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[Acute renal failure and 2,8-dihydroxyadeninuria].

M Hoffmann1, A Talaszka, J P Bocquet

  • 1Service de néphrologie et de dialyse, Centre hospitalier de Roubaix. maxime.hoffmann@free.fr

Nephrologie
|December 9, 2004
PubMed
Summary

A rare metabolic disease, 2,8-dihydroxyadeninuria, caused acute renal failure in a 65-year-old man. Treatment with allopurinol, diet, and fluids reversed the kidney damage.

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Area of Science:

  • Nephrology
  • Metabolic Medicine
  • Biochemistry

Background:

  • Recurrent urolithiasis can present with acute renal failure.
  • Investigating renal failure requires ruling out obstructive and glomerular causes.

Observation:

  • A 65-year-old man with a history of kidney stones presented with acute renal failure.
  • Crystalluria revealed 2,8-dihydroxyadeninuria, a rare metabolic disorder.
  • The condition stems from adenine phosphoribosyltransferase deficiency, impacting purine metabolism.

Findings:

  • Diagnosis of 2,8-dihydroxyadeninuria was confirmed through crystalluria analysis.
  • The patient's acute renal failure was not caused by obstruction or glomerular disease.
  • Deficiency in the purine salvage enzyme adenine phosphoribosyltransferase leads to this condition.

Implications:

  • Early diagnosis of 2,8-dihydroxyadeninuria is crucial for managing renal complications.
  • Treatment involving allopurinol, dietary modifications, and hydration can lead to renal recovery.
  • This case highlights the importance of considering metabolic disorders in unexplained acute kidney injury.

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