Can high carbohydrate diets affect Ca and Pi serum levels by controlling their intestinal absorption in end stage renal disease?

Abstract

The product of [Ca] x [Pi] levels in the blood is a major risk factor for cardiovascular calcification and is a function of serum Pi concentration. Hyperphosphatemia is common in end stage renal disease (ESRD), and must be reduced to lower mortality risk. Since fructose (F) inhibits intestinal Pi transporter NaPi2b expression in neonates and F is a major constituent of American diet, we studied intestinal Pi and Ca absorption in 5/6 nephrectomized adult rats and determine if dietary F modulates serum [Ca] x [Pi]. Six wk after nephrectomy, rats displayed ESRD symptoms, then isocaloric and isonitrogenous glucose (G) and F diets were fed for one month to ESRD and sham‐operated rats. Blood urea nitrogen (BUN) increased in ESRD rats within 2 wk after surgery and was affected by F: ESRD (56 mg/dL vs 40) and sham (28 vs 17). ESRD rats had higher serum Pi levels, but F failed to reduce serum Pi. Kidney mass index was 35% greater in ESRD fed G, and 75% greater in ESRD fed F. NaPi2b mRNA and protein abundance as well active and passive Pi transport were independent of diet and surgery. Ca serum levels were not affected by nephrectomy or diet. However, while duodenal transport of Ca was independent of surgery, this transport and calbindin 9K expression decreased with dietary F. Hence, dietary F exacerbates the clinical symptoms of ESRD (Pi and BUN) and alters intestinal Ca absorption, perhaps by reductions in calbindin expression (NIH RDK075617).