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Acute Interstitial Nephritis (AIN)

Acute Interstitial Nephritis (AIN) is a cause of intrinsic Acute Kidney Injury (AKI) characterized by inflammation and edema of the renal interstitium, usually triggered by medications, infections, or autoimmune disease

Also called

Acute tubulointerstitial nephritis

ICD-10

N12

Specialty

Nephrology

Onset

Acute

Reviewed

August 2026
On This Page

Overview

-Acute Interstitial Nephritis (AIN) results from an inflammatory reaction within the kidney interstitium, leading to tubular dysfunction and reduced kidney function.

-The main causes are:

  • Medications — the most common cause
  • Infections
  • Autoimmune diseases

-AIN commonly presents as unexplained Acute Kidney Injury (AKI), often with pyuria and other urinary abnormalities

Etiology & Risk Factors

-Etiology

–Medications 

Common drug causes Acute Interstitial Nephritis (AIN) include:

  • Antibiotics, especially beta-lactams
  • NSAIDs
  • Proton Pump Inhibitors
  • Rifampicin
  • Diuretics

 

-Other Causes

  • Bacterial or viral infections
  • Systemic lupus erythematosus
  • Sjögren syndrome
  • Sarcoidosis
  • Other immune-mediated diseases

 

-Risk Factors for Acute Interstitial Nephritis (AIN):

  • Recent medication exposure
  • Polypharmacy
  • NSAID use
  • Proton pump inhibitor use
  • Autoimmune disease
  • Recent infection

Pathophysiology

Drug, infection, or autoimmune trigger → immune-mediated interstitial inflammation → infiltration by inflammatory cells → interstitial edema and tubular injury → impaired tubular function → reduced GFR → Acute Kidney Injury (AKI)

Clinical Presentation

-Symptoms:

  • Many patients have no specific symptoms apart from those related to Acute Kidney Injury (AKI).

    Possible symptoms include:

    • Fatigue
    • Nausea
    • Reduced urine output
    • Fever
    • Rash
    • Arthralgia

 

-Signs:

  • Fever
  • Maculopapular rash
  • Peripheral eosinophilia
  • Signs of Acute Kidney Injury (AKI)
Ureteral Stones overview
Ureteral Stones overview

History Taking

-Ask about:

  • Recent new medications
  • Antibiotic use
  • NSAID use
  • Proton pump inhibitor use
  • Diuretic use
  • Timing of symptoms after medication exposure
  • Fever or recent infection
  • Rash
  • Arthralgia
  • Previous kidney disease
  • Autoimmune disease

Physical Examination

-General Examination

  • Blood pressure
  • Temperature
  • Volume status
  • Skin examination for rash

 

-System-Specific Examination:

  • Assessment for peripheral edema or fluid overload
  • Examination for signs of systemic autoimmune disease
  • Assessment for signs of infection

Investigations

-Complete Blood Count

May show:

  • Eosinophilia

  • Leukocytosis when infection or inflammation is present

 

-Biochemistry / Specific Tests

  • Serum creatinine and eGFR

  • Serum urea

  • Serum electrolytes

  • Serum bicarbonate

  • Urinalysis

  • Urine microscopy

 

Possible urinary findings include:

  • Pyuria

  • Sterile pyuria

  • White blood cell casts

  • Mild to moderate proteinuria

  • Microscopic hematuria

Urine eosinophils are not sufficiently reliable to confirm or exclude AIN.

 

-Imaging

Renal ultrasound may be used to exclude urinary obstruction or assess kidney size.

There are no specific imaging findings that confirm Acute Interstitial Nephritis (AIN).

 

-Special / Confirmatory Tests

Kidney biopsy is the definitive diagnostic test.

Typical findings include:

  • Interstitial edema

  • Inflammatory cell infiltration

  • Tubulitis

Diagnosis

-Suspect Acute Interstitial Nephritis (AIN) in a patient with:

  • Unexplained Acute Kidney Injury (AKI)
  • Recent medication exposure, infection, or autoimmune disease
  • Pyuria or white blood cell casts
  • Possible eosinophilia or rash
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Management

1. First-Line / Emergency Management

  • Immediately stop the suspected offending medication

  • Treat severe electrolyte abnormalities

  • Manage fluid overload

  • Treat severe metabolic acidosis

  • Start dialysis when standard indications are present

 

2. Definitive Treatment

  • Identify and remove the underlying cause

  • Treat the underlying infection or autoimmune disease when present

Early withdrawal of the offending drug is the most important intervention in drug-induced Acute Interstitial Nephritis (AIN).

 

3. Medical Treatment

  • Corticosteroids may be considered in selected patients, particularly when kidney function does not improve after stopping the offending drug and active Acute Interstitial Nephritis (AIN) is strongly suspected or confirmed

  • Cause-specific treatment for autoimmune or infectious AIN

  • Appropriate electrolyte management

 

4. Surgical / Procedural Treatment

No routine surgical treatment.

Kidney biopsy may be performed to confirm the diagnosis.

 

5. Supportive Management

  • Monitor serum creatinine and electrolytes

  • Monitor urine output

  • Maintain appropriate fluid balance

  • Avoid further nephrotoxic medications

  • Adjust drug doses according to kidney function

Complications

  • Persistent Acute Kidney Injury (AKI)
  • Hyperkalemia
  • Metabolic acidosis
  • Fluid overload
  • Uremia
  • Dialysis requirement
  • Chronic Kidney Disease (CKD)
  • Persistent tubular dysfunction
  • Recurrent injury after drug re-exposure

Prognosis

-Acute Interstitial Nephritis (AIN) generally has a good prognosis when the underlying cause is identified and treated early.

-Most patients experience substantial recovery of kidney function after withdrawal of the offending drug,

-although recovery may take several weeks to months. Severe or prolonged AIN can result in incomplete renal recovery and Chronic Kidney Disease (CKD), particularly when significant interstitial fibrosis has developed.

Key Points / Clinical Pearls

  • Acute Interstitial Nephritis (AIN) is inflammation of the renal interstitium causing Acute Kidney Injury (AKI).
  • Medications are the most common cause, especially antibiotics, NSAIDs, and proton pump inhibitors.
  • Other causes include infections and autoimmune diseases.
  • Common symptoms include fever, rash, arthralgia, and reduced urine output.
  • The classic triad of fever + rash + eosinophilia is uncommon and its absence does not exclude AIN.
  • Urinalysis commonly shows pyuria, sterile pyuria, and mild-to-moderate proteinuria.
  • White blood cell casts may be present.
  • Peripheral eosinophilia can occur but is not required for diagnosis.
  • Urine eosinophils are not reliable for confirming or excluding AIN.
  • Kidney biopsy is the definitive diagnostic test when the diagnosis is uncertain.
  • The most important treatment is immediate withdrawal of the offending drug.