Bicarbonate renal excretion

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. 

The early compensatory response to acute respiratory acidosis is chemical buffering. If respiratory acidosis is prolonged (more than 12 to 24 hours), renal excretion of H+ increases, which generates new bicarbonate. 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

Mechanism of Action A carbonic anhydrase inhibitor that reduces formation of hydrogen and bicarbonate ions from carbon dioxide and water by inhibiting, in proximal renal tubule, the enzyme carbonic anhydrase, thereby promoting renal excretion of sodium, potassium, bicarbonate, and water. Ocular Reduces rate of aqueous humor formation, lowers intraocular pressure. Therapeutic Effect Produces anticonvulsant activity. 

Uric acid, cystine, and some other weak acids are relatively insoluble in, and easily reabsorbed from, acidic urine. Renal excretion of these compounds can be enhanced by increasing urinary pH with carbonic anhydrase inhibitors. In the absence of continuous bicarbonate administration, these effects of acetazolamide are of relatively short duration (2-3 days). Prolonged therapy requires bicarbonate administration. 

MEMANTINE SODIUM BICARBONATE Possible t memantine levels 1 renal excretion Watch for early features of memantine toxicity... 

LITHIUM SODIUM BICARBONATE L plasma concentrations of lithium with risk of lack of therapeutic effect Due to t renal excretion of lithium Monitor clinically and by measuring blood lithium levels to ensure adequate therapeutic efficacy... 

TETRACYCLINE SODIUM BICARBONATE 1 tetracycline levels and possible therapeutic failure It is suggested that when sodium bicarbonate alkalinizes the urine, the renal excretion of tetracycline is t The interaction can be minimized by separating their dosing by 3-4 hours... 

Sodium bicarbonate is metabolized to the sodium cation, which is eliminated from the body by renal excretion, and the bicarbonate anion, which becomes part of the body s bicarbonate store. Any carbon dioxide formed is eliminated via the lungs. Administration of excessive amounts of sodium bicarbonate may thus disturb the body s electrolyte balance, leading to metabolic alkalosis or possibly sodium overload with potentially serious consequences. The amount of sodium present in antacids and effervescent formulations has been sufficient to exacerbate chronic heart failure, especially in elderly patients. ... 

Excessive loss of bicarbonate because of increased renal excretion (decreased tubular reclamation) or excessive loss of duodenal fluid (as in diarrhea). Plasma CHCO3 falls the fall is associated with a rise in the concentration of inorganic anions (mostly chloride) or a concomitant fall in the sodium concentration. 

Major functions of the distal nephron include the regeneration of bicarbonate, the excretion of acid (hydrogen ion), the secretion of potassium, and the reabsorption of water. Damage to this portion of the nephron may present as significant acidemia and either hypo-or hyperkalemia, depending on the mechanism of injury. For example, amphotericin B produces small pores in the luminal membrane of distal tubular cells. These pores allow small molecules such as potassium to leak out the molecules are then wasted in the urine. Consequently, amphotericin B nephrotoxicity is characterized by hypokalemia secondary to renal potassium wasting. ATN is associated with urinary sediment characterized by the presence of tubular cells, coarse granular casts, and rarely, RBC casts. 

No matter which condition initiated the metabolic alkalosis, abnormalities in renal function underlie its maintenance. Normally, the kidneys are capable of excreting all of the excess bicarbonate presented to them, even during periods of increased bicarbonate loads. As the serum bicarbonate concentration increases, the filtered bicarbonate load exceeds the maximal rate for bicarbonate reabsorption, and the excess bicarbonate is excreted in the urine. Under normal circumstances, the excess bicarbonate is rapidly excreted and metabolic alkalosis does not occur, or is corrected in a matter of hours... 

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. 

In type II renal tubular acidosis there is a defect in the secretion of hydrogen ions by the proximal tubule. Because the proximal tubule is the major site of bicarbonate reabsorption (4000 mEq of bicarbonate per day as compared to 70 mEq in the distal tubule), the defect in secretion of hydrogen ions in this condition leads to the flooding of the distal tubule with bicarbonate. The capacity of hydrogen ions secreted by the distal tubule to buffer this massive efflux of bicarbonate is soon overwhelmed and, as a result, large quantities of bicarbonate are excreted in the urine. Much more bicarbonate needs to be administered in this condition to correct the acidosis than is necessary in type I renal tubular acidosis. In general, in renal tubular acidosis the impairment in hydrogen ion secretion leads to excretion of potassium ions in urine. 

Mild hyperventilation occurs from early pregnancy, probably due to a centrally mediated effect of progesterone, and PCO. falls. However, blood hydrogen ion concentration is maintained within non-pregnant limits, since the plasma bicarbonate falls due to an increased renal excretion of bicarbonate. Oxygen consumption increa.scs by about 2091, but PO, is relatively unchanged. 

Fig. 2 The recovery and regeneration of bicarbonate by excretion of H in the renal tubular cell. Note that H is actively secreted into the urine while CO, diffuses along its concentration gradient.

The bicarbonate ion (HCO3A is the second-largest anionic contributor to maintaining acid-base balance, and its secretion from the pancreas helps to neutralize the contents of the small intestine. Respiration controlling the carbon dioxide concentration of the blood (PaCOj) and renal excretion of bicarbonate are the two main homeostatic influences on plasma bicarbonate. Within the renal tubular lumen, carbonic anhydrase converts carbonic acid into carbon dioxide, which diffuses into the epithelial cells and forms carbonic acid, which later dissociates to bicarbonate. 

Altered renal excretion including aminoglycosides, antineoplastic agents, and diuretics Reduced renal reabsorption of bicarbonate and increased potassium excretion Carbonic anhydrase inhibitors Alteration of ECFrICF ratio... 

Therapeutic doses of salicylate produce definite changes in the acid—base balance and electrolyte pattern. Compensation for the initial event, respiratory alkalosis, is achieved by increased renal excretion of bicarbonate, which is accompanied by increased Na and excretion plasma bicar-... 

The low plasma PCO2 leads to decreased renal tubular reabsorption of bicarbonate and increased renal excretion ofNa , K, and water. Water also is lost by salicylate-induced sweating (especially in the presence of hyperthermia) and hyperventilation dehydration, which can be profound, particularly in children, rapidly occurs. Because more water than electrolyte is lost through the lungs and by sweating, the dehydration is associated with hypernatremia. Prolonged exposure to high doses of salicylate also causes depletion ofK due to both renal and extrarenal factors. 

B. Effects The major renal effect is bicarbonate diuresis (ie, sodium bicarbonate is excreted) body bicarbonate is depleted, and metabolic acidosis results. As increased sodium is presented to the cortical collecting tubule, some of the excess sodium is reabsorbed and potassium is se-... 

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