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Potassium, calcium, and phosphate homeostasis is discussed in Chapter 36. Figure 36.21 provides an overview of the major hormones that regulate plasma calcium levels, including fibroblast growth factor 23 (FGF-23) and parathyroid hormone (PTH). PTH has various effects on calcium and phosphate homeostasis, including stimulating bone resorption, increasing urinary phosphate excretion, decreasing urinary calcium excretion, and promoting the production of calcitriol. Calcitriol, the active form of vitamin D, also plays a crucial role in maintaining calcium and phosphate balance.

The primary action of calcitriol is to enhance calcium and phosphate absorption in the intestine. It also works in conjunction with PTH to release calcium and phosphate from bone and reduce calcium excretion by the kidneys. Overall, calcitriol increases plasma calcium and phosphate levels. The production of calcitriol is primarily stimulated by hypocalcemia via PTH and hypophosphatemia.

In the absence of glucocorticoids, such as in Addison's disease, the excretion of phosphate is reduced, along with the kidneys' ability to excrete titratable acid and generate new bicarbonate ions. Growth hormone increases the reabsorption of phosphate by the proximal tubule, leading to positive phosphate balance in growing children compared to adults.

Figure 36.22 illustrates the activation of calcitriol and its effect on calcium and phosphate homeostasis. Hypocalcemia and hypophosphatemia are the major stimuli for the metabolism of calcifediol to calcitriol in the kidneys, resulting in an increase in plasma calcium and phosphate levels.

Potassium homeostasis is maintained by the kidneys, insulin, epinephrine, and aldosterone. These factors regulate the distribution of potassium between the intracellular fluid (ICF) and extracellular fluid (ECF) compartments. Various events, such as cell lysis, exercise, and changes in acid-base balance and plasma osmolality, can disrupt potassium homeostasis and plasma potassium levels.

The excretion of potassium by the kidneys is determined by the rate and direction of potassium transport in the distal tubule and collecting duct. Plasma potassium levels, aldosterone, and antidiuretic hormone (ADH) regulate the secretion of potassium in these tubular segments. On the other hand, changes in tubular fluid flow and acid-base disturbances can affect potassium excretion by the kidneys. In states of potassium depletion, the secretion of potassium is inhibited, and the distal tubule and collecting duct reabsorb potassium.

The kidneys, along with the intestinal tract and bone, play a crucial role in the regulation of plasma calcium and phosphate levels.

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CHAPTER 36 Potassium, Calcium, and Phosphate Homeostasis 667 • Fig. 36.21 Overview of the major hormones regulating plasma [Ca++]. Dashed lines indicate negative feedback. FGF-23, fibroblast growth factor 23; PTH, parathyroid hormone. (From Koeppen BM, Stanton BA. Renal Physiology. 5th ed. Philadelphia: Elsevier; 2013.)
Integrative Review of Parathyroid Hormone and Calcitriol on Ca++ and Pi Homeostasis
Fig. 36.21 , PTH has numerous effects on Ca++ and Pi homeostasis. Hypocalcemia is the major stimulus of PTH secretion. PTH stimulates bone resorption, increases urinary Pi excretion, decreases urinary Ca++ excretion, and stimulates production of calcitriol, which stimulates Ca++ and Pi absorption by the intestine. Because changes in Pi handling in bone, intestines, and kidneys tend to balance out, PTH increases plasma [Ca++] while having little effect on plasma [Pi]. Overall a rise in plasma PTH levels in response to hypocalcemia returns plasma [Ca++] to the normal range. A decline in plasma [Ca++] has the opposite effect.
Calcitriol (the active form of vitamin D) also plays an important role in Ca++ and Pi homeostasis (
Fig. 36.22
The primary action of calcitriol is to stimulate Ca++ and Pi absorption by the intestine. To a lesser degree it acts with PTH to release Ca++ and Pi from bone and to decrease Ca++ excretion by the kidneys. The net effect of calcitriol is to increase plasma [Ca++] and [Pi]. Thus the major stimuli of calcitriol production are hypocalcemia via PTH and hypophosphatemia (i.e., a low plasma [Pi]).
In the absence of glucocorticoids (e.g., in Addison’s disease), excretion of Pi is depressed, as is the ability of the kidneys to excrete titratable acid and to generate new HCO3 − . Growth hormone increases reabsorption of Pi by the proximal tubule. As a result, growing children are in positive Pi balance and have a higher plasma [Pi] than adults, and this elevated [Pi] is important for bone formation.
• Fig. 36.22 Activation of calcitriol (vitamin D3) and its effect on Ca++ and Pi homeostasis. Hypocalcemia (via PTH) and hypophosphatemia are the major stimuli of the metabolism of calcifediol to calcitriol in the kidneys. The net effect of calcitriol is to increase plasma [Ca++] and [Pi]. (From Koeppen BM, Stanton BA. Renal Physiology. 5th ed. Philadelphia: Elsevier; 2013.) 1.
K+ homeostasis is maintained by the kidneys, which adjust K+ excretion to match dietary K+ intake, and by the hormones insulin, epinephrine, and aldosterone, which regulate the distribution of K+ between the ICF and ECF compartments. Other events, such as cell lysis, exercise, and changes in acid-base balance and plasma osmolality, disturb K+ homeostasis and plasma [K+].
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Excretion of K+ by the kidneys is determined by the rate and direction of K+ transport by the distal tubule and collecting duct. Secretion of K+ by these tubular segments is regulated by plasma [K+], aldosterone, and AVP. In contrast, changes in tubular fluid flow and acid-base disturbances perturb K+ excretion by the kidneys. In K+-depleted states, K+ secretion is inhibited and the distal tubule and collecting duct reabsorb K+ .
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The kidneys, in conjunction with the intestinal tract and bone, play a vital role in regulating plasma [Ca++] and [Pi].
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