Why does serum phosphorus level increase in Chronic Kidney Disease (CKD)?

From the Guidelines

Phosphorus levels rise in chronic kidney disease (CKD) primarily because the kidneys lose their ability to excrete excess phosphorus through urine, leading to accumulation in the bloodstream, as supported by the most recent evidence from 2018 1. As kidney function declines, phosphorus elimination becomes impaired while dietary intake continues, leading to accumulation in the bloodstream. This process begins when kidney function drops below about 30-40% of normal (CKD stage 3-4). The kidneys normally filter phosphorus from the blood and excrete the excess, but damaged kidneys cannot maintain this balance. Some key points to consider in the management of phosphorus levels in CKD include:

• Dietary phosphorus restriction, such as limiting dairy, processed foods, and cola
• Phosphate binders, such as calcium acetate, sevelamer, or lanthanum, taken with meals to prevent phosphorus absorption
• Avoiding hypercalcemia, as higher calcium concentrations have been linked to increased mortality and nonfatal cardiovascular events in adults with CKD 1
• Using a dialysate calcium concentration between 1.25 and 1.50 mmol/L (2.5 and 3.0 mEq/L) in patients with CKD stage G5D 1 Untreated hyperphosphatemia contributes to bone disease, vascular calcification, and increased cardiovascular risk in CKD patients. Current evidence does not show benefit to maintaining normal serum phosphate levels in patients not receiving dialysis, and there are safety concerns associated with aggressive phosphate-lowering therapy, thus treatment should focus on patients with overt hyperphosphatemia 1.

From the Research

Causes of Increased Serum Phosphorus Level in CKD

• The kidneys play a crucial role in regulating phosphorus levels in the body, and in CKD, the kidneys are unable to effectively remove excess phosphorus from the blood, leading to hyperphosphatemia 2, 3, 4, 5.
• Dietary sources of phosphorus, including phosphate additives in food, can contribute to increased phosphorus levels in CKD patients 3, 4, 5.
• The phosphorus-protein ratio in food is an important factor in controlling dietary phosphorus intake, and a low phosphorus-protein ratio can help reduce intestinal phosphorus load 3.

Pathophysiology of Hyperphosphatemia in CKD

• Hyperphosphatemia can lead to secondary hyperparathyroidism, vascular calcification, and increased mortality risk in CKD patients 2, 5, 6.
• The complex interplay between the kidneys, intestinal tract, and bone, as well as the endocrine system, regulates phosphate homeostasis in the body 5.
• Phosphate-based additives in industrialized foods can contribute to increased phosphorus levels in CKD patients 5.

Management of Hyperphosphatemia in CKD

• Dietary phosphate restriction, reduction of intestinal phosphate absorption, phosphate removal by dialysis, and management of renal osteodystrophy are all important strategies for controlling hyperphosphatemia in CKD patients 3, 4, 5.
• Phosphate binders, such as calcium acetate, can be effective in reducing serum phosphorus levels in CKD patients 6.
• Individualized approaches to managing hyperphosphatemia, involving a combination of dietary advice, phosphate-binder use, and adjustments to dialysis prescription, are necessary to control phosphorus levels in CKD patients 4, 5.