Staphylococcus-Induced Glomerulonephritis Following Burn Injury: A Case Report

Abstract

Patient: Female, 65-year-old

Final Diagnosis: Infection-related glomerulonephritis

Symptoms: Burns • infection • nausea • renal failure

Clinical Procedure: —

Specialty: Critical Care Medicine • Infectious Diseases • Nephrology

Objective: Unusual clinical course

Background

Infection-related glomerulonephritis occurs when immune complexes formed in response to bacterial infection injure the glomerular basement membrane. Here, we describe a rare case of Staphylococcus-induced glomerulonephritis following burn injury.

Case Report

A 65-year-old woman was admitted to the Emergency Department after sustaining multiple burns from boiling water. She had second-degree burns covering 19% of her total body surface area and received conservative treatment. On day 4, she developed a burn wound infection caused by methicillin-susceptible Staphylococcus aureus and Pseudomonas aeruginosa. Antibiotic therapy was initiated; however, she developed a sudden and rapid deterioration in kidney function on day 15. Sepsis-associated acute kidney injury was initially suspected, and the fluid infusion rate was increased accordingly. However, her kidney function deteriorated further, and she subsequently developed generalized edema. After considering the staphylococcal wound infection, marked hematuria and proteinuria, and hypocomplementemia, the diagnosis was revised to Staphylococcus-induced glomerulonephritis secondary to the burn wound infection. Fluid restriction and intermittent hemodialysis were initiated on day 19 of hospitalization. Her clinical condition improved approximately 1 month later, and a kidney biopsy result on day 74 was consistent with the recovery phase of infection-related glomerulonephritis. The patient was discharged 94 days after admission.

Conclusions

Acute kidney injury secondary to a burn wound infection should be distinguished from infection-related glomerulonephritis and sepsis-associated acute kidney injury. Source control and fluid restriction are recommended when infection-related glomerulonephritis is suspected in older patients with staphylococcal wound infections, marked proteinuria or hematuria, and hypocomplementemia.

Introduction

Infection-related glomerulonephritis (IRGN) is an immune-mediated condition caused by non-kidney bacterial infections [1]. It develops through the formation of immune complexes by nephritogenic antigens, which activate the complement pathway, metalloproteinases, and collagenases, leading to glomerular basement membrane damage [2,3]. Classic acute post-infectious glomerulonephritis secondary to group A beta-hemolytic Streptococcus infection – commonly referred to as acute post-streptococcal glomerulonephritis – has long been considered the prototypical bacterial IRGN [4–6]. Owing to the improved treatment of streptococcal infections, the incidence of acute post-streptococcal glomerulonephritis has declined in most developed countries; however, IRGN is more frequently caused by staphylococcal infections [7]. IRGN caused by Staphylococcus aureus is known as Staphylococcus-induced glomerulonephritis (SIGN). SIGN secondary to methicillin-resistant S. aureus bacteremia has been associated with burns [8]; however, based on a PubMed search conducted in March 2025, no previous case reports have clearly linked IRGN to primary burn wound infections.

This case highlights the diagnostic challenge of distinguishing IRGN from sepsis-associated acute kidney injury (sepsis-AKI) in burn patients, particularly when early kidney biopsy is not feasible. Careful monitoring of the clinical course and laboratory data can facilitate early recognition and guide appropriate management.

Case Report

A 65-year-old woman with a history of hypertension was admitted to our Emergency Department after sustaining multiple burns from boiling water. Her vital signs were stable on arrival, and she had second-degree burns involving 19% of her total body surface area, including the chest, upper arms, back, and buttocks (Figure 1). Blood test results showed a serum creatinine level of 0.72 mg/dL, with no other abnormalities. Fluid resuscitation was initiated according to the Parkland formula, and conservative therapy was selected for burn management.

Figure 1.

Clinical appearance of the trunk on the day of the burn injury. Most blisters had already ruptured upon arrival. The wound was consistent with a second-degree burn.

The patient developed burn wound infections on her chest and both arms (Figure 2); therefore, cefazolin was initiated on day 4. It was subsequently changed to piperacillin on day 8 after wound cultures revealed methicillin-susceptible S. aureus (MSSA) and Pseudomonas aeruginosa colonization, with negative blood cultures. The wounds produced considerable exudate, and the patient’s oral intake decreased owing to nausea and vomiting. Therefore, intravenous infusion was resumed on day 9. On day 15, the patient developed hypertension, anuria, and kidney dysfunction (serum creatinine: 4.67 mg/dL). Sepsis-AKI or dehydration were initially suspected, and the infusion rate was accordingly increased. However, kidney function deteriorated further, and generalized edema increased oxygen demand. Hypocomplementemia (complement C3: 63 mg/dL; complement C4: 11 mg/dL), proteinuria (urine protein-to-creatinine ratio of 43 g protein/g creatinine), and hematuria (>100 red blood cells per high-powered field) led to a diagnosis of IRGN secondary to MSSA burn wound infection (ie, SIGN). Therefore, we initiated fluid restriction on day 19, and intermittent hemodialysis was started because of diuretic resistance and fluid overload. The necrotic wound was debrided, and antibiotics were administered for source control.

Figure 2.

Clinical appearance of the trunk on day 6 after the burn injury. The infected burn area turned black and emitted a foul odor. Methicillin-susceptible Staphylococcus aureus and Pseudomonas aeruginosa were detected in the wound culture.

Although the patient’s serum creatinine level peaked at 9.62 mg/dL, fluid restriction and 12 intermittent hemodialysis sessions performed over approximately 1 month led to clinical improvement (Figure 3). She recovered from anuria by day 40, and hemodialysis was discontinued on day 46; however, serum creatinine level did not return to baseline. Immunofluorescence staining of a kidney biopsy sample obtained on day 74 revealed C3 and IgA deposits in the mesangium and glomerular capillary loops, consistent with the recovery phase of IRGN (Figure 4). Electron microscopy revealed endothelial cell swelling, loss of fenestrations, and focal effacement of podocyte foot processes (data not shown). After completing physical rehabilitation, the patient was discharged on day 94. At the 5-year follow up, her condition had not progressed to end-stage renal disease; however, mild kidney dysfunction persisted (serum creatinine: 1.1 mg/dL).

Figure 3.

Clinical course from admission to day 47. Hypertension, anuria, and kidney dysfunction developed around day 15. Sepsis associated acute kidney injury was initially diagnosed, and fluid infusion was increased accordingly. However, kidney function did not improve, and the patient developed generalized edema, weight gain, and increased oxygen demand. On day 19, Staphylococcus-induced glomerulonephritis secondary to burn wound infection was diagnosed, prompting initiation of fluid restriction and intermittent hemodialysis. Although clinical symptoms improved after approximately 1 month, kidney function did not return to baseline. SBP – systolic blood pressure; DBP – diastolic blood pressure; Cr – creatinine; BW – body weight.

Figure 4.

Immunofluorescence staining of kidney tissue for complement C3 and IgA. (A) Immunofluorescence staining for complement protein C3 showing moderate granular staining in the mesangium and glomerular capillary loops. (B) Immunofluorescence staining for IgA showing moderate granular staining in the mesangium and glomerular capillary loops.

Discussion

Herein, we describe a rare case of SIGN following burn injury, successfully managed with fluid restriction and multiple hemodialysis sessions. This report can be useful for identifying AKI secondary to burn wound infections.

According to a review of IRGN, symptomatic patients most commonly present with acute nephritic syndrome, characterized by new-onset hematuria, proteinuria, edema, hypertension, and reduced kidney function [1,9]. Hypocomplementemia is observed in 35% to 80% of adult cases, with most patients showing depressed C3 levels [1]. Immunofluorescence typically reveals C3-dominant or co-dominant glomerular staining, and most cases of SIGN show mild-to-moderate IgA and moderate-to-strong C3 staining [10]. Nasr’s diagnostic criteria require at least 3 of the following: (1) evidence of infection preceding or at the onset of glomerulonephritis, (2) low serum complement, (3) endocapillary proliferative and exudative glomerulonephritis, (4) C3-dominant or co-dominant glomerular immunofluorescence staining, and (5) hump-shaped subepithelial deposits on electron microscopy [1]. In our case, early kidney biopsy was precluded due to overlapping burn wounds. Despite the delayed biopsy, our case met key criteria: MSSA wound infection, hypocomplementemia, and C3-dominant glomerular immunofluorescence staining. Therefore, the diagnosis of IRGN was confirmed.

Treatment of IRGN focuses on infection control and management of nephritic complications [1]. Most older patients require acute dialysis for uremic symptoms or fluid overload [1]. A substantial proportion of adults do not recover kidney function; approximately 40% to 77% of patients with SIGN experience persistent kidney damage, and up to 43% progress to end-stage renal disease [1,10]. In line with previous evidence, our patient exhibited persisting mild kidney dysfunction at the 5-year follow up, although her condition did not progress to end-stage renal disease.

Notably, in cases of AKI secondary to burn wound infection, it is important to differentiate IRGN from sepsis-AKI, particularly with respect to the time of onset. Table 1 summarizes the distinguishing features between IRGN and sepsis-AKI. Multiple mechanisms contribute to injury in sepsis-AKI, including inflammation, mitochondrial dysfunction, and tubular necrosis [11,12]. IRGN is associated with a high incidence of nephrotic syndrome, whereas nephrotic syndrome is rare in sepsis-AKI. Serum complement levels tend to be preserved in sepsis-AKI but are typically reduced in IRGN. Although treatment for both conditions involves controlling the source of infection, the fluid management differs. Sepsis-AKI is managed with fluid administration for resuscitation, especially in the setting of septic shock, unless excessive fluid retention occurs. In contrast, fluid restriction is required in IRGN, owing to the presence of nephrotic syndrome. The presence of staphylococcal wound infections, hypocomplementemia, and marked hematuria or proteinuria associated with nephrotic syndrome can aid in the early differentiation of IRGN from sepsis-AKI.

Table 1.

Comparison of sepsis-associated acute kidney injury (sepsis-AKI) and infection-related glomerulonephritis (IRGN).

	Sepsis-AKI	IRGN
Injury site	Tubular epithelial cell death Acute tubular necrosis [12]	Glomerular basement membranes [1]
Frequency	Approximately 10–67% of patients with sepsis [12]	Approximately 0.3–2/100 000 people [1]
Nephrotic syndrome	Rare	Frequent Hypertension Generalized edema Hematuria and proteinuria
Complement	High	Low
treatment	Source control and fluid administration for resuscitation, especially in septic shock	Source control and fluid restriction
Prognosis of kidney function	Higher rate of recovery [13]	Persistent renal dysfunction, 8–54%; end-stage renal disease, 4–33% [1]

In our case, the patient developed nausea and vomiting on day 9 of admission, which may have reflected symptoms of intestinal edema. However, the infusion rate was increased because of suspicion of sepsis-AKI and prerenal AKI caused by dehydration, resulting in exacerbated generalized edema. The lack of improvement in creatinine levels despite fluid therapy raised suspicion of IRGN. AKI secondary to burn wound infections is initially considered sepsis-AKI; however, IRGN can be latent if the clinical symptoms and serum creatinine levels do not improve following fluid administration. Careful monitoring and consideration of clinical features are essential for distinguishing IRGN from sepsis-AKI, particularly when biopsy is not immediately feasible.

Conclusions

We describe a rare case of SIGN following burn injury. Sepsis-AKI and IRGN should be considered in cases of AKI associated with burn wound infections. IRGN should be suspected, particularly in older patients with staphylococcal wound infections, marked proteinuria or hematuria, and hypocomplementemia. Prompt source control and appropriate fluid restriction are recommended when IRGN is suspected.