Introduction Hyperphosphatemia is associated with increased morbidity and mortality in patients with chronic kidney disease. The aim of this study was to assess whether a meal with high phosphorus content would affect plasma phosphate in the hours that follow among subjects with end-stage kidney disease on peritoneal dialysis. Methods This was a single-blinded randomized cross-over trial of 12 subjects on maintenance peritoneal dialysis, in which subjects were randomized to consume a meal with either high or low phosphorus content on 2 separate trial days. On each trial day, plasma phosphate was measured immediately before consumption of the standardized meal and after 1, 2, 3, and 5 hours. Results The mean fasting plasma phosphate at baseline was 1.69 ± 0.22 mmol/l. Plasma phosphate was similar between the 2 meals at baseline, as well as at 1, 2, 3, and 5 hours after consumption. The largest observed difference in plasma phosphate between the 2 meals was 0.15 mmol/l, which occurred 5 hours after consumption (high-phosphorus meal 1.75 ± 0.32 mmol/l vs. low-phosphorus meal 1.60 ± 0.14 mmol/l ( P = 0.06)). Using summary analyses for repeated measures, we observed a significant difference in the plasma phosphate between the 2 meals ( P = 0.03). Conclusion Our results show that in subjects with end-stage kidney disease, a meal with high phosphorus content has only a negligible effect on plasma phosphate compared to a meal with low phosphorus content. Thus, large increases in plasma phosphate cannot be accounted for by a high intake of phosphorus in the hours before blood sampling.

<b><i>Introduction:</i></b> Shortened erythrocyte life span and erythropoietin-stimulating agents may affect hemoglobin A_1c (HbA_1c) levels in patients receiving peritoneal dialysis (PD). We compared HbA_1c with interstitial glucose measured by continuous glucose monitoring (CGM) in patients with type 2 diabetes receiving PD. <b><i>Methods:</i></b> Fourteen days of CGM (Ipro2, Medtronic) were performed in 23 patients with type 2 diabetes receiving PD and in 23 controls with type 2 diabetes and an estimated glomerular filtration rate over 60 mL/min/1.73 m². Patients were matched on gender and age (±5 years). HbA_1c (mmol/mol), its derived estimate of mean plasma glucose (eMPG_A1c) (mmol/L), and fructosamine (µmol/L) were measured at the end of the CGM period and compared with the mean sensor glucose (mmol/L) from CGM. <b><i>Results:</i></b> In the PD group, mean sensor glucose was 0.98 (95% con­fidence interval (CI): 0.43–1.54) mmol/L higher than the eMPG_A1c compared with the control group (<i>p</i> = 0.002) where glucose levels were nearly identical (−0.05 (95% CI: −0.35–0.25) mmol/L). A significant association was found between fructosamine and mean sensor glucose using linear regression with no difference between slopes (<i>p</i> = 0.89) or y-intercepts (<i>p</i> = 0.28). <b><i>Discussion/Conclusion:</i></b> HbA_1c underestimates mean plasma glucose levels in patients with type 2 diabetes receiving PD. However, the clinical significance of this finding is undetermined. Fructosamine seems to more accurately reflect glycemic status. CGM or fructosamine could complement HbA_1c to increase the accuracy of glycemic monitoring in the PD population.

Question: The patient was diagnosed with Crohn's disease of the colon at the age of 39 years and had a chronic active disease course with rapid response to infliximab. Biopsies from the colon showed extensive inflammation with granulomas. The patient had secondary loss of response to infliximab due to formation of antidrug antibodies (ADA). She did not tolerate azathioprine or 6-mercaptopurine owing to pancreatitis and had severe hair loss when treated with methotrexate. Owing to previous good response to anti-TNF treatment, the patient was given adalimumab and subsequently certolizumab pegol, both with good initial responses, but unfortunately with subsequent loss of response caused by ADA formation. The patient also had significant extraintestinal manifestations (iridocyclitis, sacroiliitis, and peripheral arthropathies) that tended to respond to biologics. At the age of 45, the patient was switched to golimumab with good symptomatic control of the disease and extraintestinal manifestations, but fluctuating Creactive protein levels between 0.5 and 2.5 mg/dL. At the age of 48, her estimated glomerular filtration rate decreased to <60 mL/min with more rapid decreases in periods with elevated inflammatory markers (Figure A). Urinalysis revealed proteinuria and no occult blood. Urinary excretion of protein was between 0.2 and 0.6 g/d. An initial ultrasound examination of the kidneys and urinary tracts was normal and a Tc-99-MAG3 renography showed bilateral decreased kidney function. A kidney biopsy was performed (Figure B). What is the diagnosis and treatment? Look on page 59 for the answer and see the Gastroenterology website (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and images in GI.