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Low Potassium Diet Pdf Uk
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Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan
Received: 19 March 2021 / Revised: 14 May 2021 / Accepted: 17 May 2021 / Published: 21 May 2021
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(This article belongs to the expansion of the special issue on healthy life expectancy of dialysis patients in the era of 100 years of life)
Potassium (K), the most important cation in cells, plays a role in the maintenance of cellular osmolarity and acid-base balance, as well as the transmission of nerve impulses and the regulation of heart and muscle functions. Recently, K has also been shown to have an antihypertensive effect by promoting sodium excretion, while also attracting attention as an important component that can suppress hypertension associated with excessive sodium intake. Since most of the ingested K is excreted through the kidneys, a decrease in renal function is a major factor in the increase in serum levels, and target values for its consumption have been determined according to the degree of renal insufficiency. In elderly people with impaired renal function, not only hyperkalaemia but also hypokalaemia is expected to develop as a result of anorexia, K loss on dialysis and the effects of various drugs. Therefore, it is necessary to pay attention to K management adapted to the individual conditions. Because disturbances in K metabolism can also cause fatal arrhythmia or sudden cardiac death, it is extremely important to monitor patients at high risk of hyper- or hypokalemia and attempt to provide early and appropriate intervention.
Abnormalities in potassium (K) metabolism are caused by a variety of factors. However, since K metabolism is largely regulated by the kidneys, most cases of hyper- and hypokalemia are caused by renal mechanisms [1]. Impaired renal function increases the risk of developing abnormal K metabolism, although the aging of affected patients and the increasing complexity of different drugs and dialysis treatments make the pathogenesis more complicated (Figure 1). This article reviews the basics of K metabolism, the pathogenesis of abnormal K metabolism, and the relationship between K-related factors and its dynamics, together with a review of relevant literature.
About 60% of adult body weight is water, two-thirds of which is intracellular and one-third extracellular. The largest cation in the intracellular fluid is K, while the largest cation in the extracellular fluid is sodium (Na). The total amount of K in the body is about 50-55 m3/kg, of which about 98% is contained in cells (skeletal muscle, red blood cells, liver, etc.) and 1-2% in extracellular fluid. This concentration gradient (intracellular concentration: 150 mEq/L, extracellular concentration: 3.5-5.0 mEq/L) regulates excitatory conduction in nerve and muscle cells, as well as maintaining osmotic pressure in body fluids and acid-base balance [2].
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The normal daily intake of K in adults is 50-100 m3, most of which is absorbed from the small intestine Increased K in the blood is absorbed into the cells by active transport through Na-K ATPase, when about 90% of the excess K is excreted in the urine and about 10% in faeces When the kidneys are functioning normally, serum K does not rise rapidly or significantly after K intake [3].
Of the freely filtered K in the glomerulus, approx. 70% in the proximal tubule and approx. 20% in the ascending limb (TAL) of the loop of Henle, while the remaining 10% is either secreted (excreted) regularly or reabsorbed by cortical collecting duct. (CCD). In the proximal tubules, reabsorption occurs by passive transport together with reabsorption of water and Na, and in the TAL by active transport by Na-K-2Cl cotransporters (NKCCs). In CCD, several K channels, such as the renal outer medullary potassium channel (ROMK), Maxi-K and Kv1.3, are expressed in the lumen and on both sides of the vessels. K excretion is regulated by changes in the amount of K reaching the CCD lumen in response to changes in blood K concentration, as well as the flow rate (urine volume) and the negative potential in the lumen [4].
As serum K concentration increases, water and Na reabsorption decreases due to increased K reabsorption in the proximal tubule and TAL, resulting in an increase in flow rate (urine volume) and Na arrival volume due to water diuresis in the CCD. The flow-dependent increase in K secretion is mediated by Maxi-K channels on the luminal side of principal CCD cells (PC) and intercalated cells (ICs) [5]. When the flow rate in the lumen increases, transient receptor potential vanilloid (TRPV)-4 channels, which are also present in PC and IC cells, release stored intracellular calcium (Ca) and stimulate Ca influx from the lumen into the cells [6 ], thereby activating Maxi-K and improving K secretion [7]. When Na is reabsorbed in the collecting tubules due to an increased amount of Na reaching the lumen, K secretion is increased by promoting the exchangeable secretion of K by the same cation.
A decrease in serum K concentration leads to a decrease in ROMK expression in PC cells of CCD, to endocytosis of ROMK protein and degradation of the channel protein from the luminal side membrane [8], as well as to translocation of ROMK into cells upon activation of intracellular tyrosine kinase. in the luminal side membrane of the TAL, resulting in a decrease in K secretion [9]. Meanwhile, Maxi-K expression on the luminal side of the collecting duct [10] and Maxi-K-mediated renal K excretion [11] increase as K intake increases. In IC cells, K reabsorption is increased by H-K ATPase activation in the luminal membrane when serum K concentration is reduced. Although there is also a suggestion of the existence of a K secretory function of IC cells during K uptake [12], such a mechanism is currently unclear.
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An increased level of K in serum stimulates the secretion of aldosterone from the globular layer of the adrenal cortex, then aldosterone increases the epithelial sodium channel (ENaC) and ROMK expression on the luminal side of PC cells, as well as Na-K ATPase on the vascular side. , resulting in K excretion with Na reabsorption as the driving force [13]. In addition, hyperkalemia increases kallikrein production in junctional tubules, which increases ENaC activity in PC cells and thereby promotes K secretion from ROMK and Maxi-K, and suppresses K reabsorption via H-K ATPase in IC cells.
AVP and insulin increase K secretion by increasing and activating ENaC, respectively [13]. While AVP also directly activates ROMK, K excretion is reduced during antidiuresis due to decreased flow rate (urine volume); Thus, the effects on K excretion are balanced and suppressed. On the other hand, glucocorticoids appear to increase glomerular filtration rate (GFR) and increase K excretion through increased CCD intraluminal flow rate and Na arrival.
Most of the ingested K is absorbed in the small intestine, where around 10% is excreted in the faeces. There are two pathways for ion transport in the intestinal epithelium; The intercellular pathway, a passive transport pathway through the tight junction, and the transcellular pathway, an active transport pathway. K permeability tends to be greater in the upper small intestine (jejunum > ileum) and most of it is rapidly absorbed by the intracellular pathway. The permeability of the intercellular safety pathways in the colon is lower than that of the small intestine, although there are regulatory mechanisms in the colon for K absorption through H-K-ATPase in the cellular pathway and K secretion through ROMK on the side of the colon. the lumen. The presence of a gut-derived factor that increases renal K excretion by allowing K into the gastrointestinal tract has also been suggested [14].
In the case of VIPoma and pseudo-obstruction of the colon, which causes prominent watery diarrhea, the excretion of K in feces is abnormally high, indicating the involvement of vasoactive intestinal peptide (VIP) in the K regulation of the intestine [15] . Although Maxi-K
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