Sodium retention

Studies have shown that aldosterone (19) (112,113) from adrenal extracts was intensely active in the survival and sodium retention assays in the adrenalectomized rat. 

Sodium bicarbonate is a gastric antacid that may cause systemic alkalosis on overdose and may contribute to edema owing to sodium retention. It is useful for systemic acidosis because both deficient ions are present in the same molecule, and it can be used topically as a moist paste or in solution as an antipmritic. Sodium bicarbonate also is an ingredient of many effervescent mixtures, alkaline solutions, etc. One gram of NaHCO neutralizes 115 mL 0.1 NHCl. 

The volume of extracellular fluid is direcdy related to the Na" concentration which is closely controlled by the kidneys. Homeostatic control of Na" concentration depends on the hormone aldosterone. The kidney secretes a proteolytic enzyme, rennin, which is essential in the first of a series of reactions leading to aldosterone. In response to a decrease in plasma volume and Na" concentration, the secretion of rennin stimulates the production of aldosterone resulting in increased sodium retention and increased volume of extracellular fluid (51,55). 

Two AT-II receptors, AT and AT2 are known and show wide distribution (27). The AT receptor has been cloned and predominates ia regions iavolved ia the regulation of blood pressure and water and sodium retention, eg, the aorta, Hver, adrenal cortex, and ia the CNS ia the paraventricular nucleus, area postrema, and nucleus of the soHtary tract. AT2 receptors are found primarily ia the adrenal medulla, utems, and ia the brain ia the locus coeruleus and the medial geniculate nucleus. AT receptors are GCPRs inhibiting adenylate cyclase activity and stimulating phosphoHpases C, A2, and D. AT2 receptors use phosphotyrosiae phosphatase as a transduction system. 

The natural compounds cortisol [50-23-7], cortisone [53-06-5], and corticosterone [50-22-6] vary only slightly in stmctures and pharmacologic properties (see Steroids). The synthetic analogues inmore modem practice, prednisolone [52438-85-4], dexamethasone [50-02-2], triamcinolone [124-94-7], and betamethasone have greater antiinflammatory potency, and their effects on sodium retention tend to be less severe. 

Hydralazine. Hydrala2iae causes vasodilation ia all primary vascular beds and has more pronounced effects on capacitance than on resistance blood vessels. Despite the hypotension it produces, hydrala2iae iacreases renal blood flow and cardiac output. PRA iacreases with its use. Tachycardia, headache, di22iaess, and water and sodium retention are principal side effects of hydrala2iae therapy. 

It was known for some time that even after the corticoids had been separated from crude extracts of the adrenal cortex, the remaining material, the so-called "amorphous fraction" still possessed considerable mineralocorticoid activity. Aldosterone (250), one of the last steroids to be isolated from this fraction, proved to be the active principle. This compound proved to be an extremely potent agent for the retention of salt, and thus water, in body fluids. An antagonist would be expected to act as a diuretic in those edematous states caused by excess sodium retention. Although aldosterone has been prepared by both total and partial synthesis, the complexity of the molecule discouraged attempts to prepare antagonists based directly on the parent compound. 

In addition to excess sodium intake, abnormal renal sodium retention may be the primary event in the development of hypertension, and it includes abnormalities in the pressure-natriuresis mechanism. In hypertensive individuals, this theory proposes a shift in the control mechanism preventing the normalization of blood pressure. The mechanisms behind the resetting of the pressure-natriuresis curve may include afferent arteriolar vasoconstriction, decreased glomerular ultrafiltration, or an increase in tubular sodium reabsorption.4 Other theories supporting abnormal renal sodium retention suggest a congenital reduction in the number of nephrons, enhanced renin secretion from nephrons that are ischemic, or an acquired compensatory mechanism for renal sodium retention.9... 

Overactivation of the sympathetic nervous system (SNS) may also play a role in the development and maintenance of primary hypertension for some individuals. Among other effects, direct activation of the SNS may lead to enhanced sodium retention, insulin resistance, and baroreceptor dysfunction.9 Regardless of which mechanism(s) underlie the role the SNS may play in the development of primary hypertension, the SNS remains a target of many antihypertensive agents. 

Diuretics have been the mainstay for HF symptom management for many years. 0 Diuretics are used for relief of acute symptoms of congestion and maintenance of euvolemia. These agents interfere with sodium retention by increasing urinary sodium and free water excretion. No prospective data exist on I the effects of diuretics on patient outcomes.14 Therefore, the... 

To reduce mortality, administration of an aldosterone antagonist, either eplerenone or spironolactone, should be considered within the first 2 weeks following MI in all patients who are already receiving an ACE inhibitor (or ARB) and have an EF of equal to or less than 40% and either heart failure symptoms or diagnosis of diabetes mellitus.3 Aldosterone plays an important role in heart failure and in MI because it promotes vascular and myocardial fibrosis, endothelial dysfunction, hypertension, left ventricular hypertrophy, sodium retention, potassium and magnesium loss, and arrhythmias. Aldosterone antagonists have been shown in experimental and human studies to attenuate these adverse effects.70 Spironolactone decreases all-cause mortality in patients with stable, severe heart failure.71... 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

Several adaptive mechanisms by the kidney limit effectiveness of loop diuretic therapy. Postdiuretic sodium retention occurs as the concentration of diuretic in the loop of Henle decreases. This effect can be minimized by decreasing the dosage interval (i.e., dosing more frequently) or by administering a continuous infusion. Continuous infusion loop diuretics may be easier to titrate than bolus dosing, requires less nursing administration time, and may lead to fewer adverse reactions. 

Sodium bicarbonate tablets are administered in increments of 325 and 650 mg tablets. A 650 mg tablet of sodium bicarbonate contains 7.7 mEq (7.7 mmol) each of sodium and bicarbonate. Sodium retention associated with sodium bicarbonate can cause volume overload, which can exacerbate hypertension and chronic heart failure. Patient tolerability of sodium bicarbonate is low because of carbon dioxide production in the GI tract that occurs during dissolution. 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

Patients at increased risk of NSAID-induced gastrointestinal adverse effects (e.g., dyspepsia, peptic ulcer formation, and bleeding) include the elderly, those with peptic ulcer disease, coagulopathy, and patients receiving high doses of concurrent corticosteroids. Nephrotoxicity is more common in the elderly, patients with creatinine clearance values less than 50 mL/minute, and those with volume depletion or on diuretic therapy. NSAIDs should be used with caution in patients with reduced cardiac output due to sodium retention and in patients receiving antihypertensives, warfarin, and lithium. 

The zona glomerulosa is responsible for the production of the mineralocorticoids aldosterone, deoxycorticosterone, and 18-hydroxy-deoxycorticosterone. Aldosterone promotes renal sodium retention and excretion of potassium. Its synthesis and release are regulated by renin in response to decreased vascular volume and renal perfusion. Adrenal aldosterone production is regulated by the renin-angiotensin-aldosterone system. 

Vitamin Bl2 hyperuricemia, hypokalemia, and sodium retention (rare)... 

Caucasians (Okpaku et al, 2005 Strickland etal, 1995). Presumably this difference is a result of the tendency of African Americans to retain sodium. Sodium retention offered a selective survival advantage for slaves bought to America over the middle passage since hyponatremia was believed the major cause of mortality (Hildreth 8c Saunders, 1991). 

Vasodilators. Hydralazine causes direct relaxation of arteriolar smooth muscle. An important consequence of this vasodilation, however, is reflex tachycardia (T CO). It may also cause sodium retention (T plasma volume). The resulting increase in CO tends to offset effects of the vasodilator. Therefore, these drugs are most effective when administered along with sympathetic agents such as P-adrenergic receptor antagonists, which prevent unwanted compensatory responses by the heart. 

Minoxidil is a more potent vasodilator than hydralazine, and the compensatory increases in heart rate, cardiac output, renin release, and sodium retention are more dramatic. Severe sodium and water retention may precipitate congestive heart failure. Minoxidil also causes reversible hyper-... 

Renal function can be grossly assessed by hourly measurements of urine output, but estimation of creatinine clearance based on isolated serum creatinine values in critically ill patients may yield erroneous results. Decreased renal perfusion and aldosterone release result in sodium retention and, thus, low urinary sodium (<30 mEq/L). 

Theory Cortisol (or hydrocortisone) was introduced in the year 1951, for the treatment of rheumatoid arthritis. It has a significant effect on protein metabolism. It also exerts widespread effects on carbohydrates, lipid and protein synthesis (or anabolism). The cardinal side effects such as excessive potassium excretion and sodium retention, enhanced gastric acidity, oedema, psychosis and negative nitogen balance are some of the exaggerated manifestations of the normal metabolite functions of cortisol. 

Angiotensin-II AT, Human cDNA Artherosderosis, cardiac hypertrophy, congestive heart failure, hypertension, myocardial infarction, renal disease, cancer, diabetes, obesity, glaucoma, cystic fibrosis, Alzheimer s disease, Parkinson s disease Smooth muscle contraction, cell proliferation and migration, aldosterone and ADH release, central and peripheral sympathetic stimulation, extracellular matrix formation, tubular sodium retention, neuroprotection... 

The dose of aciclovir in patients with renal impairment should be reduced as aciclovir is eliminated by the renal system. Most penicillins are eliminated by the renal system and hence dose reduction of amoxicillin is required in cases of renal impairment. Non-steroidal anti-inflammatory drugs cause the inhibition of the biosynthesis of prostaglandins involved in the maintenance of renal blood flow. This may precipitate acute renal insufficiency in patients with renal impairment. Furthermore non-steroidal anti-inflammatory drugs tend to cause water and sodium retention and hence aggrevate renal impairment. 

Mineralocorticoids are endogenous compounds that have an effect on fluid and electrolytic balance in the body, mainly by promoting sodium retention in the kidney. 

Fluid/Solute overload Excessive amounts of sodium chloride by any route may cause hypokalemia and acidosis. Administration of IV solutions can cause fluid or solute overload resulting in dilution of serum electrolyte concentrations, CHF, overhydration, congested states, or acute pulmonary edema, especially in patients with cardiovascular disease and in patients receiving corticosteroids or corticotropin or drugs that may give rise to sodium retention. 

Renal function impairment Infusions of sodium ions may result in excessive sodium retention administer with care. 

Special risk patients Administer cautiously to patients with decompensated cardiovascular, cirrhotic, and nephrotic disease circulatory insufficiency hypoproteinemia hypervolemia urinary tract obstruction CHF and to patients with concurrent edema and sodium retention those receiving corticosteroids or corticotropin and those retaining salt. 

Renal function //T pa/m enf. Administration of solutions containing sodium ions may result in sodium retention. Use with caution. Also use cautiously in oliguria or anuria. 

M/sce/Zaneows-Allergic reactions. Sodium retention and edema may occur, particularly if previously poor metabolic control is improved by intensified insulin therapy. Antibody production. 

CHF- Management of edema and sodium retention also indicated with digitalis. 

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