The woman initially developed a fever two weeks before admission following a long-haul flight. Nausea, diarrhea and loss of appetite accompanied the fever, which reached 38.8°C, and her symptoms partly improved after she took acetaminophen and rifaximin. During the following week, she developed oliguria, producing 350 mL of urine per day, and dyspnea. She was admitted after the breathlessness worsened. On examination, she had a heart rate of 106 beats per minute and a respiratory rate of 28 breaths per minute, with bilateral pulmonary crackles, moderate pitting edema in the lower limbs and dullness to percussion over the bladder. She was normothermic and normotensive at admission and had no abdominal tenderness, rebound tenderness or renal tenderness.

Her medical history included 20 years of type 2 diabetes mellitus and 10 years each of hypertension and hyperlipidemia. She was taking felodipine, atorvastatin and aspirin, along with metformin and insulin injections for glucose control. Her serum creatinine had been 65 μmol/L six months before admission, within the stated reference range of 53–97 μmol/L, and the investigators described her renal function as normal at that time. On admission, serum creatinine had risen to 689 μmol/L. Other notable findings included blood potassium of 7.11 mmol/L, a urine protein-to-creatinine ratio of 1,655 mg/g, pyuria, anemia and marked inflammation. C-reactive protein was 96 mg/L and procalcitonin was 5.9 ng/mL. The oliguria, hyperkalemia and acute rise in creatinine required urgent hemodialysis, while the overall clinical picture met the reported criteria for sepsis.

Next-generation sequencing detected E. coli in both whole blood and urine, with 5,033 and 2,522 organism-specific reads, respectively, supporting the presence of bloodstream infection and an upper urinary tract infection. Conventional blood and urine cultures were negative, although both samples had been collected after a single 0.5 g intravenous dose of meropenem had been given on the day of admission, which may have reduced culture yield. Antimicrobial susceptibility testing was therefore unavailable, and meropenem treatment was empirical. Non-contrast abdominal computed tomography showed enlarged kidneys with marked cortical thickening, more pronounced on the left, and an ill-defined area of relative hypoattenuation in the upper pole of the left kidney. Ultrasound confirmed bilateral enlargement and substantial cortical swelling without hydronephrosis or a discrete abscess.

The investigators could not perform contrast-enhanced CT because of the acute kidney injury, and MRI could not be completed because the patient’s clinical instability precluded safe transport and examination. As a result, the typical wedge-shaped renal hypodense lesions used to establish a definitive diagnosis of acute focal bacterial nephritis could not be demonstrated. The designation “presumed” acute focal bacterial nephritis was therefore used, based on the combination of E. coli infection, sepsis, urinary abnormalities, enlarged kidneys and marked cortical swelling. The normal serum creatinine six months earlier and reported absence of abnormalities in previous routine urinalyses supported the view that the renal failure represented an acute event rather than progression of established chronic kidney disease.

The patient received intravenous meropenem at 1 g every 12 hours, with the dose adjusted according to creatinine clearance and the scheduled dose administered after dialysis on dialysis days. After four weeks of antibiotic therapy, blood next-generation sequencing was negative for E. coli. Urinary sediment white blood cells fell from 41,905 to 573 cells per microliter, urine bacteria fell from 7,698 to 219 organisms per microliter, and procalcitonin declined to 0.105 ng/mL. Ultrasound showed resolution of the left renal cortical swelling, with left-kidney cortical thickness decreasing to 1.2 cm and right-kidney cortical thickness to 0.9 cm. Despite these microbiological and radiological improvements, urine output increased only to approximately 1,000 mL per day with low-dose diuretics, and serum creatinine remained elevated. The mismatch between infection control and persistent kidney failure prompted the clinicians to consider a process beyond uncomplicated infection-associated acute tubular injury.

Renal biopsy was performed on the same day that empirical oral methylprednisolone was started at 24 mg per day for suspected acute interstitial nephritis. During the 14-day course, urine output rose above 2,000 mL per day without diuretics, but serum creatinine did not recover. The biopsy showed that two of nine glomeruli were ischemic and sclerotic. The remaining glomeruli exhibited mild diffuse mesangial expansion, focal and segmental endocapillary proliferation and occasional neutrophil infiltration. Immunofluorescence revealed granular IgA and C3 deposits, each scored 3+, along with weaker IgG, IgM and light-chain deposits. Electron microscopy showed mesangial hypercellularity and matrix expansion, subendothelial and mesangial electron-dense deposits, and extensive effacement of podocyte foot processes.

The tubules showed epithelial simplification, protein casts, crystalloid structures, small foci of atrophy and acute injury. The interstitium was edematous and contained small foci of lymphocytic, mononuclear and neutrophilic infiltration with early fibrosis. Small arteries showed wall thickening. In the setting of a recent microbiologically documented E. coli infection, the combination of endocapillary proliferation, neutrophil infiltration and dominant granular IgA and C3 deposition was considered most consistent with IgA-dominant infection-related glomerulonephritis accompanied by tubulointerstitial injury. Meropenem was discontinued after the four-week course, and corticosteroids were tapered once biopsy results supported that diagnosis. The distinction was clinically important because IgA-dominant infection-related glomerulonephritis can present with critical acute kidney injury requiring dialysis and has been associated with progression to chronic kidney disease and death.

The authors considered several possible contributors to the kidney injury. The initial diarrheal episode probably contributed to hypovolemia, while E. coli sepsis and presumed acute focal bacterial nephritis may also have played roles. Their individual contributions could not be distinguished because the factors were closely intertwined in the clinical course. The report also notes that corticosteroids and other immunosuppressive agents have not shown significant benefit in improving renal outcomes or reducing mortality in IgA-dominant infection-related glomerulonephritis, and such treatment carries a risk of exacerbating infection or triggering recurrence. Risk factors associated with poor prognosis include elevated serum creatinine and uric acid, as well as crescents, endocapillary proliferation, tubulointerstitial fibrosis and tubular atrophy. In this patient, the severe dialysis-requiring acute kidney injury and endocapillary proliferation were considered likely contributors to persistent kidney failure.

At discharge, the patient’s urine volume had reached 1,500 mL per day without diuretics, but she remained hemodialysis-dependent. Her serum creatinine remained approximately 500 μmol/L during the one-year follow-up. Several limitations prevent the diagnosis from being regarded as definitive. Imaging did not demonstrate the characteristic wedge-shaped hypodense lesions that contrast-enhanced CT or MRI would normally identify, and pre-admission serum IgA levels and urinalysis results were unavailable. Although the clinical history and biopsy favored infection-related disease, the investigators said pre-existing IgA nephropathy could not be definitively excluded. As a single-patient case, the report cannot establish how often this combination occurs or whether any intervention improved the prognosis. Its principal value is diagnostic: persistent acute kidney injury despite credible infection control prompted a kidney biopsy that revealed superimposed glomerular inflammation and helped distinguish it from simple acute tubulointerstitial injury.

Subject of Research: A case report of persistent acute kidney failure in presumed acute focal bacterial nephritis with biopsy-confirmed IgA-dominant infection-related glomerulonephritis.

Article Title: Acute kidney injury in an elderly patient with presumed acute focal bacterial nephritis: a case report highlighting diagnostic challenges

Article References: Li, Q., Bao, D., Zhang, H., Cui, Z., Yao, Y., Lu, M., Zheng, D., & Wang, Y. (2026). Acute kidney injury in an elderly patient with presumed acute focal bacterial nephritis: a case report highlighting diagnostic challenges. Frontiers in Medicine, 13, Article 1948946. https://doi.org/10.3389/fmed.2026.1948946

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1948946

Keywords: acute kidney injury, acute focal bacterial nephritis, Escherichia coli, IgA-dominant glomerulonephritis, renal biopsy, hemodialysis, sepsis, tubulointerstitial injury, case report, kidney inflammation, Acute, kidney