Low-potassium diet

Mild and uncomplicated hyperkalemia is commonly observed in patients taking ciclosporin and is generally prevented by a low potassium diet. A reduction in distal nephron potassium secretion and tubular flow rate, with insensitivity to exogenous mineralocorticoids, and leakage of cellular potassium into the extracellular fluid are possible mechanisms (SED-13, 1124) (64). 

Effect of potassium and lysine supplementation on performance of young pi fed low potassium diets. 

Description of Method. Salt substitutes, which are used in place of table salt for individuals on a low-sodium diet, contain KCI. Depending on the brand, fumaric acid, calcium hydrogen phosphate, or potassium tartrate also may be present. Typically, the concentration of sodium in a salt substitute is about 100 ppm. The concentration of sodium is easily determined by flame atomic emission. Because it is difficult to match the matrix of the standards to that of the sample, the analysis is accomplished by the method of standard additions. 

Ascites. Patients with cirrhosis, especially fiver cirrhosis, very often develop ascites, ie, accumulation of fluid in the peritoneal cavity. This is the final event resulting from the hemodynamic disturbances in the systemic and splanchnic circulations that lead to sodium and water retention. When therapy with a low sodium diet fails, the dmg of choice for the treatment of ascites is furosemide, a high ceiling (loop) diuretic, or spironolactone, an aldosterone receptor antagonist/potassium-sparing diuretic. 

It may be taken for granted that, if there is a wide variance in the potassium needs of individuals, the sodium needs vary also. We shall, however, dismiss this subject by commenting that the human consumption of sodium chloride is said to vary from 2 to 30 gm. per day,5 and that sodium salts become highly toxic when there is a potassium deficiency.6 It seems to the writer extremely unlikely that variations in sodium consumption should be attributed wholly to differences in "habit." The whole subject of low-salt diets needs to be re-examined with these facts in mind. 

These two elements are the main cations of the cell. Persons with high blood pressures are usually placed on a low sodium diet. Although potassium deficiency in normal adults is rare,... 

This can often be avoided by having the patient reduce sodium intake, thus decreasing sodium delivery to the K+-secreting collecting tubule. Patients who are noncompliant with a low sodium diet must take oral KC1 supplements or a potassium-sparing diuretic or must stop using the thiazide diuretic. 

Effective treatment of nephrotic edema requires adherence to a low-sodium diet (containing preferably only about 50 mmol of sodium per day) and administration of potent loop diuretics (e.g., furosemide), sometimes in high doses several times per day and/or in combination with thiazides and potassium-sparing diuretics (e.g., amiloride). Plasma ultrafiltration should be reserved for patients with refractory nephrotic edema and massive sodium and water retention. 

After the plasma Mg levels had decreased, plasma calcium levels began to drop. The drop in plasma Ca was moderate compared with that in Mg, Plasma Ca levels decreased even though the subjects were receiving adequate amounts of calcium and vitamin D. Neuromuscular symptoms developed after about 4 weeks of the diet. These symphims included tetany, lack of reflexes, tremors, and muscle lAreak-ness. Tetany may be mild, as in mouth twitches, or more severe, as in painful spasms. Hypocalcemia produces a tetany similar to that produced by Mg defi cicncy however. Mg deficiency induced tetany can occur with normal serum calcium levels. The tetany of Mg deficiency can be reversed by administration of Mg but not calcium. Tetany can result from low concentrations of Ca or Mg in the extracellular fluids which surround the nerves) or from an alkaline pH. Low potassium levels in the extracellular fluids, however, do not result in tetany. 

Sodium and potassium (supplement) Adverse in cases of low sodium/potassium diet, stomach upset, diarrhea. Phlebitis and injection pain with potassium [7,14]... 

A 72-year-old man was treated with ceftriaxone (2 g bd) and gentamicin (80 mg tds) for a severe urinary tract infection (75). On day 5 his serum potassium concentration was 3 mmol/1 with a normal serum creatinine and urine examination. Despite treatment with oral potassium chloride plus a high potassium diet, his serum potassium fell to 2.3 mmol/1 4 days later, accompanied by inappropriate kaliuresis, hypouricemia with inappropriate uri-cosuria, and hypophosphatemia with inappropriate phosphaturia. There was no bicarbonate wasting, but there was proteinuria 1.2 g/day, with a predominance of low molecular weight proteins in contrast, serum creatinine was normal and creatinine clearance was 78 ml/minute. The aminoglycoside was withdrawn with subsequent progressive improvement in renal proximal tubular function, which normalized 9 days later. 

Foscarnet competitively inhibits Na -Pj cotransport in animal and human kidney proximal tubule brush border membrane vesicles, reversibly inhibiting sodium-dependent phosphate transport [48, 49]. Renal cortical Na-K-ATPase and alkaline phosphatase activity are not inhibited by foscarnet, nor is proline, glucose, succinate, or Na" transport [48,49]. Foscarnet induces isolated phosphaturia without hypophosphatemia in thyroparathyroidectomized rats maintained on a low phosphorus diet, without affecting glomerular filtration rate, urinary adenosine 3 5 -cyclic monophosphate (cAMP) activity, or urinary calcium, sodium or potassium excretion [48,50]. Sodium-Pj cotransport in brush border membrane vesicles from human renal cortex was reported to be even more sensitive to inhibition by foscarnet than in rat renal brush border membrane vesicles [49]. 

Chronic renal failure is treated by dialysis, kidney transplants, and drugs, as well as by low-protein diets. For this reason, an outline of chronic renal failure occurs in this chapter. The normal glomerular filtration rate (GFR) is 80 to 120 ml/min. In severe renal disease, the GFR can be reduced to 10 ml/min or less. This represents a 90% loss of renal function. Diabetes mellitus and hypertension (high blood pressure) are the main causes of chronic renal failure. Sustained and chronic injury to the kidneys leads to the destruction of the nephrons, where this destruction is usually not reversible. The nephron, which is the smallest unit of kidney function, is detailed in the section on Sodium, Potassium, Chloride, and Water. The severe loss of nephrons results in alterations of functions of many other organs of the body. The collection of abnormalities that results is called uremia. 

Procedure The patient should be on a low-sodium, high-potassium diet and receiving a diuretic for 3 days before the procedure. Under fluoroscopic guidance, percutaneous catheterization is performed, and blood samples are obtained from both renal veins and the inferior vena cava for determination of PRA. 

A high intake of table salt, sodium chloride, the major source of sodium in the diet, is one factor that may cause high blood pressure, hypertension, in susceptible individuals. There has been considerable emphasis on "low-salt" diets as a means of avoiding hypertension. However, it appears that sodium is not the only culprit. It is the sodium ion-to-potassium ion ratio that appears to be important in controlling blood pressure. Ideally, the Na+/K+ ratio should be about 0.6, but the Na+/K+ ratio consumed by the average American is greater than 1.0. To avoid h)rperten-sion in later life, it is important to reduce the amount of sodium in the diet and increase the amount of potassium. 

Potassium chloride is present in some foods in small amounts. The compound is also used as a food additive to increase the acidity and to stabilize, thicken, or soften some food products, such as jams and jellies and preserves that are artificially sweetened. Many infant formulas also contain potassium chloride. Potassium chloride is also used as a nutrient for yeast cultures and in making beer. The compound is used as a salt substitute for people who are on low-salt (meaning low-sodium) diets. Some brand names of these products are LoSalt , Reheis Less Salt Blend , and Morton Lite Salt . 

Following 6 weeks on his low-salt diet and drug therapy, BD s condition seems to be greatly improved. His serum potassium levels, however, have decreased from 4.2 to 3.1 mEq/L (normal value, 3.8-5.6 mEq/L). What caused his serum potassium levels to decrease over time Why is this change a concern What can be done to remedy this problem ... 

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