Abstract
Hyperphosphatemia - The Risk Factor for Adverse Outcome in Maintenance Hemodialysis PatientsHyperphosphatemia is a potent stimulator of vascular and valvular calcifications in hemodialysis patients. To determine the prevalence of hyperphosphatemia and assess its effect on the outcome of hemodialysis patients, a total of 115 chronic hemodialysis patients were studied. Laboratory parameters were determined at baseline, and after 12 and 24 months of follow-up. Valvular calcification was assessed with echocardiography. Laboratory parameters were statistically analyzed with ANOVA. Survival analysis was performed with the Kaplan-Meier test and Log-Rank test. Hyperphosphatemia was present in 31.30% of the patients, high calcium-phosphate (Ca × P) product in 36.52% and valvular calcifications in 48.70%. Patients with serum phosphate >2.10 mmol/L and Ca × P product >5.65 mmol2/L2at baseline were at high risk for all-cause and cardiovascular mortality. Hyperphosphatemia is a risk factor for adverse outcome in patients on regular hemodialysis.
Highlights
Phosphate is a predominantly intracellular anion, either complexed or bound to proteins or lipids
Laboratory parameters were statistically analyzed with ANOVA
Hyperphosphatemia was present in 31.30% of the patients, high calcium-phosphate (Ca x P) product in 36.52% and valvular calcifications in 48.70%
Summary
Phosphate is a predominantly intracellular anion, either complexed or bound to proteins or lipids. It is essential for most cellular processes. Several transport proteins enable the intracellular uptake of phosphate. Type 1 and Type 2 sodium phosphate cotransporters are expressed in the kidneys, bones and intestines. 240 Petrovi} et al.: Hyperphosphatemia in hemodialysis patients participate in the regulation of renal and intestinal transepithelial transport [1, 2]. The kidney is a key player in the phosphate balance. Hyperphosphatemia can occur as a result of: excessive phosphate intake in the setting of impaired renal phosphate excretion (renal failure, milk-alkali syndrome); vitamin D intoxication (excessive gastrointestinal absorption and increased renal reabsorption); decreased excretion (mostly due to acute or chronic renal failure) or shift from intracellular to extracellular space (rhabdomyolysis, tumor lysis, insulin deficiency, acute acidosis) [3]
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