CHAPTER 36 of the medical textbook focuses on Potassium, Calcium, and Phosphate Homeostasis. The chapter explains that the excretion of potassium (K+) in the kidneys depends on the rate and direction of transport in the late segment of the distal tubule and collecting duct. The amount of K+ reabsorbed or secreted in each nephron segment is expressed as a percentage. In cases of dietary K+ depletion, approximately 1% of the filtered load of K+ is excreted. However, with normal or increased dietary K+ intake, the amount of K+ excreted ranges from 15% to 80% of the filtered load. The different segments involved in K+ transport along the nephron are the cortical collecting duct (CCD), distal tubule (DT), inner medullary collecting duct (IMCD), proximal tubule (PT), and thick ascending limb (TAL).

Exercise-induced changes in plasma potassium levels usually do not cause symptoms and can be reversed after a few minutes of rest. However, intense exercise can lead to life-threatening hyperkalemia in individuals who have endocrine disorders affecting insulin, epinephrine, or aldosterone release, impaired K+ excretion (e.g., due to renal failure), or take certain medications like β1-adrenergic blockers. For instance, individuals taking β1-adrenergic receptor antagonists for hypertension may experience an increase of 2 to 4 mEq/L in plasma potassium levels during vigorous exercise. Acid-base balance, plasma osmolality, cell lysis, and exercise do not contribute to K+ homeostasis or help maintain normal plasma potassium levels.

As K+ is not bound to plasma proteins, it can freely pass through the glomerulus and be filtered. Normally, when individuals consume 100 mEq of K+ per day, about 15% of the filtered amount is excreted in urine, and the remaining K+ must be reabsorbed along the nephron. However, with an increase in dietary K+ intake, K+ excretion can surpass the amount filtered, leading to K+ secretion.

Under most conditions, the proximal tubule reabsorbs around 67% of the filtered K+, while the loop of Henle reabsorbs approximately 20%. Unlike these segments, the distal tubule and collecting duct have the ability to both reabsorb and secrete K+. The rate of K+ reabsorption or secretion in these segments is influenced by various hormones and factors. In the case of ingesting 100 mEq/day of K+, the distal tubule and collecting duct secrete K+. Higher dietary K+ intake results in increased K+ secretion, leading to urinary excretion approaching 80% of the filtered amount. Conversely, a low-K+ diet stimulates K+ reabsorption in the distal tubule and collecting duct, causing urinary excretion to decrease to approximately 1% of the glomerular filtered K+.
CHAPTER 36 Potassium, Calcium, and Phosphate Homeostasis 3% 10% to 50% 9% 5% to 30% • Fig. 36.4 K+ transport along the nephron. Excretion of K+ depends on the rate and direction of K+ transport by the late segment of the distal tubule and collecting duct. Percentages refer to the amount of filtered K+ reabsorbed or secreted by each nephron segment. Arrows indicate direction of transport. Left, Dietary K+ depletion. An amount of K+ equal to 1% of the filtered load of K+ is excreted. Right, Normal and increased dietary K+ intake. An amount of K+ equal to 15% to 80% of the filtered load is excreted. CCD, cortical collecting duct; DT, distal tubule; IMCD, inner medullary collecting duct; PT, proximal tubule;
TAL, thick ascending limb.
Exercise-induced changes in plasma [K+] do not usually produce symptoms and are reversed after several minutes of rest. However, vigorous exercise can lead to life-threatening hyperkalemia in individuals (1) who have endocrine disorders that affect release of insulin, epinephrine (a β-adrenergic agonist), or aldosterone; (2) whose ability to excrete K+ is impaired (e.g., renal failure); or (3) who take certain medications, such as β1-adrenergic blockers. For example, during vigorous exercise, plasma [K+] may increase by at least 2 to 4 mEq/L in individuals who take β1-adrenergic receptor antagonists for hypertension. Because acid-base balance, plasma osmolality, cell lysis, and exercise do not maintain plasma [K+] at a normal value, they do not contribute to K+ homeostasis (see
Box 36.1 ). The extent to which these pathophysiological states alter plasma [K+] depends on the integrity of the homeostatic mechanisms that regulate plasma [K+] (e.g., secretion of epinephrine, insulin, and aldosterone).
Because K+ is not bound to plasma proteins, it is freely filtered by the glomerulus. When individuals ingest 100 mEq of K+ per day, urinary K+ excretion is about 15% of the amount filtered. Accordingly K+ must be reabsorbed along the nephron. When dietary K+ intake increases, however, K+ excretion can exceed the amount filtered. Thus K+ can also be secreted.
The proximal tubule reabsorbs about 67% of the filtered K+ under most conditions. Approximately 20% of the filtered K+ is reabsorbed by the loop of Henle, and as with the proximal tubule, the amount reabsorbed is a constant fraction of the amount filtered. In contrast to these segments, which can only reabsorb K+ , the distal tubule and collecting duct are able to reabsorb or secrete K+ . The rate of K+ reabsorption or secretion by the distal tubule and collecting duct depends on a variety of hormones and factors. When 100 mEq/day of K+ is ingested, it is secreted by these nephron segments. A rise in dietary K+ intake increases K+ secretion. K+ secretion can increase the amount of K+ that appears in urine so that it approaches 80% of the amount filtered (see
Fig. 36.4 , right panel). In contrast, a low-K+ diet activates K+ reabsorption along the distal tubule and collecting duct so that urinary excretion falls to about 1% of the K+ filtered by the glomerulus (see