Potassium urinary

The total body potassium of the average 70 kg man is approximately 3600 mmol. Almost all is insidecclls(Fig. I). Potassium intake is variable. 30-100 mmol/day in the UK. but much higher in other countries. Potassium losses are equally variable. The kidney excretes the hulk of ingested potassium. Urinary potassium excretion rises in response to increased intake. Potassium excretion by the kidney is primarily dependent upon glomerular filtration. The most important factor which regulates potassium excretion in the urine is the plasma potassium concentration. 

Velazquez, D.V., H.S. Xavier, J.E. Batista, and C. de Castro-Chaves. 2005. Zea mays L. extracts modify glomerular function and potassium urinary excretion in conscious rats. Phytomedicine 12(5) 363-369. 

ACE inhibitors lower the elevated blood pressure in humans with a concomitant decrease in total peripheral resistance. Cardiac output is increased or unchanged heart rate is unchanged urinary sodium excretion is unchanged and potassium excretion is decreased. ACE inhibitors promote reduction of left ventricular hypertrophy. 

Methybcanthine Diuretics. The mild diuretic effect of drinking coffee, from caffeine, and tea, mainly from theophylline, has been recogni2ed for along time. But the methylxanthines (Table 5) are of very limited efficacy when used as diuretics. The excretion of sodium and chloride ions are increased, but the potassium excretion is normal. Methylxanthines do not alter the urinary pH. Even though the methylxanthines have been demonstrated to have minor direct effects in the renal tubules, it is beUeved that they exert their diuretic effects through increased renal blood flow and GER (71). 

Dihydropyridine Z0947 (108) has been identified as a potassium channel opener for use in urinary urge incontinence and an asymmetric synthesis was required for long-... 

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. 

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. 

Monitor the patient for resolution of hematuria after each successive therapeutic intervention. Frequency of monitoring is based on the severity of hemorrhaging. Monitor urinary output and serum chemistries (including sodium, potassium, chloride, blood urea nitrogen, and serum creatinine) daily for renal dysfunction. Check the CBC at least daily to monitor hemoglobin and platelet count. 

Massey, L. K., Wise, K. J., The effect of dietary caffeine on urinary excretion of calcium, magnesium, sodium and potassium in healthy young females, Nutrition Research, 4, 43, 1984. 

A negative correlation was found between PbB and systolic pressure in Belgian men in the Cadmibel study (a cross-sectional population study of the health effects of environmental exposure to cadmium) (Staessen et al. 1991). In this study, blood pressure and urinary cation (positive ions found in the urine, such as sodium, potassium, and calcium) concentration data were obtained from 963 men and 1,019 women multiple stepwise regression analyses were conducted adjusting for age, body mass index, pulse... 

Chromium compounds interact synergistically or antagonistically with many chemicals. For example, potassium dichromate administered by subcutaneous injection potentiated the effects of mercuric chloride, citrinin, and hexachloro-1,3-butadiene on rat kidneys (USPHS 1993). Chromium effects were lessened by ascorbic acid and Vitamin E, and N-acetyl cysteine was effective in increasing urinary excretion of chromium in rats (USPHS 1993)... 

When rats were given 2 mg CN /kg [14C]potassium cyanide, urinary excretion of radioactivity reached 47% of the dose within 24 hours following administration (Farooqui and Ahmed 1982). When [ 14C] sodium cyanide was injected subcutaneously into rats at a level of 8.3 pmol, no difference in radioactivity eliminated was observed between the group pretreated for 6 weeks with a diet containing 0.7 mg CNTkg as potassium cyanide and their matching controls (Okoh 1983). Most of the radioactivity was detected in... 

The barium ion is a physical antagonist of potassium, and it appears that the symptoms of barium poisoning are attributable to Ba -induced hypokalemia. The effect is probably due to a transfer of potassium from extracellular to intracellular compartments rather than to urinary or gastrointestinal losses. Signs and symptoms are relieved by intravenous infusion ofKh ... 

A rhythmic variation has been observed in levels of plasma hydroxy-corticosteroids (A9, B13, D9) and in the excretion of 17-ketosteroids (P7). As shown in Table 5, urinary excretions of potassium, sodium, chloride, 17-hydroxycorticosteroids and water have been reported to be greatest between 10 am to noon and lowest between 4 am and 6 am (S21). In this study it was shown that within 5 weeks subjects could acclimate to similar patterns for a 21-hour, rather than a 24-hour, day. Heilman and his associates reported that about half of the day s cortisol production is achieved in the early morning hours during sleep and that production is minimal between noon and 10 pm (H7). In one study the plasma cortisol in normal men was 24.6 5.5 /xg/100 ml at 7 am 13.1 3.4 fig/100 ml at 9 am 11.8 fig/100 ml at noon 9.1 2.3 jag/100 ml at 7 PM and 6.3 /ig/100 ml at 10 pm (A9). 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Pharmacology Thiazide diuretics increase the urinary excretion of sodium and chloride in approximately equivalent amounts. They inhibit reabsorption of sodium and chloride in the cortical thick ascending limb of the loop of Henie and the early distal tubules. Other common actions include Increased potassium and bicarbonate excretion, decreased calcium excretion and uric acid retention. At maximal therapeutic dosages all thiazides are approximately equal in diuretic efficacy. 

Urinary alkalinization- Urates tend to crystallize out of an acid urine therefore, a liberal fluid intake is recommended, as well as sufficient sodium bicarbonate (3 to 7.5 g/day) or potassium citrate (7.5 g/day) to maintain an alkaline urine continue alkalization until the serum uric acid level returns to normal limits and tophaceous deposits disappear. Thereafter, urinary alkalization and the restriction of purine-producing foods may be relaxed. 

Drugs that may affect tetracyclines include antacids containing aluminum, calcium, or magnesium iron salts zinc salts barbiturates bismuth salts carbamazepine cholestyramine colestipol phenytoin rifamycins urinary alkalinizers (eg, sodium lactate, potassium citrate). 

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