Emphysematous pyelonephritis: The silent March to mycotic aortic aneurysm— A catastrophic vascular complication in a diabetic patient

Abstract

Emphysematous pyelonephritis (EPN) complicated by mycotic aortic aneurysm remains exceptionally rare; only one prior case exists in the literature (1993). We describe the second — a middle-aged diabetic male with EPN Class I/II and obstructive urolithiasis who improved following ureteral stenting and antibiotics. Two months later, CT aortogram showed complete resolution of renal gas but new peri-aortic inflammation and a saccular mycotic aneurysm at L3, confirming insidious vascular seeding despite apparent urological recovery. Extensive iliofemoral venous thrombosis was noted. The patient succumbed despite maximal management. This case highlights vigilance for vascular complications in diabetic EPN patients with aortic calcification, DVT.

1. Introduction

Emphysematous pyelonephritis (EPN) is a rare, life-threatening necrotizing infection of the renal parenchyma characterized by gas formation within the collecting system, renal parenchyma, or perinephric tissue.¹ It predominantly affects females and patients with uncontrolled diabetes mellitus, who account for up to 90% of cases.² The pathophysiology involves gas-forming organisms, most commonly Escherichia coli or Klebsiella pneumoniae, fermenting glucose in a hypoxic, hyperglycemic environment.³ Historically associated with mortality rates as high as 40–50%,^1,4,5 outcomes have improved substantially with modern multimodal management strategies combining early percutaneous drainage,⁶ targeted antibiotics, and meticulous glycemic control.⁷

Mycotic aneurysms, or infected arterial aneurysms, represent a localized dilation of an arterial wall due to destruction by microorganisms. They are rare entities, comprising only 0.7–2.6% of all aortic aneurysms.⁸ The pathogenesis typically involves hematogenous seeding of the vessel wall, contiguous spread from an adjacent infectious focus, or septic embolization to the vasa vasorum.⁹ Pre-existing aortic wall disease — particularly aortic calcification and atherosclerosis — is recognized as a key predisposing factor, as diseased intima is more susceptible to bacteremic seeding.^8,9

The convergence of these two devastating pathologies is virtually undocumented. A review of the English literature reveals only a single prior case report by Christensen and Bistrup in 1993, describing a patient with EPN caused by Clostridium septicum who developed a mycotic aneurysm.¹⁰ More recently, rare vascular complications involving the iliac arteries have been noted,¹¹ but the progression from EPN to a mycotic aortic aneurysm remains an exceptionally rare trajectory.

We herein report a unique case of a diabetic male with significant cardiovascular comorbidities — including pre-existing aortic calcification and prior DVT — who developed a mycotic aortic aneurysm two months following an episode of E. coli-associated emphysematous pyelonephritis, with no other identifiable source of infection.

2. Case presentation

• 1.Background and Pre-August 2025 History

A middle-aged male patient presented with a complex medical background significant for uncontrolled type 2 diabetes mellitus, hypertension, coronary artery disease (CAD), ischemic dilated cardiomyopathy, and recurrent ventricular tachycardia which necessitated an intracardiac defibrillator. His urological history first came to attention in April 2025, when he presented with right-sided obstructive uropathy and underwent percutaneous nephrostomy (PCN) placement followed by ureteroscopy. This hospitalization was complicated by acute kidney injury (AKI), with serum creatinine peaking at 10 mg/dL, necessitating three cycles of hemodialysis via femoral venous access. This femoral catheterization was subsequently complicated by a left femoral artery pseudoaneurysm and deep vein thrombosis (DVT) involving the common femoral vein (CFV) with partial luminal obstruction. The prior DVT and femoral vascular injury are postulated — though not proven — as additional predisposing factors that may have compromised systemic vascular integrity, potentially rendering the aortic wall more susceptible to bacteremic seeding.

• 2.August–October 2025: Urolithiasis and Recurrent Interventions

In August 2025, the patient re-presented with recurrent right-sided obstructive uropathy secondary to a calculus at the pelvi-ureteric junction (PUJ). He underwent right primary instrument retrieval of stone (PIRS) with Double-J (DJ) ureteric stenting. Post-operatively, the patient required multiple PCN exchanges over subsequent months. In October 2025, complications arose from a migrated and fragmented silicone stent (30% fragmentation), which was successfully retrieved endoscopically. Notably, CT imaging from this period demonstrated evidence of aortic wall calcification — a finding of critical retrospective significance, as calcified, atherosclerotic aortic walls are known to be particularly vulnerable to hematogenous bacterial seeding during bacteremic episodes.^8,9,12

• 3.First Episode: Emphysematous Pyelonephritis (January 2026)

In January 2026, the patient presented with a three-day history of severe abdominal pain and right flank pain. He was afebrile on presentation but hemodynamically fragile, consistent with his underlying severe cardiomyopathy. Non-contrast CT of the abdomen and pelvis revealed the in-situ DJ stent, a 4.5 × 5.3 mm calculus in the right distal ureter, and pathognomonic air pockets along the right renal pelvis and parenchyma — diagnostic of emphysematous pyelonephritis (EPN Class I/II per the Huang classification). Urine cultures yielded growth of Escherichia coli. Importantly, CT imaging at this juncture demonstrated no evidence of aortic aneurysm and no peri-aortic air, confirming that the aorta was intact and EPN was the sole active infectious focus at this time (Fig. 1).

Fig. 1.

Non-contrast CT abdomen/pelvis (January 2026). Gas pockets are visible within the right renal pelvis and parenchyma, diagnostic of emphysematous pyelonephritis (EPN) class I/II per Huang classification. The aorta is intact with no peri-aortic air at this time point.

Management consisted of culture-directed intravenous antibiotics, rigorous glycemic control, and continued ureteral drainage via the existing DJ stent. Following these interventions, the patient's severe abdominal pain settled significantly and he demonstrated marked clinical improvement. He was discharged on a prolonged course of oral antibiotics with close outpatient follow-up.

• 4.Second Episode: Mycotic Aortic Aneurysm (March 2026)

Two months after apparent urological improvement, the patient re-presented in March 2026 with new-onset abdominal discomfort. Urgent vascular imaging was performed. A CT aortogram (March 13, 2026) yielded two findings of exceptional and juxtaposed clinical significance (Fig. 2A and B).

Fig. 2.

CT aortogram (March 13, 2026): sequential comparison demonstrating the radiological shift of the infective focus from kidney to aorta. (A) Right kidney showing complete resolution of intrarenal air, indicating that EPN had settled. The renal parenchyma is free of gas compared with Fig. 1. (B) Abdominal aorta at the L3 level showing peri-aortic air (white arrow), fat stranding, and a saccular outpouching (red arrow) of the aortic wall consistent with mycotic aneurysm. No other infective foci are identified on this CT.

Finding 1 — EPN Resolution: Complete resolution of intrarenal gas — confirming that the emphysematous pyelonephritis had both radiologically and clinically settled. There was no residual air within the renal parenchyma or pelvis.

Finding 2 — Mycotic Aneurysm: New peri-aortic fat stranding, extraluminal air in the peri-aortic region at the L3 vertebral level, and a saccular outpouching of the abdominal aortic wall — consistent with a mycotic aortic aneurysm. This finding was entirely absent on all prior imaging. Three-dimensional reconstruction further demonstrated focal aortic outpouching consistent with emphysematous aortitis/mycotic aneurysm (Fig. 3).

Fig. 3.

Three-dimensional reconstructive image showing focal aortic outpouching consistent with emphysematous aortitis/mycotic aneurysm.

This radiological dissociation — resolution of renal air concurrent with the emergence of peri-aortic air — is of paramount clinical importance. It demonstrates that while the patient's pain had settled and EPN appeared to be resolving, the infective process had silently and insidiously migrated to the aortic wall. The absence of any other focus of active infection on the CT aortogram firmly establishes EPN as the primary and sole source of aortic seeding (Fig. 2B).

Additional findings included extensive thrombosis of the CFV and iliac veins bilaterally, likely representing progression of pre-existing DVT. No other infective foci — pulmonary, hepatic, splenic, or soft tissue — were identified on CT.

In patients with prohibitive surgical risk, endovascular approaches — including covered stent placement — may offer a temporizing palliative option to prevent catastrophic aortic rupture, though their role in the context of active infection remains debated.^13,14 In our patient, endovascular intervention was discussed in detail with the patient and his family, with all available options, risks, and potential benefits comprehensively explained. The family declined any interventional procedure, citing both financial constraints and an informed unwillingness to accept the procedural risks — a decision that reflects the complex interplay of economic barriers and patient autonomy in resource-limited healthcare settings. Conservative medical management with prolonged antibiotics therefore remained the only feasible recourse, with the attendant universally poor prognosis. Despite maximal conservative management, the patient's condition deteriorated progressively, culminating in refractory sepsis and multi-organ dysfunction syndrome (MODS), to which he ultimately succumbed.

3. Discussion

To the best of our knowledge, this is only the second reported case in the English literature of emphysematous pyelonephritis complicated by a mycotic aortic aneurysm. The first such case, reported by Christensen and Bistrup in 1993, involved Clostridium septicum as the causative organism.¹⁰ Our case is distinguished by its E. coli etiology, a two-month latency between the initial EPN episode and aneurysm presentation, and the radiological documentation of infective focus migration — from kidney to aorta — as evidenced by sequential CT findings.

3.1. Pathogenesis and the role of aortic calcification

Three pathways of aortic seeding are postulated: (1) hematogenous bacteremia during the acute EPN episode seeding a vulnerable aortic wall; (2) contiguous lymphatic spread from the retroperitoneal infection to the para-aortic tissues; or (3) persistent low-grade bacteremia from incompletely treated EPN causing progressive endovascular infection.8, 9, 10 In our patient, pre-existing aortic wall calcification identified on CT imaging during August–October 2025 is proposed as a critical predisposing factor. Calcified, atherosclerotic aortic walls have disrupted endothelial integrity and impaired local immune surveillance, rendering them significantly more susceptible to bacteremic seeding.^8,12 We submit that the calcified aorta served as the 'fertile ground' upon which the bacteremic storm of E. coli EPN sowed the seeds of aneurysm formation.

3.2. The role of DVT and vascular vulnerability

The patient's prior DVT — a sequela of femoral venous catheterization during hemodialysis — is another possible factor of significance. Patients with prior vascular injury and endothelial damage are at heightened risk for metastatic infection during bacteremic episodes.^9,15 The prior femoral pseudoaneurysm and venous thrombosis suggest a systemic vascular vulnerability.

It must be noted, however, that while these associations are grounded in established pathophysiological principles,^9,15 a definitive causal relationship between prior DVT, vascular injury, and mycotic aneurysm formation cannot be conclusively established from a single case report; these factors are therefore best regarded as postulated risk modifiers rather than proven determinants.

Pre-existing endothelial disruption, combined with the immunosuppressive effects of uncontrolled diabetes and the bacteremic load of E. coli EPN, created a synergistic milieu highly conducive to infected aneurysm development. Clinicians should be particularly vigilant for vascular seeding in EPN patients with a prior history of DVT, vascular catheterization, or endovascular injury.

3.3. EPN as the sole infectious source

A key observation in this case is that the CT aortogram in March 2026 revealed no other identifiable focus of active infection — no pulmonary, hepatic, splenic, osseous, or soft tissue infection. The absence of any alternative infective nidus firmly establishes EPN as the primary and sole source of hematogenous seeding responsible for the mycotic aortic aneurysm, distinguishing this case from presentations where multiple concurrent infective foci might confound attribution of vascular seeding.

3.4. The radiological signature: from renal air to peri-aortic air

In January 2026, CT demonstrated intrarenal air with an intact aorta. By March 2026, renal air had completely resolved, but peri-aortic air had emerged — a radiological 'signature of migration.' This pattern, where apparent clinical improvement masked an ongoing infective process at a new vascular site, exemplifies the insidious nature of mycotic aneurysm development and the danger of premature reassurance after EPN treatment. Monitoring for resolution of fever and inflammatory markers alone is insufficient; vascular imaging should be considered in high-risk patients even after apparent urological improvement.

3.5. Clinical and management implications

Management of mycotic aortic aneurysm ideally involves surgical resection and vascular reconstruction with prolonged antibiotic coverage.¹³ In patients with prohibitive surgical risk, conservative medical management with prolonged antibiotics is the only recourse, with universally poor outcomes.^13,14 The concurrent DVT and anticoagulation requirement adds a further layer of complexity — anticoagulation may increase aneurysm rupture risk, while its omission risks pulmonary embolism — as reflected in our patient's fatal outcome.

This case raises an important question regarding post-EPN surveillance. We suggest that in diabetic patients with EPN who have significant cardiovascular risk factors, pre-existing aortic calcification, or prior vascular injury, a follow-up CT aortogram at 6–8 weeks post-EPN may be warranted to detect subclinical aortic seeding before aneurysm expansion or rupture occurs.¹⁰

4. Conclusion

This is only the second reported case in the English literature of emphysematous pyelonephritis complicated by a mycotic aortic aneurysm, and the first caused by Escherichia coli. The case highlights four critical teaching points: (1) EPN can give rise to catastrophic vascular sequelae even after apparent clinical improvement; (2) the sequential radiological shift from intrarenal air to peri-aortic air — with no alternative infective focus — demonstrates the silent march of infection from kidney to aorta; (3) pre-existing aortic calcification and prior DVT represent important vascular vulnerability factors predisposing to mycotic aneurysm formation following bacteremic urological infections; and (4) the fatal outcome illustrates the lethal potential of this rare combination in patients with prohibitive surgical risk. A high index of suspicion, timely vascular imaging, and consideration of surveillance protocols after severe EPN in high-risk patients are essential.

CRediT authorship contribution statement

K.P. Nirmal: Writing – review & editing, Writing – original draft, Supervision, Formal analysis, Data curation, Conceptualization. G. Manoj Kumar: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Investigation, Formal analysis, Data curation, Conceptualization. K.B. Vismaya: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Funding acquisition, Formal analysis, Data curation, Conceptualization. Sreenath Sreedharan: Writing – original draft, Visualization, Data curation, Conceptualization. Sharoo Shaneej: Formal analysis, Conceptualization. Ramkumar Aiyappan: Data curation, Conceptualization. Anith P. Sen: Data curation, Conceptualization. Ritu Raj: Data curation, Conceptualization. B. Shilpa: Writing – review & editing, Writing – original draft, Visualization.