Phosphate intake, hyperphosphatemia, and kidney function

Abstract

Phosphate is essential in living organisms and its blood levels are regulated by a complex network involving the kidneys, intestine, parathyroid glands, and the skeleton. The crosstalk between these organs is executed primarily by three hormones, calcitriol, parathyroid hormone, and fibroblast growth factor 23. Largely due to a higher intake of ultraprocessed foods, dietary phosphate intake has increased in the last decades. The average intake is now about twice the recommended dietary allowance. Studies investigating the side effect of chronic high dietary phosphate intake suffer from incomplete dietary phosphate assessment and, therefore, often make data interpretation difficult. Renal excretion is quickly adapted to acute and chronic phosphate intake. However, at the high ends of dietary intake, renal adaptation, even in pre-existing normal kidney function, apparently is not perfect. Experimental intervention studies suggest that chronic excess of dietary phosphate can result in sustained higher blood phosphate leading to hyperphosphatemia. Evidence exists that the price of the homeostatic response (phosphaturia in response to phosphate loading/hyperphosphatemia) is an increased risk for declining kidney function, partly due by intraluminal/tubular calcium phosphate particles that provoke renal inflammation. High dietary phosphate intake and hyperphosphatemia are progression factors for declining kidney function and are associated with higher cardiovascular disease and mortality risk. This is best established for pre-existing chronic kidney disease, but epidemiological and experimental data strongly suggest that this holds true for subjects with normal renal function as well. Here, we review the latest advances in phosphate intake and kidney function decline.

Phosphate induces inflammation and exacerbates injury from cigarette smoke in the bronchial epithelium

“…2 ), various groups have previously described hyperphosphatemia as a potent contributor to inflammation in other organs 44 – 46 . Increased vascular calcification as a result of high serum and tissue phosphate concentrations have been shown to contribute to renal and cardiovascular inflammation in patients with CKD 44 , 45 . Additionally, excess dietary phosphate and adenine-induced CKD led to increased liver inflammation through stimulation of hepatic production of IL6 and IL1B in mice 8 .…”

Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins

“…During high phosphate loading, CPP formation in the tubular lumen is greatly affected by the amount of phosphate reached per single nephron, independent of changes in blood phosphate concentrations 22 . In humans, the number of nephrons declines with age, with approximately 50% fewer nephrons in the 70s than in the 20s 23 .…”

Mechanism of Malignancy Development When the Metabolism of the Human Body Deteriorates

“…Also, the kidneys are also responsible for maintaining a constant pH level by removing inorganic phosphate and pH from the blood into the urine [31,32]. It is known that kidney function declines with age, and the increase or decrease in inorganic phosphate in urine can be used as an indicator of the activity of the body's mitochondria or the synthesis of ATP from inorganic phosphate and ADP through anaerobic respiration, while an increase or decrease in urine pH can be used as an indicator of metabolism, as acid is released into the blood when nutrients are metabolized.…”