Fulminant Multisystem IgA Vasculitis With Diffuse Alveolar Hemorrhage, Severe Gastrointestinal Hemorrhage, Paralytic Ileus, and Renal Involvement in an Adolescent: A Case Report

ABSTRACT

A 17‐year‐old girl with IgA vasculitis developed diffuse alveolar hemorrhage, severe gastrointestinal hemorrhage with paralytic ileus, and clinical renal involvement. Early bronchoscopy demonstrated diffuse airway bleeding, supported the diagnosis, enabled microbiological sampling, and informed postponement of pharmacological thromboprophylaxis.

Key Clinical Message

Fulminant multisystem IgA vasculitis requires rapid recognition and coordinated multidisciplinary management. When pulmonary hemorrhage, severe gastrointestinal involvement, and renal abnormalities occur together, early bronchoscopy, organ‐specific assessment, and integrated treatment planning can support timely decisions.

Abbreviations

ANA

Antinuclear antibody

ANCA

Antineutrophil cytoplasmic antibody

Anti‐GBM

Anti‐glomerular basement membrane

ARDS

Acute respiratory distress syndrome

CT

Computed tomography

DAH

Diffuse alveolar hemorrhage

FiO₂

Fraction of inspired oxygen

GGOs

Ground‐glass opacities

HRCT

High‐resolution computed tomography

ICU

Intensive care unit

IgAV

Immunoglobulin A vasculitis

PaO₂

Partial pressure of oxygen

RBC

Red blood cell

1. Introduction

Immunoglobulin A vasculitis (IgAV), formerly Henoch–Schönlein purpura, is an immune complex‐mediated small‐vessel vasculitis characterized by nonthrombocytopenic palpable purpura, arthralgia or arthritis, gastrointestinal involvement, and renal manifestations [1, 2]. Although usually self‐limiting in children, IgAV may cause severe systemic disease, particularly when the kidneys, gastrointestinal tract, or lungs are involved [2, 3]. Diffuse alveolar hemorrhage (DAH) is a rare but life‐threatening pulmonary manifestation that may present with rapidly progressive hypoxemia, hemoptysis, anemia, and diffuse pulmonary infiltrates [4, 5, 6]. These findings overlap with infection, cardiogenic pulmonary edema, and acute respiratory distress syndrome, which may delay recognition [4, 5, 6]. Bronchoscopic evaluation and exclusion of major alternative causes, including ANCA‐associated vasculitis and anti‐glomerular basement membrane disease, are therefore important when DAH is suspected.

IgAV‐associated DAH has been reported in children and adolescents, but fulminant presentations with simultaneous pulmonary, gastrointestinal, and renal involvement remain clinically challenging. We describe an adolescent with bronchoscopy‐supported DAH, gastrointestinal hemorrhage with paralytic ileus, and marked clinical renal involvement requiring intensive care. The case illustrates the value of early pulmonary evaluation, integrated multisystem assessment, and individualized post‐stabilization immunosuppression.

2. Case History/Examination

A 17‐year‐old previously healthy girl presented with a 7‐day history of palpable purpura on the lower extremities, abdominal pain, and progressive abdominal distension. She reported no recent infection, medication exposure, or allergy. Despite treatment with oral prednisone 1 mg/kg/day at a local hospital from Day −5, her condition continued to deteriorate. Coffee‐ground emesis developed on Day −3. On Day 0, she developed acute dyspnea and hemoptysis and underwent endotracheal intubation at the referring hospital. She was transferred to the intensive care unit (ICU) on Day 1.

On admission, she was tachycardic and tachypneic. Oxygen saturation was 90% despite mechanical ventilation with an FiO₂ of 100%. Examination showed diffuse bilateral crackles, extensive nonblanching palpable purpura over the lower extremities (Figure 1), and abdominal distension with mild tenderness.

FIGURE 1.

Cutaneous manifestations of IgA vasculitis. (a–c) Extensive palpable purpura, ecchymoses, and petechiae over the lower extremities at ICU admission. Some lesions coalesced into large nonblanching patches.

3. Methods

3.1. Investigations

Arterial blood gas analysis showed severe hypoxemia, with a PaO₂/FiO₂ ratio of 183 mmHg. The white blood cell count was 12.79 × 10⁹/L, with 89.4% neutrophils, and hemoglobin was 62 g/L. C‐reactive protein was 37.58 mg/L, and interleukin‐6 was 7.39 pg/mL.

Clinical renal involvement was indicated by proteinuria (3+), occult blood (3+), 2781 urinary red blood cells/μL, hyaline and granular casts, a urinary total protein‐to‐creatinine ratio of 1101.6 mg/g, a urinary albumin‐to‐creatinine ratio of 535 mg/g, an N‐acetyl‐β‐D‐glucosaminidase‐to‐creatinine ratio of 35.67 U/g, 24‐h urinary microalbumin excretion of 612 mg/day, and 24‐h urinary protein excretion of 1.26 g/day. Serum creatinine increased from 67.65 to a peak of 77.9 μmol/L, with corresponding estimated glomerular filtration rates of 86.4 and 74.9 mL/min/1.73 m². Although KDIGO criteria for acute kidney injury were not met, the urinary abnormalities indicated substantial clinical renal involvement. Renal biopsy was deferred during the acute phase because active pulmonary and gastrointestinal bleeding increased procedural risk.

Fibrin degradation products were 81.1 mg/L, and D‐dimer was 20.2 mg/L. Tests for ANCA, ANA, and anti‐GBM antibodies were negative. Chest radiography showed bilateral perihilar patchy opacities in a “butterfly” distribution and bilateral pleural effusions (Figure 2). High‐resolution computed tomography showed diffuse ground‐glass opacities, interlobular septal thickening, and dependent consolidations compatible with pulmonary hemorrhage in the clinical context (Figure 3), together with massive pleural effusions and compressive atelectasis (Figure 4).

FIGURE 2.

Anteroposterior chest radiograph. Extensive bilateral perihilar opacities show an alveolar filling pattern compatible with pulmonary hemorrhage in the clinical context. Blunting of both costophrenic angles indicates pleural effusions. A markedly dilated gastric bubble is visible in the left upper quadrant.

FIGURE 3.

High‐resolution computed tomography of the chest, lung window. (a, b) Axial images of the upper lungs show centrally distributed ground‐glass opacities with superimposed interlobular septal thickening, producing a crazy‐paving pattern. (c–f) Images of the middle and lower lungs show confluent consolidation, most pronounced in the dependent posterior regions, with air bronchograms.

FIGURE 4.

High‐resolution computed tomography of the chest, mediastinal window. Axial images (a–f) demonstrate large, symmetric bilateral pleural effusions with compressive atelectasis of the lower lobes. The mediastinum remains midline, with no pericardial effusion.

Because of ongoing hemoptysis, severe anemia, diffuse bilateral pulmonary infiltrates, and severe hypoxemia, flexible bronchoscopy with bronchoalveolar lavage was performed on day 1, one day after intubation at the referring hospital. Diffuse fresh, frothy blood was present throughout the tracheobronchial tree, and the lavage fluid was bloody, strongly supporting DAH (Figure 5). Samples were submitted for bacterial, fungal, mycobacterial, and viral testing; fungal culture was negative. The finding of active pulmonary bleeding contributed to the postponement of pharmacological thromboprophylaxis.

FIGURE 5.

Flexible bronchoscopy on day 1. (a, b) Abundant fresh, frothy blood is present in the main bronchi. (c, d) Blood extends diffusely from the main carina into the distal bronchi. (e, f) Diffuse mucosal erythema and hemorrhage are visible. In the clinical context of hemoptysis, severe anemia, diffuse pulmonary infiltrates, and hypoxemia, these findings strongly supported diffuse alveolar hemorrhage.

A skin biopsy obtained from an older arm lesion on ICU day 3 showed leukocytoclastic vasculitis, with dense perivascular neutrophilic infiltration, leukocytoclasis, fibrinoid necrosis of small‐vessel walls, and erythrocyte extravasation (Figure 6). Direct immunofluorescence for vascular IgA deposition was unavailable through the institutional pathology workflow; therefore, the biopsy provided morphological evidence of small‐vessel vasculitis but not IgA‐specific histopathological confirmation. Abdominal computed tomography showed generalized bowel dilatation and marked wall edema, consistent with severe enteropathy and paralytic ileus (Figure 7). Upper gastrointestinal endoscopy showed hemorrhagic‐purpuric gastroduodenitis with multiple erosions, ulcers, and markedly thickened duodenal folds (Figure 8).

FIGURE 6.

Skin biopsy histopathology, hematoxylin and eosin staining. (a, b) The superficial dermis shows dense perivascular neutrophilic infiltration around postcapillary venules, with leukocytoclasis, fibrinoid necrosis of vessel walls, and erythrocyte extravasation, consistent with leukocytoclastic vasculitis.

FIGURE 7.

Abdominal computed tomography. (a) Axial image showing marked transverse‐colon dilatation and diffuse wall edema. (b) A lower section shows generalized dilatation and wall thickening of small‐bowel loops, consistent with severe enteropathy and paralytic ileus.

FIGURE 8.

Upper gastrointestinal endoscopy. (a–c) The gastric antrum and body show diffuse hyperemia, edema, purpuric lesions, hemorrhage, and aphthous‐like ulcers. (d–f) The descending duodenum shows markedly thickened, coarse, edematous folds with loss of the normal feather‐like appearance; the pyloric ring appears narrowed by edema.

3.2. Differential Diagnosis

The diagnostic assessment integrated the negative ANCA, ANA, and anti‐GBM antibody results with the characteristic multisystem presentation. Lower‐limb–predominant palpable purpura, severe gastrointestinal involvement, hematuria and proteinuria, and compatible skin histopathology supported a clinical diagnosis of severe multisystem IgAV complicated by DAH, gastrointestinal hemorrhage with paralytic ileus, and renal involvement. Because direct immunofluorescence for vascular IgA deposition was unavailable, the diagnosis was clinically supported rather than IgA‐specific histopathologically confirmed.

3.3. Treatment

The patient had received oral prednisone 1 mg/kg/day from day −5. After ICU admission, intravenous methylprednisolone 40 mg once daily was administered from day 1 to day 15, and intravenous immunoglobulin 1 g/kg/day was given from day 1 for 5 consecutive days. Supportive care included lung‐protective mechanical ventilation, prone positioning, blood transfusion, and gastrointestinal support.

3.4. Conclusions and Results (Outcome and Follow‐Up)

Clinical findings improved gradually. By day 7, the purpura was resolving, gastrointestinal function had recovered, and repeat bronchoscopy showed clearance of the previous diffuse airway blood and clots, with patent segmental bronchi (Figure 9). Residual mucosal erythema and petechiae remained, but no fresh blood, clots, or purulent secretions were seen in the distal airways. The PaO₂/FiO₂ ratio increased to 398 mmHg, and the patient was extubated.

FIGURE 9.

Follow‐up flexible bronchoscopy. (a, c) The main bronchi and carina are patent, with clearance of the previous blood and clots. (b, d) The segmental and distal bronchi contain no fresh blood or frothy secretions. Residual mucosal erythema and scattered petechiae remain, without visible active bleeding.

On day 9 (August 20, 2024), she was transferred to the general gastroenterology ward. Follow‐up chest computed tomography showed near‐complete resolution of the diffuse ground‐glass opacities and consolidations (Figure 10). Oral cyclosporine 50 mg twice daily was introduced after clinical stabilization as maintenance immunosuppression and a steroid‐sparing strategy, not as acute rescue therapy.

FIGURE 10.

Follow‐up chest computed tomography, lung window, after transfer to the general ward. (a–f) The previously diffuse bilateral ground‐glass opacities and consolidations have largely resolved. Only minimal scattered opacities and mild dependent linear atelectasis remain.

At discharge, treatment was transitioned to oral prednisone 50 mg/day, with a planned taper of 5 mg weekly to 40 mg/day, 5 mg every 2 weeks to 30 mg/day, and then 2.5 mg every 2 weeks. At the outpatient visit on September 14, 2024, serum creatinine was 52.7 μmol/L, and eGFR was 110.8 mL/min/1.73 m². Urinalysis showed no proteinuria, casts, or leukocytes; urinary protein‐to‐creatinine and albumin‐to‐creatinine ratios were not reassessed.

At telephone follow‐up on October 21, 2025, the patient reported no recurrence of purpura, abdominal pain, hemoptysis, or dyspnea and had resumed school. No further laboratory or imaging data were available after the September 2024 outpatient assessment; thus, the later follow‐up reflected patient‐reported status rather than objectively confirmed long‐term remission. The clinical course is summarized in Table 1.

TABLE 1.

Clinical timeline of presentation, treatment, and outcomes.

Time point	Clinical events and findings	Management and outcomes
Day −7	Palpable purpura developed over the lower extremities, with abdominal pain and progressive abdominal distension.	No specific immunosuppressive treatment was reported.
Day −5	Symptoms persisted and progressed at the referring facility.	Oral prednisone 1 mg/kg/day was initiated.
Day −3	Coffee‐ground emesis developed, indicating overt gastrointestinal bleeding.	Treatment continued at the local hospital.
Day 0	The patient developed acute dyspnea, hemoptysis, and worsening hypoxemic respiratory failure.	Endotracheal intubation and mechanical ventilation were initiated at the referring hospital.
Day 1	She was transferred to our ICU with severe hypoxemia and anemia. Chest imaging and bronchoscopy with bronchoalveolar lavage supported DAH. Abdominal imaging and upper gastrointestinal endoscopy demonstrated severe gastrointestinal involvement. Urinary findings indicated clinical renal involvement.	Lung‐protective mechanical ventilation, prone positioning, blood transfusion, gastrointestinal support, and other intensive supportive measures were provided. Intravenous methylprednisolone 40 mg once daily and intravenous immunoglobulin 1 g/kg/day were initiated.
Day 3	A skin biopsy obtained from an older lesion on the arm demonstrated leukocytoclastic vasculitis. Direct immunofluorescence for vascular IgA deposition was unavailable.	The histopathological findings supported the clinical diagnosis but did not provide IgA‐specific confirmation.
Days 1–5	Severe multisystem IgAV with pulmonary, gastrointestinal, and renal involvement was managed in the ICU.	Intravenous immunoglobulin, corticosteroid therapy, and intensive supportive care were continued.
Day 7	Purpura was resolving, gastrointestinal function had recovered, and repeat bronchoscopy showed clearance of diffuse airway blood and clots. The PaO2/FiO2 ratio increased to 398 mmHg.	The patient was extubated.
Day 9	The patient was transferred to the general gastroenterology ward. Follow‐up chest CT showed near‐complete resolution of the diffuse ground‐glass opacities and consolidations.	Oral cyclosporine 50 mg twice daily was introduced after clinical stabilization as maintenance immunosuppression and a steroid‐sparing strategy.
Day 15	The course of intravenous methylprednisolone was completed.	Treatment was transitioned to oral prednisone according to the discharge plan.
Discharge	The patient was clinically stable, without recurrent hemoptysis, respiratory failure, or active gastrointestinal bleeding.	Oral prednisone 50 mg/day was prescribed, with tapering by 5 mg weekly to 40 mg/day, 5 mg every 2 weeks to 30 mg/day, and then 2.5 mg every 2 weeks.
September 14, 2024 outpatient follow‐up	Serum creatinine was 52.7 μmol/L and eGFR was 110.8 mL/min/1.73 m2. Urinalysis showed no proteinuria, casts, or leukocytes. Urinary protein‐to‐creatinine and albumin‐to‐creatinine ratios were not reassessed.	No further objective laboratory or imaging follow‐up was available.
October 21, 2025 telephone follow‐up	The patient reported no recurrence of purpura, abdominal pain, hemoptysis, or dyspnea and had resumed school.	No contemporaneous laboratory or imaging examinations were available; the assessment was based on patient‐reported symptoms and functional status.

4. Discussion

This case represents a fulminant multisystem phenotype of adolescent IgAV rather than an isolated pulmonary complication. Concurrent severe pulmonary, gastrointestinal, and renal involvement required invasive mechanical ventilation, repeated bronchoscopy, and multidisciplinary intensive care.

Several features are clinically relevant. First, DAH occurred with severe gastrointestinal hemorrhage, paralytic ileus, and marked renal involvement. Early bronchoscopy was prompted by hemoptysis, severe anemia, diffuse bilateral pulmonary opacities, and marked hypoxemia. Diffuse fresh airway blood and bloody bronchoalveolar lavage fluid supported a diffuse pulmonary bleeding process, helped exclude a focal central‐airway source, and enabled microbiological sampling [7, 8]. Because progressively bloodier sequential aliquots and hemosiderin‐laden macrophages were not documented, the findings were considered strongly supportive rather than definitive for DAH. Visualization of active bleeding also led to postponement of pharmacological thromboprophylaxis, while serial bronchoscopy documented subsequent clearance of blood and clots.

Second, renal involvement was clinically significant despite the absence of KDIGO‐defined acute kidney injury. The modest change in serum creatinine contrasted with marked hematuria, proteinuria, urinary casts, and abnormal quantitative urinary indices. IgAV‐related renal involvement may therefore be evident even when glomerular filtration remains relatively preserved [9, 10]. Because renal biopsy was not performed, these findings were classified as clinical renal involvement rather than histologically confirmed IgAV nephritis.

Third, the simultaneous pulmonary, gastrointestinal, renal, and cutaneous manifestations required early multidisciplinary coordination. Critical care and respiratory teams managed hypoxemic respiratory failure and pulmonary bleeding; gastroenterology and gastrointestinal surgery evaluated gastrointestinal hemorrhage and paralytic ileus; rheumatology and nephrology assessed systemic and renal involvement and immunosuppressive options; and dermatology and pathology supported tissue evaluation. This approach integrated bleeding risk, organ‐specific priorities, and treatment alternatives. Although team composition varies by institution, prompt cross‐specialty communication is important when several organ‐threatening manifestations evolve concurrently.

No standard regimen has been established for IgAV‐associated DAH. High‐dose intravenous methylprednisolone pulse therapy, cyclophosphamide, rituximab, and plasma exchange have been reported, alone or in combination, mainly in case reports and literature reviews [5, 6, 11, 12]. Experience in systemic lupus erythematosus‐associated DAH also emphasizes early recognition and prompt treatment but cannot be directly extrapolated to IgAV [13]. The multidisciplinary team discussed these escalation strategies; however, oxygenation and pulmonary and gastrointestinal bleeding improved during treatment with methylprednisolone 40 mg/day, intravenous immunoglobulin, and intensive supportive care, so further escalation was not undertaken.

After clinical stabilization, cyclosporine A was introduced on day 9 as maintenance immunosuppression and a steroid‐sparing strategy rather than as acute rescue therapy.

Cyclosporine A was selected for two patient‐specific reasons. First, the patient was an adolescent girl, and avoiding cyclophosphamide was considered relevant because of its dose‐dependent gonadal toxicity and potential effects on future fertility [14, 15]. Second, prolonged systemic corticosteroid exposure was considered undesirable in the setting of severe vasculitic enteropathy, gastrointestinal hemorrhage, and paralytic ileus, given the risks of ischemia, necrosis, and perforation in severe intestinal disease [16, 17]. Cyclosporine A has been used in selected children with IgAV nephritis, but the evidence is limited and does not address DAH or severe gastrointestinal involvement [18]. Its use here should therefore be viewed as an individualized post‐stabilization, steroid‐sparing approach. Because pulmonary and gastrointestinal improvement preceded cyclosporine initiation, no causal inference can be made regarding acute disease control.

The concurrent pulmonary and gastrointestinal manifestations may reflect systemic immune‐mediated injury to different small‐vessel beds. IgA‐containing immune complexes, complement activation, and neutrophil‐mediated endothelial injury have been implicated in IgAV [19, 20]. Alveolar capillary injury may cause pulmonary hemorrhage, whereas injury to gastrointestinal mucosal and submucosal vessels may produce vascular leakage, bowel‐wall edema, hemorrhage, and ischemia. This provides a plausible framework for the simultaneous DAH, gastrointestinal bleeding, and paralytic ileus, but remains inferential because pulmonary and gastrointestinal tissue confirmation was unavailable.

DAH in systemic autoimmune disease commonly presents with acute respiratory deterioration, hypoxemia, a fall in hemoglobin, and diffuse pulmonary infiltrates. These nonspecific findings may overlap with infection, cardiogenic pulmonary edema, or acute respiratory distress syndrome [6, 7, 8]. A recent single‐center study of systemic lupus erythematosus‐associated DAH likewise emphasized its life‐threatening nature and the importance of early recognition [13]. Although the underlying disease differs, this general diagnostic context is relevant to IgAV. DAH should be considered promptly when patients with IgAV develop hemoptysis, rapidly worsening hypoxemia, diffuse pulmonary opacities, or otherwise unexplained anemia.

In this patient, lower‐limb–predominant palpable purpura, severe gastrointestinal involvement, hematuria and proteinuria, leukocytoclastic vasculitis on skin histopathology, and negative ANCA, ANA, and anti‐GBM antibody tests supported the clinical diagnosis of IgAV. The patient fulfilled the EULAR/PRINTO/PRES classification criteria through purpura combined with abdominal pain and renal involvement, without reliance on histological IgA deposition [10]. These criteria supported classification in the clinical context but were not treated as a diagnostic gold standard.

Direct immunofluorescence could have strengthened the histopathological attribution by demonstrating IgA‐predominant vascular deposition, but it was unavailable through the institutional pathology workflow. The specimen was also obtained from an older lesion, which may have reduced the expected diagnostic yield [21]. Because leukocytoclastic vasculitis on routine histology is not specific to IgAV, the absence of direct immunofluorescence limits histopathological certainty. We therefore describe the diagnosis as clinically supported rather than pathologically confirmed.

Pulmonary hemorrhage has been reported in children and adolescents with IgAV, often with renal abnormalities and sometimes with abdominal manifestations or respiratory failure. In a review of 17 pediatric cases, proteinuria and abdominal pain occurred in 82% and 76%, respectively, and nine patients required intubation. A later review identified 23 pediatric cases with pulmonary involvement, predominantly DAH [4, 5]. Thus, none of the individual organ manifestations in this patient was unprecedented.

The distinctive feature of this case is the simultaneous severity and detailed documentation of multisystem involvement. Bronchoscopy‐supported DAH caused severe hypoxemic respiratory failure requiring mechanical ventilation. Gastrointestinal involvement included overt hemorrhage, endoscopically documented hemorrhagic‐purpuric gastroduodenitis, and paralytic ileus. Renal involvement was marked by hematuria, proteinuria, urinary casts, and abnormal urinary indices despite the absence of KDIGO‐defined acute kidney injury. Although pulmonary–renal disease, gastrointestinal bleeding, and mechanical ventilation have each been reported [22, 23, 24, 25, 26], their concurrence, together with serial bronchoscopic, endoscopic, and radiological documentation, provides a detailed view of fulminant multisystem IgAV. We therefore present the case as a well‐documented severe phenotype rather than as the first report of IgAV‐associated DAH. Selected pediatric and adolescent cases are compared in Table 2.

TABLE 2.

Phenotypic comparison of selected pediatric and adolescent cases of IgA vasculitis‐associated pulmonary hemorrhage.

Study	Age/Sex	GI involvement	Renal involvement	Evidence of DAH	Mechanical ventilation
Payton et al. [22].	17/F	Not prominent	Proteinuria, hematuria, elevated serum creatinine	Chest radiography; BAL not performed	Not reported
Carter et al. [23].	15/M	Abdominal pain and blood in stools	Hematuria, proteinuria, hypertension, elevated serum creatinine	Chest radiography; BAL not performed	Yes
Vats et al. [24].	7/M	Abdominal pain, vomiting, bloody diarrhea	Proteinuria, hematuria, elevated serum creatinine	Chest radiography; BAL not performed	Yes
Chen et al. [5].	11/F	Abdominal pain and vomiting	Hematuria, nephrotic‐range proteinuria, acute renal failure	BAL showed numerous red blood cells and hemosiderin‐laden macrophages	Not reported
Ngobia et al. [25].	18/M	Abdominal pain	Hematuria, proteinuria, elevated serum creatinine	BAL showed hemosiderin‐laden macrophages	Not reported
Clarke et al. [26].	5/M	Abdominal pain and rectal bleeding	Proteinuria, hematuria, worsening renal function	Chest radiography; BAL not performed	Yes
Present case	17/F	Severe gastrointestinal hemorrhage, hemorrhagic‐purpuric gastroduodenitis, and paralytic ileus	Marked clinical renal involvement with hematuria, proteinuria, urinary casts, and abnormal quantitative urinary indices; KDIGO‐defined AKI was absent, and renal biopsy was not performed	Bronchoscopy‐supported DAH with diffuse fresh airway blood and bloody lavage fluid; HRCT showed diffuse ground‐glass opacities and consolidations	Yes

Note: The selected cases illustrate the pediatric and adolescent spectrum of IgAV‐associated pulmonary hemorrhage and do not constitute a systematic review.

Abbreviations: AKI, acute kidney injury; BAL, bronchoalveolar lavage; DAH, diffuse alveolar hemorrhage; GGOs, ground‐glass opacities; GI, gastrointestinal; HRCT, high‐resolution computed tomography; MV, mechanical ventilation; NR, not reported; RBCs, red blood cells.

This report has several limitations. Direct immunofluorescence for vascular IgA deposition was unavailable, and the skin biopsy was obtained from an older lesion; consequently, routine histology showed leukocytoclastic vasculitis but did not provide IgA‐specific confirmation. Renal biopsy was deferred during active pulmonary and gastrointestinal bleeding because of procedural risk and was not pursued after clinical improvement. Renal involvement was therefore assessed clinically. Lung biopsy was not performed during active DAH and critical illness, so pulmonary capillaritis was not histologically confirmed. Cyclosporine was started after stabilization, precluding assessment of its effect on acute disease control. Finally, objective follow‐up was limited to the outpatient laboratory assessment on September 14, 2024. The October 21, 2025 telephone follow‐up captured only patient‐reported symptoms and functional status, without repeat laboratory or imaging evaluation; long‐term disease activity and organ‐specific outcomes could not be determined objectively.

Adolescent IgAV may rarely present as fulminant multisystem disease involving the lungs, gastrointestinal tract, and kidneys. DAH should be considered early when rapidly progressive hypoxemia, hemoptysis, diffuse pulmonary infiltrates, or unexplained anemia develops. Early bronchoscopy, exclusion of major vasculitic mimics, and careful gastrointestinal and renal assessment can guide management. Prompt multidisciplinary coordination may support timely diagnosis and balanced, organ‐specific treatment. In this case, cyclosporine served as individualized post‐stabilization maintenance and steroid‐sparing therapy, not acute rescue treatment.

Author Contributions

Xianzhang Shan: conceptualization, methodology, software, data curation, resources, project administration, formal analysis, validation, visualization, investigation, writing – original draft. Yancui Zhu: conceptualization, supervision, writing – review and editing.

Funding

The authors have nothing to report.

Disclosure

Patient Perspective: At telephone follow‐up on October 21, 2025, the patient reported that she had resumed school and had no recurrence of purpura, abdominal pain, hemoptysis, or dyspnea. No contemporaneous laboratory or imaging assessments were available.

Ethics Statement

The study was conducted in accordance with the Declaration of Helsinki. The institutional review board waived ethical approval because the report involved a single anonymized case.

Consent

Written informed consent for publication of the case and accompanying images was obtained from the patient and her legal guardian.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.