![]() The combination of calcium oxalate crystals, secondary hyperoxaluria and newly diagnosed celiac disease made oxalate nephropathy in celiac disease the most likely diagnosis. In combination with low urine citrate, low urinary glycolic acid and glyceric acid this is consistent with secondary hyperoxaluria (Table 2). Gas chromatography analysis of plasma and urine showed a marked increase in plasma oxalate concentration (28.2 µmol/L ) and urinary oxalate excretion (1.23 mmol/24 hr and 117.23 mmol/mol creatinine ). In the outpatient setting the diagnosis was confirmed after duodenal biopsies showed partial villous atrophy and increased intraepithelial lymphocytes, consistent with celiac disease (Marsh 3a). He was treated with a gluten-free diet, with improvement of the abdominal pain and normalization of fecal pattern. It was therefore thought to be caused by celiac disease. Meanwhile, the abdominal pain was found to be primarily after ingestion of gluten-rich diets, the anti-tissue transglutaminase antibodies were positive (42 U/ml) and there was documented steatorrhea (13.6 g of total fecal fat per day). ![]() 1).īecause tubulointerstitial nephritis (TIN), without known causing agent, likely contributed to the renal failure prednisone 30 mg once daily was initiated after the renal biopsy with results pending. Various tubules contained calcium oxalate crystals and showed patchy tubulo-interstitial nephritis with subtle lymphocytic infiltrates (Fig. The tubulointerstitium contained multiple zones with atrophy, and fibrosis was present in approximately 20% of the cortical area. Remarkably, the initial screening with urine dipstick seems to be falsely negative for leucocyturia.Ī renal biopsy was done because the renal function did not improve after rehydration and normalization of defecation pattern.ģ of 13 glomeruli were globally sclerosed and did not show any abnormalities otherwise. Microscopic urinalysis showed leucocyturia of approximately 10 leukocytes per high-power field, with possible leucocyte casts, and no evidence of glomerular erythrocyturia, consistent with tubular injury. He was admitted for further evaluation of renal impairment and abdominal complaints.įluid resuscitation did not improve the renal function, which made dehydration due to diarrhea as a cause of renal impairment unlikely. The kidneys were of normal size and there was no evidence of nephrocalcinosis. Renal ultrasound did not show evidence of hydronephrosis. The urine dipstick was negative for erythrocyturia or leucocyturia. Plasma phosphate during the admission was 1.01 mmol/L. The electrolytes were within normal range. C-reactive peptide was 19 mg/L, with leukocytes of 7.2 × 10^9/L. Five months prior to presentation his creatinine was 102 µmol/L. ![]() Laboratory tests showed acute renal failure with a creatinine of 290 µmol/L with a normal anion gap metabolic acidosis and no proteinuria (Table 1). He did not use any medication at the time of presentation. At presentation in our hospital he did not have a fever (99.3 ☏ (37.4 ☌)), mild hypertension (167/83 mmHg) and a normal heart rate (62/min). He had discontinued the methotrexate he used for eczema three months ago because of these abdominal complaints, without clinical improvement. Colonoscopy in a different medical center did not show any pathology in colon and distal ileum. Celiac disease is therefore one of the intestinal diseases that can lead to hyperoxaluria and oxalate nephropathy.Ī 72-year-old Caucasian male, with a past medical history of eczema, for which he was recently treated with methotrexate, presented with a 3 month history of abdominal discomfort and diarrhea with 5 kg weight loss and fatigue. Oxalate dispositions in the kidney can lead to acute tubular injury and chronic renal insufficiency. Treatment with prednisone, and gluten-free, low oxalate and normal calcium diet, lowered the plasma oxalate levels and improved his renal function.ĭecreased absorption of free fatty acids can lead to increased free oxalate in the colon due to the binding of free fatty acids to calcium, preventing the formation of the less absorbable calcium oxalate in the colon. ![]() The abdominal complaints with steatorrhea and positive anti-tissue transglutaminase antibodies were diagnosed as celiac disease, which was confirmed after duodenal biopsies. Elevated plasma and urine oxalate levels established the diagnosis oxalate nephropathy. Renal biopsy showed calcium oxalate depositions. The clinical course, laboratory results and urinalysis were suspect for tubular injury. However, reports of oxalate nephropathy in newly diagnosed celiac disease are rare.Ī 72-year-old Caucasian male presented to the hospital with abdominal discomfort and acute renal insufficiency with a creatinine of 290 µmol/L. Oxalate nephropathy, due to secondary hyperoxaluria has widely been described in gastrointestinal diseases. ![]()
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