Sodium losses

Diuretics. The primary mechanism by which diuretics reduce blood pressure is to decrease plasma volume. Acting at the kidney, diuretics increase sodium loss and, due to the... 

Angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors not only cause vasodilation (1 TPR), but also inhibit the aldosterone response to net sodium loss. Normally, aldosterone, which enhances reabsorption of sodium in the kidney, would oppose diuretic-induced sodium loss. Therefore, coadministration of ACE inhibitors would enhance the efficacy of diuretic drugs. 

The same diet affects species differently. For instance, mountain hares, Lepus timidus, consume much hirch in their winter diet, while European hares, Lepus europaeus, do not. A high concentration of hirch phenolics in the diet causes massive sodium loss via the urine in European hares, but not in mountain hares (lason and Palo, 1991). Further, among laboratory rodents, hamsters are extremely sensitive to tannins while rats and mice easily adjust within 3 days to doses of condensed tannins that are lethal to hamsters (Mehansho etal, 1987). 

Differences in digestive ability can reflect different ecological lifestyles of related species. The mountain hare feeds on hirch in winter and grass in summer. when fed birch that is high in phenolics, the hare suffers no sodium loss but detoxifies instead. The European hare does not eat birch in winter but eats grass year round. When forced to eat a high-phenolic diet, it loses much sodium through its urine (lason and Palo, 1991). 

Mechanism of Action A mineralocorticoid that acts at distal tubules. Therapeutic Effect Increases potassium and hydrogen ion excretion. Replaces sodium loss and raises blood pressure (with low dosages). Inhibits endogenous adrenal cortical secretion, thymicactivity, and secretion ot corticotropin by pituitary gland (wit h higher dosages). 

In the treatment of low salt syndrome which may occur in presence of heart failure, renal impairment, during surgery, etc. In these cases chloride loss frequently exceeds sodium loss. 

The ion-exchange reaction of the synthetic zeolites NaX and NaY with cobalt, zinc and nickel ions is shown to be non-stoichiometric at low bivalent-ion occupancy, the hydrolytic sodium loss being about twice as large for NaX ( 5 ions/unit cell) as for NaY. The effect is more pronounced at high temperatures and disappears at high occupancies. Reversibility tests in NaX toward zinc and cobalt ions, as studied by a temperature-variation method, show the temperature history to be an important factor in the irreversibility characteristics. The low-temperature partial irreversibility, induced by a high-temperature treatment (45°C) is interpreted in terms of a temperature-dependent occupancy of the small-cage sites by divalent cations, which become irreversibly blocked at low temperature (5°C). 

Zeolite Content, gram/liter Sodium Loss, ions/unit cell... 

Additional checks were made using a dialysis procedure in which zeolite samples which had been isotopically equilibrated with a 22Na O.OlAf NaCl solution were dialyzed against distilled water. After repeated washings, the sodium loss from NaX reached a steady value of 2.8 ( 0.1) ions/ unit cell at a zeolite content of 0.44 gram/liter, i.e. a value which is nearly identical to the data in Table I for a 10 NaCl concentration. Under similar conditions, the sodium loss from NaY is much less and corresponds to 1.5 ( 0.1) ions/unit cell. These results were confirmed by electrical conductivity measurements on the respective dialysates the conductivity for NaX is about twice as large (7.5 X 10 6 mhos/cm) as for NaY (3.9 X 10 6 mhos/cm). 

Stoichiometry. The effect of bivalent ion occupancy upon the stoichiometry is shown in Figure 1. The stoichiometry factor / is defined as the number of Na+ ions desorbed/M2+ ions adsorbed and the deviation from 2 is a measure of the hydrolytic sodium loss. As before, it appears that NaX is much more sensitive to excess sodium loss than NaY at low occupancy of M2+, the data are comparable with the results of Table II 6-8 ions/unit cell (NaX) and 2.5-3 (NaY), which again differ by a factor of about 2. 

Sodium removal is the next important step—by dietary salt restriction or a diuretic—especially if edema is present. In mild failure, it is reasonable to start with a thiazide diuretic, switching to more powerful agents as required. Sodium loss causes secondary loss of potassium, which is particularly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of a potassium-sparing diuretic such as spironolactone. As noted above, spironolactone should probably be considered in all patients with moderate or severe heart failure since it appears to reduce both morbidity and mortality. 

Taylor, L.N., Wood, C.M. and McDonald, D.G. (2003) An evaluation of sodium loss and gill metal binding properties in rainbow trout and yellow perch to explain species differences in copper tolerance, Environmental Toxicology and Chemistry 22 (9), 2159-2166. 

Trimetaphan camsylate is incompatible with alkaline preparations, bromides, iodides, gallamine triethiodide, and thiopentone sodium. Loss of urokinase is reported when diluted with glucose solutions in PVC intravenous infusion sets.127... 

The incidence of classic CAH-P450c21 in the United States ranges from 1 10,000 to 1 18,000, with approximately 75% of patients with CAH-P450c21 exhibiting classic salt wasting (White and Speiser, 2000). Aldosterone is essential for normal sodium homeostasis and acts to enhance sodium absorption and potassium excretion (Fig. 33-3). In the relative absence of aldosterone, there is an increase in sodium loss... 

Q2 Eddie lost a large amount of salt and water because of excessive sweating in his furry costume. How is sodium intake and sodium loss in sweat and urine related to body water balance ... 

Fluid and sodium balance are important to the safe use of lithium. Both dehydration and a negative sodium balance (for example a low salt intake, diuretic-induced sodium loss) will reduce renal lithium clearance and predispose to toxicity (331). Hyponatremia (for example, secondary to polydipsia or SIADH) may also increase the risk of lithium toxicity (332). 

FIGURE 19.8 The time course of furosemide concentration and natriuretic effect after 3 doses of 40 mg compared with those parameters after a single dose of 120 mg. Notice that the concentrations after 120 mg are exactly three times higher than after 40 mg, but the peak effect after 40 mg is quite close to the peak after 120 mg because the 120-mg dose is limited by effects approaching Emax- The cumulative sodium loss after 120 mg is 400 mmol, wliile the three 40-mg doses produce a 600-mmol loss. 

Yu Y. and Hewins R. H. (1998) Transient heating and chondmle formation evidence from sodium loss in flash heating simulation experiments. Geochim. Cosmochim. Acta 62, 159-172. 

Some 65% of the filtered sodium is actively transported from the lumen of the proximal tubule by the sodium pump (Na", K -ATPase). Chloride is absorbed passively, accompan)dng the sodium bicarbonate is also absorbed, through the action of carbonic anhydrase. These solute shifts give rise to the iso-osmotic reabsorption of water, with the result that > 70% of the glomerular filtrate is returned to the blood from this section of the nephron. The epithelium of the proximal tubule is described as leaky because of its free permeability to water and a number of solutes. Osmotic diuretics such as mannitol are solutes which are not reabsorbed in the proximal tubule (site 1. Fig. 26.1) and therefore retain water in the tubular fluid. Their effect is to increase water rather than sodium loss, and this is reflected in their special use acutely to reduce intracranial or intraocular pressure and not states associated with sodium overload. 

The maximum efficacy in removing salt and water that any drug can achieve is related to its site of action, and it is clinically appropriate to rank diuretics according to their natriuretic capacity, as set out below. The percentages quoted in this rank order refer to the highest fractional excretion of filtered sodium under carefully controlled conditions and should not be taken to represent the average fractional sodium loss during clinical use. 

Amiloride exerts an inhibitory action on sodium channels under the influence of aldosterone in the distal tubule. Its action is therefore complementary to that of the thiazides and, used with them, it augments sodium loss and but limits potassium loss. One such combination, co-amilozide, (Moduretic) (amiloride 2.5-5 mg plus hydrochlorothiazide 25-50 mg), is used for hypertension or oedema. The maximum effect of amiloride occurs about 6 h after an oral dose with a duration of action >24h 21 h). The oral dose is 5-20 mg daily. 

Hyponatraemia may result if sodium loss occurs in patients who drink a large quantity of water when taking a diuretic. Other mechanisms are probably involved, including enhancement of antidiuretic hormone release. Such patients have reduced total body sodium and extracellular fluid and are oedema-free. Discontinuing the diuretic and restricting water intake are effective. The condition should be distinguished from hyponatraemia with oedema which develops in some pahents with congestive... 

Loop diuretics (especially as i.v. boluses) potentiate ototoxicity of aminoglycosides and nephrotoxicity of some cephalosporins. NSAIDs tend to cause sodium retention which counteracts the effect of diuretics the mechanism may involve inhibition of renal prostaglandin formation. Diuretic treatment of a patient taking lithium can precipitate toxicity from this drug (the increased sodium loss is accompanied by reduced lithium excretion). Reference is made above to drug treatments which, when combined with diuretics, may lead to hyper-kalaemia, hypokalaemia, hyponatraemia, or glucose intolerance. 

The enzyme carbonic anhydrase facilitates the reaction between carbon dioxide and water to form carbonic acid, which then breaks down to hydrogen (H" ) and bicarbonate (HCOj") ions. This process is fundamental to the production of either acid or alkaline secretions and high concentrations of carbonic anhydrase are present in the gastric mucosa, pancreas, eye and kidney. Because the number of available to exchange with Na" in the proximal tubule is reduced, sodium loss and diuresis occur. But HCOg reabsorption from the tubule is also reduced, and its loss in the urine leads within days to metabolic acidosis, which attenuates the diuretic... 

Physiological concentrations of cortisol are essential for supporting the circulation and glucose production. Physiological concentrations of aldosterone are essential to prevent excessive sodium loss. 

The amount of chloride in the diet tends to parallel the amount of sodium. Losses of chloride from the body also parallel those of sodium. The minimal requirement of Cl for the adult is about 0-75 g/day. The minimal requirement for sodium chloride for the adult is thus about 1.25 g per day. 

Selenium 400 micrograms/day for 2 weeks in a boy of 17 and 25 micrograms/day for 2 weeks in an 11-month-old infant were thought to have caused renal damage, manifested primarily by sodium loss (11). However, there is little evidence that selenium is nephrotoxic, and the patients in question had cystic fibrosis, which could have caused sodium depletion. 

One of the earliest case reports was by Butler and colleagues who reported a patient in whom a low sodium diet (9 mEq/d) exacerbated renal dysfunction, increased urinary sodium loss, and caused postural hypotension [18]. Administration of supplemental oral sodium chloride promptly reversed the defect within 12 hours. These abnormalities were confirmed on rechallenge during treatment, but were absent 13 months after completion of AmB therapy. 

Cyclophosphamide can also cause tubular necrosis in experimental animals [82]. No clinical nephrotoxicity has been described, even when carefully assessed in patients receiving high doses of cyclophosphamide [83, 84]. Although there are no detectable alterations of renal function tests, some subtle changes in tubular kidney physiology do occur. Bode and associates [85] studied the mechanism of water retention that occurs from cyclophosphamide. They determined that cyclophosphamide directly affected the tubules, causing increased water resorbtion and sodium loss. This water retention is self-limited and lasts only a day or two. It is not a major clinical problem. 

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