they include retroperitoneal fibrosis, pelvic malignancy, gynecologic pathology, and vascular compression[2]. Among vascular etiologies, iliac artery aneurysms represent a particularly rare cause, as most are surgically corrected before reaching a size sufficient to compress adjacent structures[3].

When a sufficiently enlarged iliac aneurysm does cause ureteral compression, the clinical presentation is frequently nonspecific - mimicking more prevalent urologic conditions - and may lead to diagnostic delay. In patients with preexisting chronic kidney disease (CKD), even unilateral obstruction can precipitate acute-on-chronic renal deterioration requiring urgent intervention[4].

We report a case of severe unilateral hydronephrosis with acute-on-CKD resulting from extrinsic compression of the right ureter by a large common iliac artery aneurysm. This case is notable for several reasons: (1) The diagnosis was established using noncontrast computed tomography (CT) in the setting of acute renal deterioration, without the benefit of iodinated contrast or magnetic resonance angiography; (2) The patient’s background CKD rendered her particularly vulnerable to rapid functional decline from unilateral obstruction; and (3) Management required complex multidisciplinary coordination involving urology, vascular surgery, nephrology, and cardiology - considerations that have not been consistently highlighted in previously published cases.

CASE PRESENTATION

Chief complaints

Lower pelvic pain, decreased oral intake, and vomiting of several days’ duration.

History of present illness

A 63-year-old woman presented to the emergency department with a several-day history of constant right lower pelvic pain, progressively decreased oral intake, and recurrent vomiting. The pain was non-radiating and not associated with fever, chills, dysuria, hematuria, chest pain, or dyspnea. She denied any change in bowel habits, recent trauma, urologic instrumentation, or prior similar episodes. She had no known history of urolithiasis or urologic malignancy. On directed questioning, she denied any prior awareness of a pulsatile abdominal mass or previous vascular imaging. Symptoms had worsened progressively over the preceding week, prompting emergency presentation.

History of past illness

The patient had an established history of hypertension, dyslipidemia, hypothyroidism following prior total thyroidectomy, CKD with a documented baseline serum creatinine of 1.6 mg/dL on outpatient records obtained six weeks prior to admission, and coronary artery disease with prior cardiology follow-up on record. She had no prior history of aortic or iliac artery aneurysm, no prior vascular surgical interventions, and no prior episodes of obstructive uropathy or hydronephrosis.

Personal and family history

The patient was a 63-year-old woman residing in Lebanon. She denied current or prior tobacco use, alcohol consumption, or illicit drug use. Her regular medications included antihypertensive therapy, statin therapy, and levothyroxine replacement. No relevant family history of vascular aneurysms, connective tissue disease, or hereditary renal disease was reported.

Physical examination

On admission, the patient was hemodynamically stable. Vital signs were as follows: Blood pressure 135/74 mmHg, heart rate 86 beats/minute, respiratory rate 12 breaths/minute, temperature 37 °C, and oxygen saturation 96% on room air. Body mass index was 27.4 kg/m². Abdominal examination revealed right lower quadrant tenderness on palpation without guarding or rebound tenderness. A pulsatile abdominal mass was not appreciated on deep palpation of the lower abdomen and pelvis. Cardiopulmonary examination was unremarkable. No peripheral edema was present. Examination of the lower extremities revealed no signs of peripheral vascular compromise.

Laboratory examinations

Laboratory evaluation demonstrated severe normocytic anemia with hemoglobin 7.3 g/dL. Serum creatinine on admission was 2.7 mg/dL, representing an acute rise of 1.1 mg/dL from the documented baseline of 1.6 mg/dL (1.69 × baseline within the preceding seven days), fulfilling Kidney Disease: Improving Global Outcomes criteria for AKI superimposed on CKD (acute-on-CKD). C-reactive protein was mildly elevated. Thyroid-stimulating hormone was within the therapeutic range. Urinalysis demonstrated no pyuria, hematuria, or bacteriuria. One blood culture yielded gram-positive cocci on initial draw; however, repeat cultures were negative, the patient remained afebrile throughout admission, and the result was deemed a contaminant following infectious disease consultation. Cardiac biomarkers including troponin levels remained within normal limits. Transthoracic echocardiography performed as part of preoperative cardiac optimization demonstrated preserved left ventricular systolic function with an ejection fraction of approximately 65% and no regional wall motion abnormalities.

Imaging examinations

Noncontrast CT of the abdomen and pelvis was performed without intravenous contrast given the acute-on-chronic renal deterioration. CT demonstrated severe right-sided hydronephrosis with hydroureter extending to the pelvic brim (Figure 1A), and a large right common iliac artery aneurysm measuring 4.8 cm at its maximal transverse diameter with peripheral mural thrombus and no evidence of rupture, causing external compression of the right ureter at the level of the pelvic brim with medial ureteral displacement (Figure 1B and C). The contralateral left kidney appeared stable and consistent with the known CKD baseline. These findings confirmed obstructive uropathy as the primary cause of the acute-on-chronic renal deterioration. A schematic illustration of the anatomical relationship between the aneurysm and the compressed ureter is provided in Figure 2. Contrast-enhanced vascular imaging was deferred at this stage; CT angiography was subsequently performed prior to the definitive vascular intervention once renal function had partially recovered.

Figure 1 Noncontrast axial computed tomography images demonstrating obstructive uropathy secondary to a right common iliac artery aneurysm. A: Right pelvicalyceal dilatation consistent with hydronephrosis (arrow); B: Right common iliac artery aneurysm with adjacent ureteral compression (arrow); C: A cut below the previous ones showing the largest part of the aneurysm. Computed tomography was performed without intravenous contrast because of acute kidney injury.

Figure 2  Schematic illustration demonstrating extrinsic compression of the right ureter by a large right common iliac artery aneurysm resulting in hydroureteronephrosis and obstructive uropathy.

MULTIDISCIPLINARY EXPERT CONSULTATION

A multidisciplinary team was convened involving urology, vascular surgery, nephrology, cardiology, and infectious disease. Urology recommended urgent urinary decompression; retrograde ureteral stenting was considered but deferred given the degree of extrinsic ureteral compression and medial displacement at the pelvic brim, which rendered retrograde cystoscopic access anatomically unreliable. Percutaneous nephrostomy was therefore recommended as the safer and more immediately effective approach. Vascular surgery confirmed the diagnosis of a right common iliac artery aneurysm causing ureteral obstruction and recommended definitive endovascular aneurysm repair (EVAR) following renal and cardiac optimization, with pre-procedural CT angiography to confirm anatomical suitability. Cardiology performed preoperative risk stratification, reviewed echocardiographic and biomarker data, and cleared the patient for the planned vascular intervention following optimization. Nephrology provided guidance on renal function monitoring and CKD management throughout the admission and post-discharge follow-up period. Infectious disease consultation confirmed the blood culture isolate as a contaminant and recommended discontinuation of empirical antibiotics.

FINAL DIAGNOSIS

Acute-on-CKD secondary to obstructive uropathy caused by extrinsic compression of the right ureter by a large right common iliac artery aneurysm (4.8 cm maximal transverse diameter), resulting in severe right-sided hydroureteronephrosis.

TREATMENT

The patient received intravenous hydration and packed red blood cell transfusion for symptomatic anemia, with subsequent improvement in hemoglobin levels. Percutaneous nephrostomy was successfully performed under imaging guidance, achieving adequate decompression of the obstructed right collecting system confirmed on post-procedure imaging. Empirical antibiotics initiated following the blood culture isolate were discontinued after infectious disease consultation confirmed a contaminant result. Following partial renal recovery, cardiac optimization was completed and pre-procedural CT angiography confirmed anatomical suitability for endovascular repair. EVAR of the right common iliac artery aneurysm was performed eight weeks after hospital discharge without major perioperative complications.

OUTCOME AND FOLLOW-UP

Following percutaneous nephrostomy, serum creatinine declined from 2.7 mg/dL on admission to 1.9 mg/dL by post-procedure day 4, establishing a new functional baseline marginally above the pre-admission CKD baseline of 1.6 mg/dL, consistent with partial acute-on-CKD recovery. The patient was discharged in stable condition with the nephrostomy tube in place and follow-up arranged with vascular surgery, nephrology, cardiology, and endocrinology. EVAR was performed at eight weeks post-discharge without complications. The nephrostomy tube was removed twelve weeks after initial insertion, following imaging confirmation of aneurysm sac decompression and restoration of ureteral patency. At three-month follow-up, serum creatinine was stable at 1.8 mg/dL, consistent with the patient's established post-obstructive CKD baseline.

DISCUSSION

Extrinsic ureteral compression from vascular aneurysms is a rare but clinically significant cause of obstructive uropathy. Iliac artery aneurysms account for a small proportion of intra-abdominal aneurysms and are frequently asymptomatic until complications arise[5]. When sufficiently enlarged, these aneurysms may compress adjacent structures including veins, nerves, and ureters. The distal ureter is particularly vulnerable given its anatomic proximity to the iliac vessels at the pelvic brim, and progressive aneurysmal enlargement may result in direct mechanical compression, leading to hydroureteronephrosis and obstructive nephropathy[6].

The present case contributes to the existing literature in several clinically meaningful ways. First, the diagnosis was established solely on noncontrast CT, as intravenous contrast was contraindicated by the acute-on-chronic renal deterioration itself - a diagnostic paradox in which the primary consequence of the underlying pathology simultaneously limits the optimal imaging approach. This challenge has not been consistently highlighted in prior reports. Second, the patient’s background CKD amplified her vulnerability to acute renal decompensation from unilateral obstruction; patients with reduced renal reserve cannot rely on contralateral compensation in the same manner as those with two normal kidneys. Third, management required complex multidisciplinary decision-making at multiple junctures, including the choice of decompression modality, timing of definitive vascular repair relative to cardiac optimization, and the sequencing of post-EVAR nephrostomy removal.

A comparison with previously published cases is instructive (Table 1). Sangey and Moledina[7] reported internal iliac aneurysm causing hydroureteronephrosis, managed with surgical repair resulting in renal improvement. Sato et al[8] described a case complicated by spontaneous ureteral rupture, managed with ureteral stenting and EVAR, with full recovery. Jalil et al[4] reported chronic ureteral compression from a thrombosed iliac aneurysm managed with serial stenting and achieving stable long-term renal function. The present case differs from these reports in the acuity of renal deterioration, the diagnostic constraint imposed by AKI precluding contrast-enhanced imaging, and the selection of percutaneous nephrostomy over retrograde stenting for initial decompression.

Table 1 Selected published cases of iliac artery aneurysm causing ureteral obstruction.

Ref.	Age/sex	Aneurysm location	Imaging	Presentation	Management	Outcome
Sangey and Moledina[7]	NR	Internal iliac artery	CT + conventional angiography	Hydroureteronephrosis	Open surgical repair	Renal function improvement
Sato et al[8]	NR	Common iliac artery	CT angiography	Spontaneous ureteral rupture	Ureteral stent + EVAR	Full recovery
Jalil et al[4]	NR	Iliac artery (thrombosed)	CT	Chronic obstruction, CKD	Serial ureteral stenting	Stable long-term renal function
Present case	63/female	Right common iliac artery	Noncontrast CT (contrast contraindicated due to AKI)	Acute-on-CKD, severe hydronephrosis + hydroureter; no pulsatile mass on exam	PCN; EVAR at 8 weeks post-discharge	Partial renal recovery (Cr 1.9 mg/dL → 1.8 mg/dL at 3 months); nephrostomy removed at 12 weeks

NR: Not reported; CT: Computed tomography; EVAR; Endovascular aneurysm repair; CKD: Chronic kidney disease; AKI: Acute kidney injury; PCN: Percutaneous nephrostomy; Cr: Serum creatinine.

Contrast-enhanced CT angiography is the standard modality for vascular characterization and operative planning. In patients with AKI or advanced CKD, noncontrast CT can reliably identify hydronephrosis and aneurysmal mass effect and should not be deferred; magnetic resonance angiography with gadolinium provides improved vascular characterization when renal function subsequently allows. Ultrasound can detect hydronephrosis but is typically insufficient to identify the underlying vascular etiology[7].

The choice between percutaneous nephrostomy and retrograde ureteral stenting for initial urinary decompression depends on the degree of ureteral deviation and extrinsic compression. In cases of severe extrinsic obstruction with significant ureteral displacement - as in the present case - retrograde cystoscopic access is anatomically challenging and less reliable, and percutaneous nephrostomy is preferred as it provides immediate, gravity-dependent drainage independent of ureteral patency[8]. This approach was appropriate here given the medial displacement and pelvic brim compression demonstrated on imaging.

Definitive management via EVAR was selected over open repair given the patient’s significant cardiac comorbidities. Although EVAR offers reduced perioperative morbidity, aneurysm sac decompression occurs gradually after endovascular exclusion, and ureteral patency must be monitored post-procedurally before nephrostomy removal[9]. In the present case, nephrostomy removal was deferred until twelve weeks post-EVAR, by which time imaging confirmed aneurysm sac shrinkage and restoration of ureteral patency, reflecting appropriate individualized management in a high-risk patient.

The absence of a clinically palpable pulsatile abdominal mass is consistent with the deep pelvic location of the common iliac artery, combined with overlying bowel gas and adipose tissue (body mass index 27.4 kg/m² in this patient), which frequently renders iliac aneurysms undetectable on routine palpation and underscores the diagnostic dependence on cross-sectional imaging[3].

Early recognition and multidisciplinary intervention are essential to prevent irreversible nephron loss. This case highlights the importance of considering vascular etiologies in patients with unexplained hydronephrosis and renal dysfunction, particularly in those with CKD and preexisting cardiovascular comorbidities.

CONCLUSION

Hydronephrosis and unexplained renal deterioration, vascular compression should be considered, particularly when imaging reveals a pelvic arterial mass adjacent to the ureter. When contrast administration is contraindicated, noncontrast CT can reliably identify hydronephrosis and aneurysmal mass effect and should not be deferred. Early multidisciplinary coordination involving urology, vascular surgery, nephrology, and cardiology is essential to achieve prompt urinary decompression and definitive aneurysm management, minimizing the risk of irreversible renal impairment.