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      Renal Amyloidosis Secondary to Tuberculosis of Cecum

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      S. Karger AG

      Tuberculosis, End-stage renal disease, Proteinuria, Nephrotic syndrome, Amyloidosis

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          Renal amyloidosis can occur as a primary or secondary, systemic or localized disorder. It is defined as a chronic infiltrative disorder characterized by impaired organ function caused by extracellular insoluble protein fibrils. Although colonic tuberculosis is not uncommon, the occurrence of reactive renal amyloidosis in such patients is not as prevalent. We report a single case of renal amyloidosis in a patient with tuberculosis of the cecum who presented with nephrotic syndrome.

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          Prognosis of Renal Amyloidosis: A Clinicopathological Study Using Cluster Analysis

          Progression of renal amyloidosis is associated with severe proteinuria or nephrotic syndrome, and various mechanisms have been postulated to explain these complications. We studied the acceleration of proteinuria and reduced renal function by cluster analysis using clinical parameters, renal histological findings, type of renal amyloidosis and follow-up data. We divided 97 cases into three groups of renal amyloidosis. Accelerated progression correlated with serum creatinine (s-Cr) levels at renal biopsy and histological grade of renal damage by amyloid deposition (p < 0.0001). The most influential prognostic factors (s-Cr level ≧2.0 mg/dl) were tubulointerstitial and vascular damage induced by amyloid deposition at biopsy (odds ratio 96.9 and 69.2, respectively). In addition, we found amyloidosis type amyloid associated (AA) correlated with more amyloid-mediated vascular and tubulointerstitial damage than amyloidosis type amyloid light chain (AL) (p < 0.001, p < 0.01, respectively). Proteinuria and nephrotic syndrome were more severe in cases of amyloidosis AL than in amyloidosis AA (p = 0.076). In conclusion, less tubulointerstitial and vascular damage was caused by amyloid deposition; this was slowly progressive. Amyloid AA was detected in tubulointerstitial tissue and vessels more frequently than amyloid AL. Heavy proteinuria and/or nephrosis were not indicators of rapid progression.

            Author and article information

            S. Karger AG
            September 2002
            26 September 2002
            : 92
            : 3
            : 708-710
            Department of Medicine, Renal Division, Coney Island Hospital, Brooklyn, N.Y., USA
            64091 Nephron 2002;92:708–710
            © 2002 S. Karger AG, Basel

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