2010Renal FailureOpen access

The spectrum of acute renal failure in IgA nephropathy

Yao‐Ko Wen, Meiling Chen

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Abstract

BACKGROUND: Acute renal failure rarely complicates the course of IgA nephropathy. In this study, we have tried to define the mode of presentation, the spectrum of morphology, and the prognostic factors for renal outcome. METHODS: Twenty patients with biopsy-proven IgA nephropathy who developed acute renal failure were identified from 2000 to 2009 at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, morphology of renal biopsy, and outcomes. RESULTS: On histology, glomerular crescents were present in 11 patients (55%), acute tubular necrosis was identified in 11 patients (55%), acute interstitial nephritis was seen in 4 patients (20%), and extensive tubular red blood cell casts were present in 4 patients (20%). At the end of follow-up, 2 patients (10%) had died, 11 patients (55%) were in remission, and 7 patients (35%) developed end-stage renal disease. The prognostic factors for renal outcome were peak serum creatinine, dialysis support requirement, morphology (prominent glomerular/tubular injury), percentage of glomeruli affected by crescents, and interstitial infiltration (p = 0.04, <0.001, 0.013, 0.05, 0.02, respectively). CONCLUSIONS: Our findings suggested that there were four pathogenic mechanisms involved in IgA nephropathy with acute renal failure including (1) crescentic IgA nephropathy; (2) acute tubular necrosis associated with microhematuria and red blood cell casts occluding tubules; (3) acute tubular necrosis not related to microhematuria; and (4) acute interstitial nephritis, apparently induced by drugs. In general, patients with prominent tubular injury had a much higher remission rate than patients with prominent glomerular injury.

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BACKGROUND: Acute renal failure rarely complicates the course of IgA nephropathy. In this study, we have tried to define the mode of presentation, the spectrum of morphology, and the prognostic factors for renal outcome. METHODS: Twenty patients with biopsy-proven IgA nephropathy who developed acute renal failure were identified from 2000 to 2009 at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, morphology of renal biopsy, and outcomes. RESULTS: On histology, glomerular crescents were present in 11 patients (55%), acute tubular necrosis was identified in 11 patients (55%), acute interstitial nephritis was seen in 4 patients (20%), and extensive tubular red blood cell casts were present in 4 patients (20%). At the end of follow-up, 2 patients (10%) had died, 11 patients (55%) were in remission, and 7 patients (35%) developed end-stage renal disease. The prognostic factors for renal outcome were peak serum creatinine, dialysis support requirement, morphology (prominent glomerular/tubular injury), percentage of glomeruli affected by crescents, and interstitial infiltration (p = 0.04, <0.001, 0.013, 0.05, 0.02, respectively). CONCLUSIONS: Our findings suggested that there were four pathogenic mechanisms involved in IgA nephropathy with acute renal failure including (1) crescentic IgA nephropathy; (2) acute tubular necrosis associated with microhematuria and red blood cell casts occluding tubules; (3) acute tubular necrosis not related to microhematuria; and (4) acute interstitial nephritis, apparently induced by drugs. In general, patients with prominent tubular injury had a much higher remission rate than patients with prominent glomerular injury.

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Available abstract

BACKGROUND: Acute renal failure rarely complicates the course of IgA nephropathy. In this study, we have tried to define the mode of presentation, the spectrum of morphology, and the prognostic factors for renal outcome. METHODS: Twenty patients with biopsy-proven IgA nephropathy who developed acute renal failure were identified from 2000 to 2009 at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, morphology of renal biopsy, and outcomes. RESULTS: On histology, glomerular crescents were present in 11 patients (55%), acute tubular necrosis was identified in 11 patients (55%), acute interstitial nephritis was seen in 4 patients (20%), and extensive tubular red blood cell casts were present in 4 patients (20%). At the end of follow-up, 2 patients (10%) had died, 11 patients (55%) were in remission, and 7 patients (35%) developed end-stage renal disease. The prognostic factors for renal outcome were peak serum creatinine, dialysis support requirement, morphology (prominent glomerular/tubular injury), percentage of glomeruli affected by crescents, and interstitial infiltration (p = 0.04, <0.001, 0.013, 0.05, 0.02, respectively). CONCLUSIONS: Our findings suggested that there were four pathogenic mechanisms involved in IgA nephropathy with acute renal failure including (1) crescentic IgA nephropathy; (2) acute tubular necrosis associated with microhematuria and red blood cell casts occluding tubules; (3) acute tubular necrosis not related to microhematuria; and (4) acute interstitial nephritis, apparently induced by drugs. In general, patients with prominent tubular injury had a much higher remission rate than patients with prominent glomerular injury.

Key concepts: Medicine, Microhematuria, Acute tubular necrosis, Interstitial nephritis, Renal biopsy, Nephropathy, Acute kidney injury, Creatinine

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