Abstract
Lanthanum carbonate (LA) is an effective phosphate binder. Previous study showed the phosphate-binding potency of LA was twice that of calcium carbonate (CA). No study in which LA and CA were given at an equivalent phosphate-binding potency to rats or humans with chronic renal failure for a long period has been reported to date. The objective of this study was to compare the phosphate level in serum and urine and suppression of renal deterioration during long-term LA and CA treatment when they were given at an equivalent phosphate-binding potency in rats with adriamycin (ADR)-induced nephropathy. Rats were divided into three groups: an untreated group (ADR group), a CA-treated (ADR-CA) group and a LA-treated (ADR-LA) group. The daily oral dose of LA was 1.0 g/kg/day and CA was 2.0 g/kg/day for 24 weeks. The serum phosphate was lower in the ADR-CA or ADR-LA group than in the ADR group and significantly lower in the ADR-CA group than in the ADR group at each point, but there were no significant differences between the ADR and ADR-LA groups. The serum phosphate was also lower in the ADR-CA group than in the ADR-LA group, and there was significant difference at week 8. The urinary phosphate was significantly lower in the ADR-CA group than in the ADR or ADR-LA group at each point. The urinary phosphate was also lower in the ADR-LA group than in the ADR group at each point, and significant difference at week 8. There were no significant differences in the serum creatinine or blood urea nitrogen among the three groups. In conclusion, this study indicated the phosphate-binding potency of LA isn’t twice as strong as CA, and neither LA nor CA suppressed the progression of chronic renal failure in the serum creatinine and blood urea nitrogen, compared to the untreated group.
Highlights
Effective control of the phosphate overload in patients with chronic kidney disease (CKD) is recognized as an important target for reducing the high mortality rate associated with this condition [1,2], and current practice guidelines recommend aggressive treatment of hyperphosphatemia to achieve lower serum phosphorus targets.A low-phosphate diet has been shown to prevent the progression of experimental renal disease [3,4,5]
Three of the eighteen rats died between weeks 8 and 16, and four rats died between weeks 16 and 24 in the ADR-Lanthanum carbonate (LA) group
The serum phosphate level was lower in the ADR-CA group and in the ADR-LA group compared to the ADR group at each point (Figure 2C)
Summary
Effective control of the phosphate overload in patients with chronic kidney disease (CKD) is recognized as an important target for reducing the high mortality rate associated with this condition [1,2], and current practice guidelines recommend aggressive treatment of hyperphosphatemia to achieve lower serum phosphorus targets.A low-phosphate diet has been shown to prevent the progression of experimental renal disease [3,4,5]. The administration of a low-phosphate diet is consistently associated with a decreased intake of protein, calories and other nutrients, the absence of which results in nutritional deficits, especially in cases of progressive renal disease with massive proteinuria. Phosphate binders are administered in order to decrease the serum phosphate levels by adsorbing phosphate in the intestine They bind phosphate, form insoluble products, and selectively suppress the intestinal absorption of phosphate without leading to a deficiency of other nutritional elements. Lumlertgul et al reported that a phosphate binder (dihydroxyaluminum aminoacetate) suppressed the progression of chronic renal failure (CRF) in rats with 5/6 nephrectomy [6]. ADR-induced nephropathy in rats is a commonly used model of chronic renal disease, characterized by persistent proteinuria and progressive reduction in renal function leading to terminal renal failure [8]. Epithelial degeneration develops as an initial lesion in the kidney, and progresses to irreversible glomerular sclerosis and tubulointerstitial changes [9]
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