Introduction: Acute lobar nephronia (ALN) is a focal renal infection without liquefaction, historically regarded as rare in the pediatric population, yet recent literature suggests it may be under-diagnosed, which may result in the formation of renal abscess and future renal scarring. Methods: The clinical presentation, investigations, treatment and long-term outcomes of 5 patients diagnosed with ALN was described and literature review was conducted by reviewing publications in PubMed using the keywords "acute lobar nephronia" and "pediatric". Results: Three patients were males, aged 1 to 11 years. The primary complaint in all cases was fever, accompanied by significantly elevated inflammatory markers. Upon presentation, none of the patients exhibited pyuria on urinalysis, and all had sterile blood and urine cultures. Diagnosis was based on CT scans for three patients and renal sonography for two. Main findings included hyperechogenic renal parenchyma, and hypodense localized parenchyma. Treatment consisted of broad-spectrum intravenous antibiotics, administered for 7 to 12 days and additional 1 week course with amoxicillin-clavulanate, resulting in similar defervescence times across all patients. None of the patients demonstrated recurrence and none had renal pathology upon repeated renal sonography and upon DMSA scintigraphy. Discussion: Clinical suspicion for ALN should arise in cases of abdominal pain and markedly increased inflammatory markers. It"s crucial to note that the absence of pyuria and negative culture results should not exclude ALN diagnosis, underscoring the need for a high index of suspicion in the pediatric population.

Background: Kingella kingae is a primary cause of pediatric osteoarticular infections. Diagnosis is challenging due to mild clinical presentations and fastidious culture growth, often mimicking viral illnesses. The MeMed BV™ assay measures C-reactive protein (CRP), interferon gamma-induced protein 10 (IP-10), and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) to differentiate bacterial from viral infections, but its utility in K. kingae has not been evaluated. Objectives: To characterize the CRP, IP-10, and TRAIL profiles in pediatric patients with confirmed K. kingae infections compared to viral and classical bacterial cohorts. Methods: This retrospective study analyzed 19 children with microbiologically confirmed K. kingae. Controls included viral (n = 20), pneumococcal (n = 17) and Gram-negative (n = 7) cohorts. Serum concentrations of the three host-response proteins were compared. Results: The median age of the K. kingae cohort was 11.0 months (IQR, 9.0–12.0 months). Compared to viral controls, K. kingae elicited significantly lower IP-10 levels (median: 100.0 pg/mL [IQR, <100.0–399.0] vs. 632.5 pg/mL [IQR, 346.3–1375.8]; p = 0.004) and a downward trend in TRAIL levels (median: 75.0 pg/mL [IQR, 66.0–95.0] vs. 169.5 pg/mL [IQR, 76.5–205.0]; p = 0.066), aligning with a bacterial profile. Conversely, K. kingae induced significantly lower inflammatory and host-response markers than typical bacterial infections; its median CRP (18.8 mg/L [IQR, 10.0–50.0]) and MeMed BV™ score (28 [IQR, 11–61]) were markedly lower than those observed in the pneumococcal cohort (CRP: 94.0 mg/L [IQR, 39.5–182.5]; MeMed BV: 89 [IQR, 51–98.5]) and the alternative bacterial cohort (CRP: 106.0 mg/L [IQR, 32.0–250.0]; MeMed BV: 73.0 [IQR, 67.0–99.0]). Conclusions: Kingella kingae infections elicit a distinct host-response fingerprint characterized by mild CRP elevation, leukocytosis, and uniquely suppressed IP-10 levels. Utilizing this three-protein signature may help distinguish K. kingae from viral mimics, preventing diagnostic delays and optimizing antibiotic stewardship.