Sodium renal absorption

Acetazolamide inhibits the enzyme carbonic anhydrase, and interferes with the ability of the renal tubules to produce and secrete hydrogen ions. And, the diuretic action is due to the decreased sodium biocarbonate absorption in proximal tubules and diminished hydrogensodium exchange in the distal tubules. 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

Re-absorption is a two-step process beginning with the active or passive extraction of substances from the mbule fluid into the renal interstitium (the connective tissue that surrounds the nephrons), followed by their transport from the interstitium into the bloodstream. These transport processes are driven by hydrostatic, oncotic, diffusion and active transport. Some key regulatory hormones for re-absorption include aldosterone, which stimulates active sodium re-absorption (and water as a result), and antidiuretic hormone, which stimulates passive water re-absorption. Both hormones exert their effects principally on the collecting ducts. 

Atrial natriuretic peptide (ANP)—which is secreted when the heart walls are stretched owing to rising blood pressure and causes sodium excretion by decreasing renal absorption, thus increasing the loss of sodium through the kidneys. 

The water solubiUty of glutaric acid fosters its toxicity. Glutaric acid is a known nephrotoxin. Renal failure has been documented ia rabbits adruinistered sodium glutarate subcutaneously (124). Dibasic ester (Du Pont), which contains primarily dimethyl glutarate, has low acute toxicity by inhalation and by ingestion, and is moderately toxic via dermal absorption. The acid is both a dermal and ocular irritant of humans. The ester is a severe skin irritant and may cause a rash ia humans (120). 

In an attempt to conserve sodium, the kidney secretes renin increased plasma renin activity increases the release of aldosterone, which regulates the absorption of potassium and leads to kafluresis and hypokalemia. Hypokalemia is responsible in part for decreased glucose intolerance (82). Hyponatremia, postural hypotension, and pre-renal azotemia are considered of tittle consequence. Hypemricemia and hypercalcemia are not unusual, but are not considered harmful. However, hypokalemia, progressive decreased glucose tolerance, and increased semm cholesterol [57-88-5] levels are considered... 

Diuretics promote the urinary excretion of sodium and water by inhibiting the absorption of filtered fluid across the renal tubular epithelium. The ensuing reduction in Na reabsorption reduces the Na content of the body, the critical determinant of extracellular and plasma fluid volumes. Thus, the use of diuretics is primarily indicated in the treatment of edematous diseases and of arterial hypertension. 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

These salts should always be given with substantial amounts of water otherwise the patient may be purged at the expense of body water, resulting in dehydration. Sodium-containing laxatives should not be used in patients with congestive heart failure, since the patient may absorb excessive sodium. Similarly, in cases of renal failure, magnesium or phosphate-containing products should not be used, since the loss of a renal clearance of these ions may result in cumulative toxic levels despite their minimal absorption. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

Fluoride taken in the form of sodium fluoride as a tablet or solution is absorbed rapidly. Only a few minutes after intake, there is a rise in plasma fluoride. The fluctuation in plasma fluoride concentration is dependent on the fluoride dose ingested, the dose frequency and the plasma half-life of fluoride. The half time for absorption is --30 min, so peak plasma concentration usually occurs within 30-60 min [64-69]. Absorbed fluoride is rapidly distributed by the circulation to the intracellular and extracellular fluids and is retained only in calcified tissues. The sensitivity of the serum fluoride concentrations to previous intake, glomerular filtration and the intensity of bone resorption suggests that the human organism exerts no direct homeostatic control and that fluoride concentrations reflect the recent intake [73]. Plasma fluoride levels increase with age, with increasing fluoride content of bone and as a consequence of renal insufficiency [2]. 

Liddle s syndrome is an autosomal dominant form of hypertension. It is a disorder of the renal epithelial sodium channel, which has three subunits, a, j, and y, and mutations within the first two are associated with increased sodium channel activity [7, 36]. This causes excessive sodium absorption in the distal nephron of the kidney. It gives rise to hypoglycemia, low -renin, and low aldosterone. 

Because acid-pepsin disease rarely occurs in the absence of gastric acid and pepsin, antacids are highly effective in its overall management. Antacids consist of a mixture of magnesium, aluminum, and calcium compounds. Their efficacy is based on their inherent ability to react with and neutralize gastric acid. Sodium bicarbonate, which may leave the stomach rapidly, can cause alkalosis and sodium retention. Calcium salts may produce hypercalcemia, which can be detrimental in patients with impaired renal function. Aluminum salts may decrease the absorption of tetracyclines and anticholinergic drugs. 

Renal plasma flow and glomerular filtration rate are usually unaffected, but free water clearance may increase. Because most sodium is reabsorbed in the proximal renal tubules, spironolactone is relatively ineffective when administered alone. Concomitant administration of a diuretic which blocks re-absorption of sodium proximal to the distal portion of the nephron (such as a thiazide or loop diuretic) is required for maximum diuretic effects. When administered with other diuretics, spironolactone produces an additive or synergistic diuretic response and decreases potassium excretion caused by the other diuretic [65],... 

Evidence also suggests that the toxicity of uranium varies according to the route of exposure and to its compounds. This finding may be partly attributable to the relatively low gastrointestinal absorption of uranium compounds. Only <0.1-6% of even the more soluble uranium compounds are absorbed in the gastrointestinal tract. On the basis of the toxicity of different uranium salts in animals, it was concluded that the relatively more water-soluble salts (uranyl nitrate hexahydrate, uranyl fluoride, uranium pentachloride) were primarily renal and systemic toxicants. The less water-soluble compounds (uranium trioxide, sodium diuranate, ammonium diuranate) were of moderate-to-low toxicity, while the insoluble compounds (uranium tetrafluoride, uranium dioxide, uranium peroxide, triuranium octaoxide) were... 

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