Predictors and significance of kidney dysfunction in patients with chronic graft-versus-host disease.

Kidney complications have been studied in allogeneic hematopoietic stem cell transplant patients but not specifically among chronic graft-versus-host disease (cGVHD) patients. Participants (n = 365) enrolled in the cross-sectional cGVHD natural history study (NCT00092235) were assessed for kidney dysfunction and overall survival. Kidney dysfunction was analyzed for associations in univariate and multivariable analyses. Kidney dysfunction (eGFR < 60) was found in 64 patients, and 29 patients had moderate-severe kidney dysfunction (eGFR < 45). Patients with kidney dysfunction were more likely treated with cyclosporine at evaluation or to have received it for GVHD prophylaxis, or prior treatment of GVHD. Patients with kidney dysfunction were less severely affected by cGVHD of skin, mouth, and joints/fascia. In multivariable modeling, history of cyclosporine use (OR = 2.19, 95% CI 1.13-4.25), angiotensin receptor blocker use (OR = 5.57, 95% CI 1.49-20.84), proteinuria (OR = 2.39, 95% CI 1.19-4.79), lower CRP (OR = 0.95, 95% CI 0.91-0.99), lower C3 (OR = 0.98, 95% CI 0.97-0.99), and lower hemoglobin (OR = 0.70, 95% CI 0.58-0.84) were jointly associated with kidney dysfunction. Overall survival was lower in those with moderate-severe kidney dysfunction (p = 0.015), demonstrating the importance of addressing kidney dysfunction in this population. The association of kidney dysfunction with less severe cGVHD suggests an etiology unrelated to cGVHD but potentially a consequence of drug-related toxicities.

Oxalate Content of Enteral Nutrition Formulas.

OBJECTIVES: Patients requiring oral and/or enteral nutrition support, delivered via nasogastric, gastric, or intestinal routes, have a relatively high incidence of calcium oxalate (CaOx) kidney stones. Nutrition formulas are frequently made from corn and/or or soy, both of which contain ample oxalate. Excessive oxalate intake contributes to hyperoxaluria (>45 mg urine oxalate/day) and CaOx stones especially when unopposed by concomitant calcium intake, gastrointestinal malabsorption is present, and/or oxalate degrading gut bacteria are limiting or absent. Our objective was to assess the oxalate content of commonly used commercial enteral nutrition formulas. METHODS: Enteral nutrition formulas were selected from the formulary at our clinical inpatient institution. Multiple samples of each were assessed for oxalate concentration with ion chromatography. RESULTS: Results from 26 formulas revealed highly variable oxalate concentration ranging from 4 to 140 mg oxalate/L of formula. No definitive patterns for different types of formulas (eg, flavored vs unflavored, high protein vs not) were evident. Coefficients of variation for all formulas ranged from 0.68% to 43% (mean ± SD 19% ±â€Š12%; median 18%). CONCLUSIONS: Depending on the formula and amount delivered, patients requiring nutrition support could obtain anywhere from 12 to 150 mg oxalate/day or more and are thus at risk for hyperoxaluria and CaOx stones.