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Renal function and biopsies were studied in 18 patients, 7 to 108 months after intestinal bypass. Enteropathy was found in 12 and hyperoxaluria in 16. Every biopsy showed a type of focal interstitial nephritis, tubular atrophy, fibrosis, and glomerular hyalinization. Damage ranged from minimal to extensive and renal function from normal to end-stage failure. Tubular injury had resulted partly from oxalate deposits. However, in 10 patients no oxalate crystals were seen. In eight others, most of the damaged areas were remote from crystal deposits. Immunoglobulin M and C3 deposits, found in glomerular capillaries and the messangium in six of 11 specimens, and the presence of circulating immune complexes in five of 10 patients, in addition to the extraintestinal organ involvement, suggested immune complex mesangial injury as one factor in bypass nephropathy. With progressive impairment of renal function, a biopsy appears justified. If damage is significant, the bypass should be dismantled.

Twenty-three of 81 intestinal bypass patients with episodes of bypass enteropathy had papulopustular or nodular skin lesions. Histologic examination of the dermal lesions showed various forms of vasculitis in nine of 14 subjects. In six of 11 patients examined by immunofluorescent microscopy, both the lesions and uninvolved sun-exposed skin areas had immunoglobulin and complement deposits in linear or granular patterns in the dermoepidermal line, giving the appearance of a positive lupus band test. Skin lesions resolved with spontaneous improvement of bypass enteropathy or in response to metronidazole therapy. After the bypass was dismantled, the eruptions disappeared permanently, and previously positive lupus band tests became negative. The skin lesions were frequently observed in association with arthritis, suggesting an immune-complex mechanism, probably originating in "blind loop" bacterial overgrowth.