Hyperphosphatemia in Chronic Kidney Disease: Causes, Symptoms, & Management

By Dr. Varun Verma in Nephrology

Feb 02 , 2024 | 2 min read

Hyperphosphatemia, an elevated level of phosphate, is frequently observed in patients with chronic kidney disease (CKD). Various factors contribute to this condition, including increased phosphate intake, reduced phosphate excretion, or a disorder that redistributes intracellular phosphate to the extracellular space. The kidneys play a major role in controlling blood phosphate levels, making their health crucial in this context.

Phosphates, the naturally occurring form of phosphorus, rank as the second most abundant element in the human body after calcium. Similar to calcium, phosphates rely on vitamin D for absorption. However, an excess of phosphorus in CKD patients raises concerns due to its potential to lower blood calcium levels, leading to health issues like cardiovascular calcification, metabolic bone disease, and the development of secondary hyperparathyroidism (SHPT).

Under normal circumstances, phosphate is absorbed from digested food in the gut, with the kidneys efficiently managing increased excretion in the case of higher-than-normal phosphate absorption. However, if kidney function is compromised, even moderately elevated phosphate absorption can result in hyperphosphatemia, a common occurrence in dialysis patients.

Moreover, phosphate absorption can be heightened by vitamin D, further contributing to hyperphosphatemia through increased gut absorption. Excessive phosphate intake can stem from various sources, including intravenous injection, overconsumption of vitamin D through diet or supplements, acute phosphorus poisoning, or the milk-alkali syndrome.

Reduced elimination of phosphate through the kidneys, particularly when coupled with a high phosphate intake, can lead to hyperphosphatemia. This is often observed in kidney problems such as acute or chronic renal failure, where parathyroid hormone (PTH) regulation of phosphate plays a significant role. Low PTH levels can increase phosphate reabsorption, contributing to retention and hyperphosphatemia.

Symptoms of hyperphosphatemia may include hypocalcemic symptoms such as muscle cramps, numbness, or tingling. Other symptoms related to the underlying cause, often uremic symptoms, may include fatigue, shortness of breath, anorexia, nausea, vomiting, and disturbed sleep.

Diagnosis involves specific blood tests to measure phosphate, calcium, magnesium, blood urea nitrogen, creatinine, vitamin D, and parathyroid hormone levels. Treatment focuses on identifying and addressing the underlying cause, with medications like phosphate binders and loop diuretics helping normalise phosphate levels. Additionally, dietary modifications, particularly a low phosphate diet, play a crucial role in managing hyperphosphatemia.

A low-phosphate diet involves avoiding or moderating the consumption of certain foods high in phosphorus, such as soft drinks, chocolates, processed meats, processed cheeses, ready-to-eat meals, ice creams, and specific vegetables and legumes. A nephrologist or renal dietician consultation is advisable before making significant dietary changes.

In managing phosphate homeostasis for CKD patients, multiple strategies, including dietary adjustments, phosphate removal via dialysis, and intensive dialysis regimens, can be implemented to ensure effective control.

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