Subclinical celiac disease and crystal-induced kidney disease following kidney transplant

Abstract

Decreased kidney function from kidney deposition of calcium oxalate has been described previously in inflammatory bowel disease and after jejuno-ileal and Roux-en-Y gastric bypass surgeries. Although celiac disease is the most prevalent bowel abnormality associated with intestinal malabsorption, its relationship to high kidney oxalate burden and decreased kidney function has not been established. We report a case of subclinical celiac disease and hyperoxaluria that presented with loss of kidney function as a result of high oxalate load in the absence of overt diarrhea, documented intestinal fat malabsorption, and nephrolithiasis. Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients. We propose that this entity should be suspected in patients with chronic kidney disease in which the cause of kidney damage has not been clearly established.

Figure 1

Native and allograft kidney biopsy. A) Light microscopy of native kidney biopsy showed a total of 17 glomeruli with 6 globally sclerotic. Left panel: No hypercellularity or crescent formation was seen. There was tubular atrophy and dropout with interstitial fibrosis, and crystals were present in the tubules. Right panel: Under polarized light, the crystals were birefringent consistent with calcium oxalate crystals. B) Allograft biopsy 3 weeks post kidney transplant: Tubule showing occasional refractile acellular deposits and birefringent crystals under a polarized lens. C) Allograft biopsy 8 weeks post kidney transplantation: calcium oxalate crystals seen within tubular lumen and within tubular epithelial cells with associated tubular injury. Birefringent calcium oxalate crystals seen in many tubular lumens and tubular epithelial cells. D) Allograft biopsy 14 weeks post kidney transplant: Large refractile acellular deposits in several tubular lumens with associated tubular injury. Extensive birefringent calcium oxalate crystals within tubular lumina and within tubular epithelial cells. Left panels: hematoxylin and eosin stain (original magnification, ×200); right panels: polarized lens (original magnification, ×100). Courtesy of Dr James Wellons.

Figure 2

Clinical course of serum creatinine concentration and urinary oxalate excretion rate in relationship to the major clinical events. A) Kidney transplant. B) Oxalate crystals on post-kidney transplant biopsies (first biopsy, 3 weeks posttransplant; second, 8 weeks; third, 14 weeks). C) Oxalate restriction. D) Gluten-free diet started. E) Nonadherence to diet. F) Resumption of gluten-free diet.

Figure 3

Architecture and SLC26A6 expression in the small intestine in biopsies from the patient (top row) and an unaffected control (bottom row). Left panels: intestinal biopsy showing normal mucosal architecture in patient and control (Hematoxylin and eosin stain; original magnification, ×100). Middle and right panels: each cluster of 4 images shows (clockwise from top left) villin staining (green), DIC image, merged image, and SLC26A6 staining (red); original magnification, ×100.