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Vapor-Induced Acute Kidney Injury Presenting as a Pulmonary–Renal Syndrome in an Adolescent

This case report describes a 14-year-old boy who developed severe acute kidney injury and pulmonary infiltrates mimicking a pulmonary–renal syndrome following electronic cigarette use, which was ultimately diagnosed as vaping-induced acute tubular injury via kidney biopsy and resolved completely after discontinuing immunosuppression.

Original authors: Cagla Cagli Piskin, Bahriye Atmis, Zahide Orhan Ok, Kıvılcım Eren Ates, Gulfiliz Gonlusen, Aysun K. Bayazit

Published 2026-06-29

📖 4 min read☕ Coffee break read

CC BY 4.0

Original authors: Cagla Cagli Piskin, Bahriye Atmis, Zahide Orhan Ok, Kıvılcım Eren Ates, Gulfiliz Gonlusen, Aysun K. Bayazit

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). ✨ This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

The Story: A Teenager's "System Crash" After Vaping

Imagine a teenager's body as a highly sophisticated, well-oiled machine. One day, this 14-year-old boy, who had never had any health problems before, started using electronic cigarettes (vaping). Just two days later, his machine began to sputter and smoke.

The Symptoms: A Triple Threat
Suddenly, the boy's body went into crisis mode in three major areas:

The Engine (Kidneys): His kidneys stopped filtering waste. His urine turned dark, he stopped producing urine, and his blood pressure skyrocketed to dangerous levels.
The Air Intake (Lungs): His lungs filled with fluid and inflammation, making it hard to breathe.
The Computer (Brain): The high blood pressure caused his brain to short-circuit, leading to seizures and confusion.

Because he had failing kidneys and failing lungs, doctors initially thought he had a rare, aggressive autoimmune disease called a "pulmonary–renal syndrome." Think of this like a "friendly fire" incident where the body's own security system (the immune system) mistakenly attacks both the kidneys and the lungs.

The Medical Detective Work

The doctors treated him as if his immune system was the enemy. They started powerful "firefighters"—strong steroids and a blood-cleaning process called plasma exchange—to stop the attack. They also put him on dialysis (an external machine acting as a temporary kidney) because his own kidneys had shut down completely.

However, the "enemy" they were looking for (autoimmune antibodies) wasn't there. The blood tests came back negative. It was like searching for a thief in a house but finding no footprints or fingerprints.

The Turning Point: Looking Under the Hood

To solve the mystery, the doctors performed a kidney biopsy. Imagine this as taking a tiny, high-resolution photo of the kidney's internal wiring to see exactly what was broken.

The Verdict:
The photo revealed the truth: The "security system" (immune system) was actually fine. The glomeruli (the kidney's main filters) were untouched. Instead, the damage was happening in the tubules (the pipes that carry the filtered fluid).

The pipes were clogged with debris and the cells lining them were dying. The doctors realized this wasn't an autoimmune attack; it was Acute Tubular Injury.

The Analogy:
Think of the kidney as a water filtration plant.

The Doctors' Initial Fear: They thought vandals (the immune system) were smashing the filters and pipes.
The Reality: The vandals weren't there. Instead, someone had dumped a toxic sludge (vaping chemicals) directly into the pipes, causing the pipes to corrode and clog from the inside out.

The Outcome: A Full Recovery

Once the doctors realized the immune system wasn't the problem, they stopped the "firefighting" steroids. This was a crucial move because those drugs have heavy side effects, and the boy didn't need them.

The result? The boy's kidneys, which had been completely shut down, began to heal.

3 Months later: His kidneys were working normally again.
18 Months later: He was completely healthy, off all medication, with normal blood pressure and normal kidney function.

The Big Takeaway

This paper teaches us three main things, using simple terms:

Vaping Can Be Toxic to Kidneys: While we know vaping hurts lungs, this case proves it can also severely damage kidneys in young people, even if they were previously healthy.
Don't Jump to Conclusions: The symptoms looked exactly like a rare autoimmune disease, but they were actually caused by direct chemical toxicity.
The "Microscope" Saves the Day: The kidney biopsy was the hero. It acted like a truth-teller, stopping the doctors from giving the boy unnecessary, heavy-duty drugs and confirming that his kidneys could fully recover.

In short: A teenager vaped, his body crashed, and doctors almost treated him for a rare immune disease. A tiny biopsy showed it was actually just chemical damage from the vape, and once they stopped the heavy treatment, his kidneys bounced back completely.

Technical Summary: Vapor-Induced Acute Kidney Injury Presenting as a Pulmonary–Renal Syndrome in an Adolescent

Problem Statement
Electronic cigarette (vaping) use among adolescents is increasingly prevalent and associated with multisystem toxicity. While vaping-associated lung injury (EVALI) is well-characterized, renal complications in this demographic remain poorly defined and are rarely confirmed histologically. Existing literature suggests that kidney involvement is exceptional in children, and the specific pathological mechanisms linking vaping to severe acute kidney injury (AKI) are not fully understood. This case addresses the diagnostic challenge of distinguishing vaping-induced renal toxicity from immune-mediated pulmonary–renal syndromes, which typically require aggressive immunosuppression.

Methodology
The study presents a detailed case report of a previously healthy 14-year-old male who developed oliguria, dark-colored urine, severe hypertension, seizures, and pulmonary infiltrates two days after regular electronic cigarette use. The clinical workup included:

Laboratory Analysis: Serial monitoring of serum creatinine, urinalysis (protein-to-creatinine ratio), complement levels, and serological testing for autoimmune markers (ANA, anti-dsDNA, ANCA). Notably, urinary $\beta_2$ -microglobulin was measured to assess tubular integrity.
Imaging: Thoracic CT revealed pulmonary consolidation and cavitary lesions; brain MRI was unremarkable despite seizures; renal ultrasound showed increased cortical echogenicity.
Intervention: The patient was initially treated empirically for a suspected pulmonary–renal syndrome (rapidly progressive glomerulonephritis or vasculitis) with pulse methylprednisolone, plasma exchange, and intermittent hemodialysis.
Definitive Diagnosis: A kidney biopsy was performed to differentiate between immune-mediated glomerular disease and tubular injury. Histopathological examination included light microscopy, immunofluorescence (testing for IgG, IgA, IgM, C3, C4, C1q, and fibrinogen), and electron microscopy assessment where applicable.

Key Results

Clinical Progression: Serum creatinine rose rapidly from 1.18 mg/dL to a peak of 10.6 mg/dL, necessitating hemodialysis. The patient exhibited active urinary sediment (hematuria and proteinuria) and severe hypertension (160/100 mmHg).
Serological Findings: All autoimmune serologies were negative, and complement levels remained normal, casting doubt on an immune-complex or pauci-immune etiology.
Tubular Markers: Urinary $\beta_2$ -microglobulin was markedly elevated (6.45 mg/L), indicating significant tubular dysfunction.
Histopathology: The kidney biopsy revealed preserved glomeruli without proliferative or crescentic lesions. The interstitium showed only minimal edema. In contrast, the tubular compartment demonstrated epithelial simplification, degenerative changes, intratubular erythrocyte casts, and necrotic cellular debris. Immunofluorescence was negative for all immune deposits.
Outcome: Upon confirmation of acute tubular injury (ATI) and exclusion of immune-mediated disease, immunosuppression was withdrawn. The patient's urine output recovered, hemodialysis was discontinued, and renal function normalized. At 18-month follow-up, the patient remained asymptomatic with normal creatinine (0.63 mg/dL), normal urinalysis, and normal blood pressure off all antihypertensive therapy.

Key Contributions

Histological Confirmation: This report provides rare, biopsy-proven evidence of vaping-associated acute tubular injury in an adolescent, distinguishing it from the more commonly reported adult cases or those lacking histological verification.
Diagnostic Differentiation: The study demonstrates that vaping toxicity can mimic a pulmonary–renal syndrome (characterized by pulmonary infiltrates, hematuria, and rapid renal failure). Crucially, it highlights that seronegative presentations with active urinary sediment may still represent non-immune tubular injury rather than vasculitis or glomerulonephritis.
Clinical Management Impact: The kidney biopsy was instrumental in redirecting management. It allowed for the cessation of unnecessary and potentially harmful immunosuppressive therapies (plasma exchange and corticosteroids) once an immune-mediated process was excluded.
Pathophysiological Insight: The findings support a primary tubular toxic mechanism. The presence of intratubular erythrocyte casts, often associated with glomerular bleeding, was reinterpreted in the context of preserved glomeruli and negative immunofluorescence as a result of severe tubular injury and necrosis.

Significance and Claims
The authors assert that electronic cigarette exposure should be considered a potential etiology for unexplained severe AKI in adolescents, particularly when accompanied by pulmonary and neurological features. The paper claims that vaping-associated acute tubular injury can present with a severity requiring dialysis but remains fully reversible if recognized early and managed appropriately.

The study emphasizes the critical value of kidney biopsy in adolescents with severe, unexplained AKI that mimics immune-mediated disease but lacks serological confirmation. By securing a definitive diagnosis of isolated tubular injury, clinicians can avoid prolonged immunosuppression and provide a more accurate prognosis. The authors conclude that while the specific toxic agent within the vaping aerosol (e.g., nicotine, heavy metals, aldehydes) could not be identified due to the lack of toxicological analysis of the product, the temporal relationship and exclusion of other causes strongly support a vaping-associated etiology. This case adds to the growing body of evidence suggesting that severe vaping toxicity involves combined neurological, pulmonary, and renal systems, with renal pathology potentially remaining unrecognized without histological examination.