Kidneys phosphorus excretion regulated

Serum phosphorus concentration is so closely regulated by the kidneys that it is unusual for hyperphosphatemia (serum phosphorus concentration >4.5 mg/dL) to develop in patients with normal renal function. The most frequent causes of hyperphosphatemia are decreases in urinary phosphorus excretion, and increases in phosphate entrance into the extracellular fluid via either exogenous administration or endogenous intracellular phosphate release. 

Calcium and phosphate enter the body from the intestine. The average American diet provides 600-1000 mg of calcium per day, of which approximately 100-250 mg is absorbed. This figure represents net absorption, because both absorption (principally in the duodenum and upper jejunum) and secretion (principally in the ileum) occur. The amount of phosphorus in the American diet is about the same as that of calcium. However, the efficiency of absorption (principally in the jejunum) is greater, ranging from 70% to 90%, depending on intake. In the steady state, renal excretion of calcium and phosphate balances intestinal absorption. In general, over 98% of filtered calcium and 85% of filtered phosphate is reabsorbed by the kidney. The movement of calcium and phosphate across the intestinal and renal epithelia is closely regulated. Intrinsic disease of the intestine (eg, nontropical sprue) or kidney (eg, chronic renal failure) disrupts bone mineral homeostasis. 

Maintenance of fluid volume, osmolarity, electrolyte balance, and acid-base status are aU regulated in large part by the kidney. Homeostasis of sodium, potassium, chloride, calcium, magnesium, and phosphorus is altered due to changes in urinary excretion that occur in patients with impaired kidney function. A comprehensive discussion... 

Phosphorus enters the body in organic form as various esters, which are present as nucleic acids, phosphoproteins, phospholipids, phosphosaccharides and vitamins (Table 11.12). Ingested P is absorbed mainly in the small intestine, as HjPO , and HPOJ , and expulsion occurs via the kidney in the form of these anions, mainly in the urine. The kidneys regulate the P level in the blood by controlling the excretion rate. 

In the kidney, the effect of PTH in promoting phosphate excretion does not depend on the presence of vitamin D. The vitamin itself, however, promotes retention of phosphate by reabsorption. High levels of vitamin D therefore enhance the blood levels of both calcium and phosphorus on account of the action of the vitamin on osteoclasts and kidney cells, respectively. Recent work suggests that the enzyme system which converts 25-HCC to 1,25-DHCC in the kidney is regulated by PTH rather than being controlled directly by the blood calcium level. It has been suggested that the formation of 1,25-DHCC may also be affected by the phosphate concentration in the kidney cells. 

EXCRETION OF PHOSPHORUS. The kidneys provide the main excretory mechanization for regulation of the serum phosphorus level. All of the plasma inorganic phosphate is filtered through the renal glomeruli, if the serum phosphorus level falls, the renal tubules return more phosphorus to the blood if the serum phosphorus level rises, the renal tubules excrete more. Also, when the diet lacks sufficient phosphorus, the renal tubules conserve phosphorus by returning it to the blood. On an average diet, an adult excretes from 0.6 to 1.0 g of phosphorus every 24 hours. 

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