Urine potassium

Most patients with autonomous aldosterone overproduction are hypokalemic, but most patients with hypokalemia do not have primary aldosteronism. In hyperaldosteronism, urinary potassium excretion is inappropriately high, and a random urine potassium >30mraol/L is usually indicative of primary aldosteronism or some type of mineralocorticoid excess condition. If hypokalemia can be shown to he due to nonrenal potassium loss, the diagnosis of aldosteronism does not need to be considered further. ... 

Normal growth requires potassium involvement in enzyme activities. It plays a part in making muscle protein from amino acids, assists in the storage of glucose in the hver, and cooperates with sodium in maintaining blood pressure. It helps in the synthesis of nucleic acids and signals the kidneys to eliminate wastes in the urine. Potassium works with sodium to regulate the heartbeat. 

I. Pharmacology. Potassium is the primary intracellular cation, which is essential for maintenance of acid-base balance, intracellular tonicity, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscle, and maintenance of normal renal function (and ability to alkalinize urine). Potassium also acts as an activator in many enzyme reactions and participates in many physiological processes such as carbohydrate metabolism, protein synthesis, and gastric secretion. Potassium is critical in regulating nerve conduction and muscle contraction, especially in the heart. A variety of toxins cause alterations in serum potassium levels (see Table 1-27, p 38). 

Supplements. Supplements of potassium in medicine are most widely used in conjunction with the most powerful classes of diuretics, which rid the body of sodium and water, but have the side effect of also causing potassium loss in urine. Potassium supplements are available as a number of different salts, including potassium chloride, citrate, gluconate, bicarbonate, aspartate, and orotate. °... 

This form of aldosteronism must be distinguished from primary aldosteronism due to adrenal hyperplasia and ordinary secondary aldosteronism. In primary aldosteronism, sodium deprivation results in a reduction of sodium in blood and potassium in urine, potassium retention is facilitated, and, as a result, hypokalemia is corrected. In the juxtaglomerular disease, uri-... 

Benedict s quantitative reagent (sugar in urine) This solution contains 18 g copper sulfate, 100 g of anhydrous sodium carbonate, 200 g of potassium citrate, 125 g of potassium thiocyanate, and 0.25 g of potassium ferrocyanide per liter 1 mL of this solution = 0.002 g sugar. 

The potassium or calcium salt form of oxaUc acid is distributed widely ia the plant kingdom. Its name is derived from the Greek o>ys, meaning sharp or acidic, referring to the acidity common ia the foflage of certain plants (notably Oxalis and Mmex) from which it was first isolated. Other plants ia which oxahc acid is found are spinach, rhubarb, etc. Oxahc acid is a product of metabohsm of fungi or bacteria and also occurs ia human and animal urine the calcium salt is a principal constituent of kidney stones. 

Potassium nitrate, essential in the manufacture of black gun powder, was produced by the Chinese, who had developed gun powder by the tenth century AD. The process involved the leaching of soil in which nitrogen from urine had combined with mineral potassium. By the early 1800s, potassium nitrate had become a strategic military chemical and was stiU produced, primarily in India, by using the ancient Chinese method. The caUche deposits in Chile are the only natural source of potassium nitrate (2). These deposits are not a rich source of potassium nitrate, purifying only to about 14% as K O. 

The leaves of the indigo plant do not contain the dye as such, but in the form of its precursor, a glycoside known as indican (109). Indican [487-60-5] is the dextrose derivative (35) of indoxyl [480-93-3] (110). Indoxyl occurs also in the urine of humans as the potassium salt of indoxyl sulfonic acid (111). 

Ion-selective electrodes are available for the electro analysis of most small anions, eg, haUdes, sulfide, carbonate, nitrate, etc, and cations, eg, lithium, sodium, potassium, hydrogen, magnesium, calcium, etc, but having varying degrees of selectivity. The most successful uses of these electrodes involve process monitoring, eg, for pH, where precision beyond the unstable reference electrode s abiUty to deUver is not generally required, and for clinical apphcations, eg, sodium, potassium, chloride, and carbonate in blood, urine, and semm. 

Litholytic agents in current use are classified as direct or indirect. Indirect type drugs decrease the C.P. of urine, thus inhibiting calculus formation. An example is citrate which helps prevent insoluble salts from crystallizing in the urinary tract. Potassium citrate is administered in pill form as a preventive drug. Direct type drugs dissolve renal calculi which have already formed. 

Biochemical characteristics (plasma levels of alanine and aspartate transminases, alkaline phosphatase, triglycerides, cholesterol, urea, uric acid, allantoin, glucose, protein, albumin, sodium, potassium, calcium, magnesium, phosphorus urine levels of protein and glucose). 

Hyperkalemia (increase in potassium in the blood), a serious event, may be seen with the administration of potassium-sparing diuretics. Hyperkalemia is most likely to occur in patients with an inadequate fluid intake and urine output, those with diabetes or renal disease tiie elderly, and those who are severely ill. In patients taking spironolactone, gynecomastia (breast enlargement in tiie male) may occur. This reaction appears to be related to both dosage and duration of therapy. The gynecomastia is usually reversible when therapy is discontinued, but in rare instances, some breast enlargement may remain. 

Potassium as a nutrient lowers blood pressure, prevents bone loss, and reduces the risk of kidney stones. Some of these effects are due to the loss of sodium in the urine when potassium is ingested. 

Each year in the United States, about 30 million prescriptions for potassium supplements are written for people with hypertension (high blood pressure). These supplements are often prescribed with diuretics. Diuretics cause increased urination and reduce the volume of retained fluids in the body, thus reducing blood pressure. Explain why potassium supplements are prescribed. 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

Measure spot urine sodium/potassium ratio to assess adherence to dietary sodium restrictions. 

Assess dietary sodium intake by patient food recall or by spot urine sodium/potassium ratio for appropriate sodium excretion. 

Develop a plan to provide symptomatic care of complications associated with ARF, such as diuretic therapy to treat volume overload. Monitor the patient s weight, urine output, electrolytes (such as potassium), and blood pressure to assess efficacy of the diuretic regimen. 

In patients with peritonitis, hypovolemia is often accompanied by acidosis, so large volumes of a solution such as lac-tated Ringers may be required initially to restore intravascular volume. Maintenance fluids should be instituted (after intravascular volume is restored) with 0.9% sodium chloride and potassium chloride (20 mEq/L) or 5% dextrose and 0.45% sodium chloride with potassium chloride (20 mEq/L). The administration rate should be based on estimated daily fluid loss through urine and nasogastric suction, including 0.5 to 1.0 L for insensible fluid loss. Potassium would not be included routinely if the patient is hyperkalemic or has renal insufficiency. Aggressive fluid therapy often must be continued in the postoperative period because fluid will continue to sequester in the peritoneal cavity, bowel wall, and lumen. 

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