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Acute Interstitial Nephritis – Kidney Quiz With Solution

Acute Interstitial Nephritis Case:

Background: An older woman was started on therapy for temporal arteritis 4 months ago. Medications include prednisone, omeprazole, empagliflozin, and vitamin D. The patient’s temporal arteritis improved, but she did not feel well. The primary provider worked up the condition, noting an increase in the serum creatinine, and a urine which showed leukocytes. The patient was treated for a presumed urinary tract infection. Results of the urine culture were negative. She is diagnosed with acute interstitial nephritis.

White blood cells in the urine suggesting acute interstitial nephritis.
White blood cells seen in the urinalysis suggesting acute interstitial nephritis.

The creatinine was 2.1 mg/dL (baseline 1.3). The CBC revealed the presence of eosinophils. The patient does not have a rash or a fever.

Please answer the following questions:

Which medication most likely caused the acute interstitial nephritis?
* empaglifozen
* vitamin D
* omeprazole
* prednisone

Describe acute interstitial nephritis (AIN).

How does the clinical presentation of AIN vary?

Define the classic triad of symptoms associated with AIN.

What is the significance of medication exposure in diagnosing AIN?

How long after drug exposure does AIN typically occur?

What might previous exposure to a drug indicate in AIN?

What are common findings seen in the urinalysis for AIN?

What is the mainstay treatment for AIN?

How does the presentation of AIN relate to proton pump inhibitors?

Explain the potential consequences of untreated drug-induced AIN.

What is the definition of AIN in terms of serum creatinine levels?

Describe medications associated with acute interstitial nephritis.

What is the prognosis for acute interstitial nephritis with early recognition and treatment?

Do glucocorticoids play a role in the treatment of acute interstitial nephritis?

Discussion:

Acute Interstitial Nephritis (AIN)

Diagnosis and Causes

AIN is often caused by a hypersensitivity reaction to medications like antibiotics, proton pump inhibitors, or NSAIDs.

  • The clinical presentation varies but may include fever, rash, eosinophilia, and elevated serum creatinine.
  • AIN is mainly triggered by drug exposure, with proton pump inhibitors linked to a more subacute course.

Signs and Symptoms

Urinalysis may reveal leukocytes, leukocyte casts, sterile pyuria, and/or erythrocytes.

Treatment and Prognosis

The mainstay of treatment is discontinuation of the offending medication.

  • Early recognition and withdrawal of the causative drug can lead to reversibility of AIN and renal failure.
  • Glucocorticoid therapy may be considered in selected patients with biopsy-proven AIN, except for NSAID-induced cases.

Drug Associations

Medications linked to AIN include proton pump inhibitors, H2 blockers, penicillins, cephalosporins, NSAIDs, diuretics, and immune checkpoint inhibitors.

Statistics and Complications

Drug-induced AIN accounts for 70-75% of cases in developed countries and is responsible for approximately 20% of renal biopsies for unexplained AKI.

  • AIN is defined by a significant increase in serum creatinine after exposure to a potential triggering medication.
  • It can lead to acute decline in renal function, potentially progressing to permanent kidney insufficiency or end-stage kidney disease.

Inspiration: Allergic and Drug-Induced Interstitial Nephritis, National Library of Medicine

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