Candida Albicans and Escherichia Coli Superinfection in Emphysematous Pyelonephritis: A Case Report of A Challenging Presentation and Management

ABSTRACT

Emphysematous pyelonephritis is a rare, life‐threatening infection of the kidney characterized by necrosis and gas formation within the renal parenchyma, collecting system, and perinephric tissue. It commonly occurs in patients with poorly controlled type 2 diabetes mellitus (T2DM) and in those with obstructive nephropathy. The most frequent causative pathogen is Escherichia coli, while Candida albicans is rarely implicated. This condition carries a high fatality rate, and early, aggressive medical interventions are recommended. We report a 66‐year‐old female with uncontrolled T2DM who presented with constitutional symptoms and abdominal pain, clinically suggestive of diabetic ketoacidosis with urinary tract infection (UTI). Urine culture revealed Candida albicans , and abdominal computed tomography (CT) revealed gas within the renal parenchyma, confirming the diagnosis of EPN. The patient initially responded well to medical therapy; however, she subsequently developed complications a few days after discharge, ultimately leading to her demise. Emphysematous pyelonephritis is a life‐threatening condition, and sequential microbial (fungal–bacterial) infection underscores its unpredictable clinical course, even after initial improvement. The challenges are further magnified in settings with limited access to advanced diagnostic and interventional resources. Sustained vigilance, along with timely and aggressive multidisciplinary management during the post‐acute phase, remains essential to prevent catastrophic outcomes.

Key Clinical Message

Emphysematous pyelonephritis due to Candida albicans and subsequent Escherichia coli superinfection is exceedingly rare yet potentially fatal, with an unpredictable clinical course. Sustained vigilance during the post‐acute phase is essential to improving outcomes.

1. Introduction

Emphysematous pyelonephritis (EPN) is a rare, severe infection of the kidneys characterized by suppurative necrosis and gas formation within the renal parenchyma, collecting system, and perinephric tissues [1]. This life‐threatening condition occurs predominantly in patients with poorly controlled diabetes mellitus, accounting for approximately 90% of cases, and less commonly in those with obstructive uropathy [2]. The infection is typically unilateral, with bilateral involvement reported in less than 10% of cases [2, 3].

Escherichia coli is the most frequently isolated pathogen, identified in up to 70% of urine or pus cultures. Other reported bacterial pathogens include Klebsiella pneumoniae , Proteus mirabilis , Group D streptococcus, and coagulase‐negative Staphylococcus. Rarely, fungal organisms such as Candida albicans, Cryptococcus neoformans , and Pneumocystis jirovecii have been implicated [4].

A related but distinct entity, emphysematous pyelitis, involves gas limited to the collecting system and generally carries an excellent prognosis with medical management. In contrast, EPN requires urgent attention due to its life‐threatening potential and frequent need of combined medical and surgical management [3].

Historically, mortality rates approached 78% in the 1970's but have since declined to approximately 20% with advances in diagnosis and treatment [5, 6]. However, in low‐ and middle‐income countries, mortality remains high [6]. Death is most commonly attributed to acute kidney injury (AKI) and septic complications [3, 6]. However, recent literature has identified hyponatremia and the need for emergency nephrectomy as additional predictors of high mortality [7].

2. Case Presentation

A 66‐year‐old female presented with a six‐day history of abdominal pain, which was sudden in onset radiating to the back. She initially sought care at a private clinic, where she was diagnosed with a UTI, treated with oral antibiotics, and discharged home. By the fifth day, however, her abdominal pain worsened and became persistent, accompanied by vomiting, low‐grade fever, and generalized malaise. These symptoms prompted her to seek further medical attention to our facility.

Her medical history was significant for T2DM for 10 years, with poor adherence to medication. She was on metformin 500 mg twice daily and gliclazide 80 mg once daily. She had reported recurrent episodes of UTIs over the past 6 months, managed with multiple courses of antibiotics. The rest of her medical history was noncontributory.

On examination, she appeared lethargic and tachypneic. Her vitals were: blood pressure (BP) 127/77 mmHg, pulse rate (PR) 106 beats per minute, respiratory rate (RR) 19 breaths per minute, oxygen saturation (SpO₂) 98% on room air, temperature (T) 36.9°C, and random blood glucose (RBG) 23 mmol/L. Urinalysis showed ketones 3+, glucose 4+, and protein 1+. Abdominal examination revealed tenderness over the epigastric, right hypochondriac, and left lumbar regions, with left renal angle tenderness and muscle guarding. Other systems examinations were unremarkable.

An initial impression of acute abdomen was made. She was initiated on intravenous (IV) crystalloids, ceftriaxone 1 g twice daily, and metronidazole 500 mg three times daily, and the surgical team was consulted. Following further investigations (Table 1), she was diagnosed with diabetic ketoacidosis (DKA), acalculous cholecystitis, stage 1 AKI and EPN which was evident by presence of gas in the left kidney with fat stranding on CT scan (Figure 1).

TABLE 1.

Relevant laboratory findings during 1st and 2nd admissions.

Variable	1st admission	At discharge	2nd admission
White blood cell count/l (4–11 × 109/L)	12.93 × 109	8.07 × 109	11.43 × 109
Neutrophil (2–6.9 × 109/L)	11.11 × 109	5.08 × 109	9.76 × 109
Hemoglobin (11.5–16.5) g/dL	10.2	8.1	6.9
Platelet count (150–500 × 103/L)	192 × 109	346 × 109	68 × 109
Blood glucose (< 11.1 mmol/L)	23	10.1	28.7
Serum creatinine (44–88 μmol/L)	125	132.27	628
Urea (0.0–8.3) mmol/L	11.25	1.23	18.11
Potassium (3.5–5.1) mmol/L	3.39	3.58	6.31
Sodium (135–145) mmol/L	131.62	132.27	129.82
Bicarbonate (22–26) mmol/L	21	—	20.1
Blood cultures	NG	NG	NG
Urine cultures	C. albicans	NG	E. coli
Serum venous lactate (0.5–2.2) mmol/L	5.9	—	3.5
Partial pressure of CO2 (35–45) mmHg	18	—	50

Abbreviations: CO₂, carbon dioxide; NA, not applicable; NG, no growth.

FIGURE 1.

Non‐contrast CT scan of the abdomen. (A) Axial (transverse) view showing gas in the left kidney with fat stranding (white arrow). (B) Coronal view showing air‐fluid level within the left renal parenchyma (white arrow) and extension into the para‐renal space consistent with Class IIIb EPN. Image courtesy of the Radiology Department, Kilimanjaro Christian Medical Centre (KCMC).

She was managed for the DKA, which resolved within 24 h. Insulin therapy was continued with soluble insulin 8 IU every 8 h for 2 days, followed by Insulatard 25 IU in the morning and 10 IU in the evening. For pain control, she received IV paracetamol 1 g every 8 h. On day three, she developed a fever, and her antibiotics were escalated to IV piperacillin tazobactam 3.375 g three times daily. The surgical and urology teams jointly decided on conservative management for both acalculous cholecystitis and EPN.

By day five, blood cultures showed no growth; however, urine culture grew Candida albicans . Oral fluconazole was initiated with a 400 mg loading dose followed by 200 mg once daily maintenance therapy. Her clinical condition improved, and she was discharged in the third week with oral fluconazole 200 mg daily for 4 weeks and scheduled for follow‐up after 2 weeks.

Five days post‐discharge, she was readmitted in a confused state, presenting with a history of high‐grade fever, rigors & chills, dyspnea, and markedly reduced urine output. On examination, she was disoriented, tachypneic, diaphoretic, and pale, with cold extremities. Her vitals were: BP 111/62 mmHg, PR 107 beats per minute, RR 32 breaths per minute, SpO₂ of 98% on room air, T of 35.5°C, and RBG of 28.7 mmol/L. She remained anuric despite urinary catheterization. Her abdominal exam revealed epigastric and left renal angle tenderness. Neurologically, she was disoriented to person, place, and time with a Glasgow Coma Scale score (GCS) of 13/15 and a best verbal response score of 3. Other systems were unremarkable.

She received an intravenous bolus of 1 L of normal saline and a stat dose of intravenous ceftriaxone 1 g, after which she was admitted under the urology team for further management.

Relevant investigations during her readmission (Table 1): urinalysis was suggestive of UTI with nitrite 1+, leucocytes 2+, numerous white blood cells, and bacteriuria; blood culture had no growth; urine culture had Escherichia coli (ESBL+) confirming bacterial superinfection, sensitive to meropenem; and chest x‐ray showed features of pulmonary edema.

Sepsis‐induced AKI was diagnosed with the need for emergency hemodialysis. She was kept on intermediate acting insulin 25 IU in the morning and 10 IU in the evening, IV meropenem 500 mg twice daily at renal adjusted dose based on culture sensitivity. She was to go for an emergency nephrectomy; however, the patient was deemed a high surgical risk due to metabolic derangements. The next of kin declined to sign the high‐risk surgery consent and opted for medical management.

On the third day, she developed multi‐organ failure involving the renal, respiratory, and cardiovascular systems, despite aggressive efforts she went into septic shock. She was transferred to the medical intensive care unit, intubated, and kept on mechanical ventilation, noradrenaline infusion at 0.5 mcg/kg/min, and the antibiotics were escalated by adding IV vancomycin 1 g every 48 h.

Point‐of‐care ultrasound at bedside revealed the presence of multiple B‐lines and left pleural effusion of approximately 400 mL using the Balik formula. Under aseptic technique, thoracocentesis was performed and drained approximately 250 mL of serous fluid. The inferior vena cava collapsibility was less than 50%, and a decision was made to restrict the fluid therapy to 500 mL of 0.9% normal saline every 6 hours. Despite the efforts, her mean arterial pressure kept deteriorating with titration of noradrenaline to 2.5 mcg/kg/min, and she sustained a cardiac arrest. Cardiopulmonary resuscitation was performed without success, and her death was certified. Autopsy was declined by the next of kin.

3. Discussion

3.1. Overview

EPN is a rare, life‐threatening necrotizing infection of the renal parenchyma and perinephric tissues, characterized by gas formation within the collecting system and adjacent structures [2]. The condition exhibits a marked female predominance with a reported female‐to‐male ratio of approximately 6:1, likely due to anatomical predisposition to UTIs. The mean age at presentation is typically between 55 and 60 years, with a left kidney preference observed in up to 67% of cases [3].

3.2. Pathophysiology and Etiology

The pathogenesis of EPN involves infection by gas‐forming organisms capable of fermenting glucose via mixed acid and butyric fermentation pathways, producing hydrogen (H₂) and carbon dioxide (CO₂) [1, 3]. This process is facilitated by hyperglycaemia, impaired immune function, and compromised renal perfusion—conditions frequently associated with uncontrolled diabetes mellitus [7, 8, 9]. Together, these factors promote bacterial proliferation, tissue ischemia, and necrosis.

Escherichia coli remains the most frequently isolated organism in EPN, followed by Klebsiella pneumoniae , Proteus mirabilis , and Pseudomonas aeruginosa . Fungal pathogens such as Candida albicans are rarely implicated [4, 7]. In the present case, C. albicans was initially isolated, followed later by E. coli . This progression may reflect the patient's immunocompromised state due to poorly controlled T2DM; E. coli —a more aggressive and competitive pathogen—appears to have superinfected and outcompeted C. albicans [10].

To our knowledge, EPN initially caused by C. albicans and subsequently complicated by E. coli superinfection resulting in fatality has not been previously reported. A similar sequential infection pattern was described by Mabadi et al., where C. albicans infection was followed by vancomycin‐resistant Enterococcus after antifungal therapy [11], although mixed bacterial–fungal infections have been described (Figure 2; Table S1).

FIGURE 2.

Number of emphysematous pyelonephritis (EPN) cases with fungal and bacterial co‐infection/superinfection that have been reported worldwide including the current case (see Table S1).

3.3. Clinical Presentation

EPN often presents with non‐specific symptoms similar to acute pyelonephritis, including fever, rigors, chills, abdominal or flank pain, nausea, and vomiting [12]. Pneumaturia, while rare, remains a distinctive and highly suggestive feature.

Unusual presentations have been reported, including pneumomediastinum and septic pulmonary emboli [13]. In our patient, concurrent acalculous cholecystitis was observed, a finding also described by Dutta et al. [12].

3.4. Diagnosis and Classification

Radiologic imaging remains the cornerstone of EPN diagnosis. Ultrasonography serves as a rapid, cost‐effective bedside modality capable of detecting intrarenal gas or obstruction; however, computed tomography (CT) remains the gold standard, providing accurate localization of gas and delineation of parenchymal destruction [7].

Two major classification systems are used to guide prognostication and management. Huang and Tseng's four‐tier classification (Classes I‐IV) stratifies disease based on the anatomical extent of gas spread, with higher classes correlating with increased mortality and need for surgical intervention [3]. Wan et al. proposed an alternative two‐type system, distinguishing between Type I (parenchymal destruction without fluid collection) and Type 2 (presence of fluid collections and localized gas), with respective mortality rates of 69% and 18% [6]. Both classification systems agree on a better outcome when EPN is confined within the collecting system (Table 2).

TABLE 2.

Classification systems of EPN.

Classification system	Radiological description
Huang and Tseng classification
Class I	Gas in the collecting system only
Class II	Gas in the renal parenchyma
Class III.A	Gas or abscess in the perirenal space
Class III.B	Gas or abscess in the para‐renal space
Class IV	Bilateral EPN or solitary kidney with EPN
Wan classification system
Type 1	Parenchymal destruction with either an absence of fluid collection or a presence of streaky or mottled gas
Type 2	Either renal or perinephric fluid collection with bubbly or localized gas or gas in the collecting system

Abbreviation: EPN, emphysematous pyelonephritis.

3.5. Management and Prognosis

Management of EPN involves prompt initiation of broad‐spectrum intravenous antibiotics, hemodynamic stabilization, and rigorous glycemic control. The choice between conservative, interventional, or surgical approaches depends on disease severity, radiologic classification, and patient comorbidities. Adjunctive supportive care is essential, particularly in patients presenting with septic shock, acute kidney injury (AKI), altered mental status, or multiorgan dysfunction—factors known to predict poor prognosis [7, 14].

While aggressive medical therapy with or without percutaneous catheter drainage (PCD) is preferred for localized disease (Huang and Tseng Class I–IIIa) [7, 15], extensive or bilateral disease (Class IIIb–IV) often necessitates nephrectomy, with reported mortality exceeding 40% [3, 9]. Huang et al. reported an 80% success rate with combined antibiotics and PCD for Class IIIa disease, whereas Dutta et al. observed only 50% [12].

In our patient, the initial indolent presentation and favorable early response to conservative therapy were followed by rapid deterioration post‐discharge, progressing to Class IIIb EPN with AKI, thrombocytopenia, anemia, hyponatremia, and septic shock. Mortality rates escalate markedly with the accumulation of the aforementioned systemic complications, reaching 27%, 75%, and 100% when one, two, or three complications are present, respectively [16]. Given the patient's instability, surgical intervention carried prohibitive risk, and despite intensive critical care, metabolic decompensation ensued, leading to death.

Although standardized treatment guidelines remain undefined, recent literature favors a stepwise approach, reserving nephrectomy for refractory or extensive disease [7]. Conservative management combined with percutaneous drainage has demonstrated mortality reduction to approximately 21% [1]. However, recent pooled analyses indicate that in carefully selected patients with limited disease, medical therapy alone can achieve even lower mortality rates of about 9.7%. This improvement may be attributed to earlier recognition, better imaging, and more effective antibiotics than those available in earlier studies [7].

4. Conclusion

EPN is a rare but fulminant renal infection associated with high mortality, predominantly affecting diabetic and immunocompromised patients. Prompt recognition, appropriate imaging, and individualized management are critical to improving survival. This case highlights the potential for sequential microbial (fungal–bacterial) EPN and underscores its unpredictable clinical course, even after initial improvement. The challenges are further magnified in settings with limited access to advanced diagnostic and interventional resources. Sustained vigilance, along with timely and aggressive multidisciplinary management during the post‐acute phase, remains essential to prevent catastrophic outcomes.

Author Contributions

Daniel P. Mujuni: conceptualization, data curation, formal analysis, investigation, methodology, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Abid M. Sadiq: data curation, formal analysis, investigation, methodology, project administration, software, supervision, validation, writing – review and editing. Kajiru G. Kilonzo: conceptualization, data curation, investigation, project administration, writing – review and editing. Raya S. Hamad: data curation, formal analysis, investigation, writing – original draft, writing – review and editing. Abel Mwanga: data curation, investigation, resources, writing – review and editing. Elphius J. Asila: data curation, investigation, resources, validation, writing – review and editing. Donald D. Lema: data curation, resources, validation, writing – review and editing. Elichilia R. Shao: data curation, project administration, resources, validation, writing – review and editing. Elifuraha W. Mkwizu: data curation, investigation, project administration, resources, writing – review and editing. Nyasatu G. Chamba: conceptualization, formal analysis, investigation, methodology, project administration, resources, supervision, validation, writing – review and editing.

Funding

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient's primary caregiver for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor‐in‐Chief of this journal on request.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Table S1: Available clinical literature on EPN bacterial and fungal co‐infection and superinfection.

Mujuni D. P., Sadiq A. M., Kilonzo K. G., et al., “ Candida Albicans and Escherichia Coli Superinfection in Emphysematous Pyelonephritis: A Case Report of A Challenging Presentation and Management,” Clinical Case Reports 14, no. 1 (2026): e71800, 10.1002/ccr3.71800.

Data Availability Statement

Data openly available in a public repository that does not issue DOIs.