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Published on: March 7, 2019
AA amyloid nephropathy with predominant vascular deposition in Crohn's disease
Noriaki Kurita1, Nagaaki Kotera, Yu Ishimoto
1Division of Nephrology, Department of Medicine, Mitsui Memorial Hospital, Tokyo, Japan. kurita_n@opal.plala.or.jp
Insights
This study highlights a rare case of kidney damage in a Crohn's disease patient due to amyloid A (AA) amyloidosis, emphasizing the need for pathological diagnosis in renal insufficiency.
Area of Science:
- Nephrology
- Gastroenterology
- Pathology
Background:
- Crohn's disease (CD) management often involves medications that can cause kidney issues.
- Renal insufficiency in CD patients necessitates careful etiological investigation.
Observation:
- A 44-year-old male with a 17-year history of CD presented with progressive renal insufficiency and mild urinary abnormalities.
- Despite controlled disease activity with 5-aminosalicylic acid and azathiopurine, serum creatinine was elevated at 1.4 mg/dl.
- Kidney biopsy revealed predominant arterial and arteriolar amyloid A (AA) deposition, atypical for AA amyloidosis.
Findings:
- The patient exhibited vascular AA amyloidosis, differing from the typical glomerular pattern.
- Renal function decline occurred with minimal proteinuria and hematuria, challenging initial diagnostic assumptions.
Implications:
- This case underscores the importance of pathological examination for diagnosing renal insufficiency in Crohn's disease patients.
- It highlights a less common presentation of AA amyloidosis, emphasizing the need to consider diverse renal pathologies in CD.
- Accurate diagnosis is crucial for appropriate management and preventing further kidney damage.
Abstract:
A 44-year-old man with a 17-year history of Crohn's disease (CD) was referred to our nephrology department on suspicion of drug-induced nephrotoxicity. Over the preceding 18 months, he had slowly progressive renal insufficiency with slight urinary abnormalities. His disease activity had been well controlled up to that point with 5-aminosalicylic acid and azathiopurine. Laboratory examination revealed slight proteinuria without hematuria and an elevated serum creatinine level of 1.4 mg/dl. Pathological examination revealed amyloid A (AA) deposition in the kidney, predominantly in the arterial and arteriolar walls with little to none in the glomerular capillaries. AA amyloidosis is typically accompanied by glomerular amyloid deposition and massive proteinuria. In the present case, however, vascular amyloid deposition was predominant, and the renal function was deteriorated with slight urinary abnormalities. The present case confirmed the importance of conducting a definitive pathological diagnosis of renal insufficiency in CD patients.
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