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Scholarly Commons > HCA Healthcare Journal > Vol. 6 > Iss. 5 (2025)

 

Keywords

acute kidney injury; hypocomplementemia; immune-mediated acute interstitial nephritis; tubulointerstitial nephritis

Disciplines

Nephrology

Abstract

Background

Acute interstitial nephritis (AIN) is the most common cause of acute kidney injury (AKI) with subsequent renal impairment and is often underdiagnosed. Acute interstitial nephritis presents with a decline in kidney function and is characterized by an inflammatory infiltrate in the kidney interstitium. It is most often induced by drug therapy and is sometimes followed by infections with unknown causes. In a typical presentation of AIN, there is no evidence of hypocomplementemia; low complement is associated most commonly with autoimmune etiologies. Renal biopsy serves as the most definitive test for both the diagnosis and prognosis of AIN.

Case Presentation

A woman in premenopause, with no significant past medical history, other than a remote history of seizures, presented to the emergency department (ED), in cardiac arrest, via emergency medical services (EMS). When EMS arrived, she was noted as hypotensive and tachycardic with agonal respirations, having received 3 rounds of defibrillation in the field. Per rapid assessment, the patient received CPR from a bystander for an unknown amount of time. Upon arrival at the ED, the patient again went into cardiac arrest, requiring 5 rounds of CPR, with 3 separate administrations of epinephrine, followed by intubation with mechanical ventilation. Initial labs presented significant results for acute respiratory acidosis without renal compensation, leukocytosis, elevated troponin consistent with myocardial infarction, mild normocytic anemia, and intrarenal AKI. Imaging was significant for a suprarenal mass, later confirmed to be pheochromocytoma. Over the next few days, the patient developed anuric kidney failure requiring dialysis, and a kidney biopsy was obtained for confirmation of AIN. However, she was also noted to have decreased complement, which is not typically found in interstitial nephritis.

Conclusion

We encountered a patient with interstitial nephritis and low complement level. The reason behind this rare phenomenon remains unclear in recent literature. As of 2024, only 11 other known cases of AIN have been found to have hypocomplementemia, making it a rare and curious pathophysiological process. More research and data are needed for further investigation into this exciting new pathology, its fundamental process, and potential treatment variations aside from those already used in AIN.

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