Abstract
BackgroundIgA nephropathy has been reported as a renal involvement in Crohn’s disease. Crescentic IgA nephropathy, which accounts for fewer than 5% of cases of IgA nephropathy, has a poorer prognosis than other forms of crescentic glomerulonephritis. We recently experienced a case of rapidly progressive IgA nephropathy concurrent with exacerbation of Crohn’s disease.Case presentationAn 18-year-old male diagnosed with Crohn’s disease underwent a hemicolectomy 2 years prior previously. He had maintained a state of Crohn’s disease remission with 5-aminosalicylic acid treatment. Four months prior to referral to the nephrology clinic, he experienced non-bloody diarrhea. He simultaneously developed proteinuria and microscopic hematuria with deterioration of renal function. Based on renal biopsy findings, the patient was diagnosed with crescentic IgA nephropathy. Immunostaining for interleukin-17 in renal tissue and previous exacerbated colonic ulcers was positive. Steroid pulse therapy was administered, followed by high-dose glucocorticoid and oral cyclophosphamide therapy. The patient’s renal function recovered and his gastrointestinal symptoms were alleviated.ConclusionsWe report a case of crescentic IgA nephropathy presenting with exacerbation of Crohn’s disease, and present a review of the literature focusing on the pathophysiologic relationship between these two conditions.
Highlights
IgA nephropathy has been reported as a renal involvement in Crohn’s disease
We report a case of crescentic IgA nephropathy presenting with exacerbation of Crohn’s disease, and present a review of the literature focusing on the pathophysiologic relationship between these two conditions
In this report, we presented a case of rapidly progressive IgA nephropathy (IgAN) concurrent with aggravation of Crohn’s disease, both of which responded to immunosuppressive treatment
Summary
Renal involvement, including tubulointerstitial nephritis, amyloidosis, and urolithiasis caused by calcium oxalate or urate, has been reported in approximately 4% to 23% of patients with Crohn’s disease [1,2]. Colonoscopy revealed geographic ulcers consistent with Crohn’s disease His blood pressure was 127/76 mmHg. Laboratory test results showed normal BUN (10.1 mg/dL) and serum creatinine (0.76 mg/dL) levels. Proteinuria (2+ by a dipstick test) and microscopic hematuria were detected by urinalysis His renal function had deteriorated, with increased BUN (30.3 mg/dL) and creatinine (3.42 mg/dL) levels. Planned intravenous cyclophosphamide therapy was canceled because the patient developed abdominal symptoms on the fifth day of steroid treatment He had watery diarrhea 10 times daily, and laboratory data revealed that he suffered from metabolic acidosis caused by severe diarrhea. The patient was switched from azathioprine to mycophenolate sodium (360 mg/day) because of bone marrow suppression His intestinal symptoms were not aggravated, and renal functions were maintained (33.8 mg/dL BUN and 2.32 mg/dL serum creatinine) while taking mycophenolate sodium (360 mg/day) and deflazacort (12 mg/day) during December 2011. Immunostaining for IL-17 was positive in both renal tissue and exacerbated colonic ulcers from the patient (Figure 1C, D), in comparison, this staining was negative in renal tissues from a patient with primary IgAN (control; Figure 1E)
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