Clinical Characteristics of Acute Lobar Nephronia in Renal Allograft
Acute lobar nephronia (ALN), also termed acute focal bacterial nephritis, represents a severe form of upper urinary tract infection (UTI) characterized by inflammatory mass lesions within the renal parenchyma without abscess formation. Positioned between acute pyelonephritis and renal abscess in the spectrum of renal infections, ALN poses diagnostic and therapeutic challenges, particularly in renal transplant recipients. This condition, first described radiologically in 1979, has gained recognition for its potential to mimic malignancies or other renal pathologies, necessitating a nuanced clinical approach to avoid misdiagnosis and inappropriate management.
Diagnostic Criteria and Clinical Presentation
The diagnosis of ALN relies on a combination of clinical and imaging findings. Key diagnostic criteria include: (1) a history of UTI accompanied by fever, chills, and localized pain or tenderness over the renal allograft; and (2) radiologic evidence of poorly defined striated or wedge-shaped lesions with decreased enhancement on contrast-enhanced computed tomography (CT). In transplant recipients, the clinical presentation is often insidious, with nonspecific symptoms such as mild dysuria or asymptomatic leukocyturia during the early phase. However, progression to acute suppurative infection manifests with high-grade fever, rigors, and marked tenderness over the graft. Laboratory findings typically reveal elevated inflammatory markers (leukocytosis, neutrophilia, elevated C-reactive protein) and pyuria. Approximately 50% of cases (7/14) exhibit transient graft dysfunction, reflected by elevated serum creatinine levels.
Epidemiology and Risk Factors
A retrospective analysis of 14 renal transplant recipients with ALN (8 from a single center, 6 from literature reviews) highlighted a female predominance (male-to-female ratio 1:6) and a median age at transplantation of 36.5 years (range: 17–65 years). Cadaveric donors accounted for 85% (11/13) of cases, with the remaining from living relatives. Underlying comorbidities included diabetes mellitus (54%, 7/13) and hepatitis B virus infection (23%, 3/13). ALN occurred at a median of 49 months post-transplantation (range: 2–180 months), underscoring its potential to develop years after engraftment.
Microbiologic Profile
Gram-negative bacteria predominated among identified pathogens (77%, 10/13 species), with Escherichia coli (4/13), Klebsiella pneumoniae (3/13), and Proteus mirabilis (2/13) being the most frequent isolates. Gram-positive organisms, including Enterococcus faecalis and Staphylococcus aureus, accounted for 23% (3/13) of cases. Blood and urine cultures were critical for guiding targeted antibiotic therapy, although 29% (4/14) of cases lacked microbiologic confirmation.
Radiologic and Pathologic Features
Imaging studies play a pivotal role in distinguishing ALN from other renal pathologies. In the acute phase (Phase II), ultrasonography demonstrates hyperechoic or hypoechoic lesions with indistinct margins, often localized to the upper pole of the allograft (73%, 8/11 cases). CT reveals wedge-shaped hypodense areas with heterogeneous enhancement, while positron emission tomography (PET)-CT shows hypermetabolic foci indicative of active inflammation. Histopathologic examination of biopsy specimens from three patients revealed dense acute and chronic inflammatory infiltrates without evidence of malignancy or rejection. Chronic-phase biopsies (Phase III) demonstrated tubulointerstitial fibrosis and scarring, correlating with ultrasonographic findings of echogenic regions and hypoechoic heterogeneity.
Disease Progression and Phases
The clinical course of ALN post-transplantation can be stratified into three distinct phases:
- Phase I (Early Chronic UTI Exacerbation): Subclinical or mild symptoms, such as intermittent dysuria or asymptomatic leukocyturia, characterize this stage. Imaging and laboratory parameters often remain normal, leading to underdiagnosis.
- Phase II (Acute Suppurative Infection): Marked by abrupt onset of fever (>38.5°C), graft tenderness, and systemic inflammation, this phase necessitates prompt imaging to confirm ALN. Radiologic findings peak during this stage, with CT and PET-CT providing definitive evidence of parenchymal involvement.
- Phase III (Scar Formation): Following resolution of acute infection, chronic scarring develops, detectable via ultrasound as echogenic foci with heterogeneous density. PET-CT normalizes, but histology reveals irreversible fibrotic changes. Recurrent infections may lead to granuloma formation or progression to renal abscess.
Treatment Outcomes and Follow-Up
Initial management involves broad-spectrum antibiotics tailored to culture results, with a mean treatment duration of 15.6 ± 8.9 days. Urine sterilization (negative leukocyte counts) was achieved within 4.6 ± 3.0 days in patients from the institutional cohort. Intravenous followed by oral regimens ensured resolution of acute symptoms, although 21% (3/14) experienced recurrence during a median follow-up of 72.5 months (range: 2–188 months). Chronic allograft scarring developed in 88% (7/8) of the center’s patients, with two cases showing granulomatous changes on biopsy. Graft loss occurred in 25% (2/8) due to chronic rejection unrelated to ALN. Literature-reported cases demonstrated complete radiologic resolution within 2 weeks to 6 months, with preserved graft function.
Clinical Implications and Challenges
ALN in renal allografts is frequently misdiagnosed as malignancy due to its mass-like appearance, risking unnecessary nephrectomy. Key diagnostic clues include a history of recurrent UTIs, temporal association with strenuous activity (a potential trigger for bacterial dissemination), and rapid response to antibiotics. Regular post-transplant surveillance with ultrasound is recommended to monitor for scar formation and detect recurrences. Persistent lesions despite therapy should raise suspicion for abscess formation, warranting drainage or surgical intervention.
Conclusion
Acute lobar nephronia in renal transplant recipients represents a diagnostically challenging entity with distinct clinical, microbiologic, and radiologic features. Early recognition and prolonged antibiotic therapy are critical to preventing progression to abscess formation or chronic fibrosis. Integration of imaging findings with histopathologic and microbiologic data ensures accurate diagnosis and avoids graft loss from misdiagnosis. Long-term follow-up remains essential to monitor for recurrence and assess allograft function.
doi.org/10.1097/CM9.0000000000001997
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