Acid-base balance renal

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Excretion into urine of ammonia produced by renal mbu-lar cells facilitates cation conservation and regulation of acid-base balance. Ammonia production from intracellular renal amino acids, especially glutamine, increases in metabolic acidosis and decreases in metabolic alkalosis. 

Along with the respiratory system, the renal system maintains acid-base balance by altering the excretion of hydrogen and bicarbonate ions in the urine. When the extracellular fluid becomes acidic and pH decreases, the... 

Kidney Failure, Chronic An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body s electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH]... 

Pharmacology Potassium participates in a number of essential physiological processes, such as maintenance of intracellular tonicity and a proper relationship with sodium across cell membranes, cellular metabolism, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscle, acid-base balance, and maintenance of normal renal function. Normal potassium serum levels range from 3.5 to 5 mEq/L. 

Alkalinization of urine Hematuria, renal colic, costovertebral pain, and formation of urate stones associated with use in gouty patients may be prevented by alkalization of urine and liberal fluid intake monitor acid-base balance. 

Mechanism of Action An electrolyte that is necessary for multiple cellular metabolic processes. Primary action is intracellular. Therapeutic Effect Needed for nerve impulse conduction and contraction of cardiac, skeletal, and smooth muscle maintains normal renal function and acid-base balance. 

Mechanism of action The thiazide derivatives act mainly in the distal tubule to decrease the reabsorption of Na+ by inhibition of a Na+/CI cotransporter on the luminal membrane (see Figure 23.2). They have a lesser effect in the proximal tubule. As a result, these drugs increase the concentration of Na+ and Cl- in the tubular fluid. The acid-base balance is not usually affected. [Note Because the site of action of the thiazide derivatives is on the luminal membrane, these drugs must be excreted into the tubular lumen to be effective. Therefore, with decreased renal function, thiazide diuretics lose efficacy.]... 

The kidneys not only secrete hydrogen ions but they also regenerate bicarbonate ions. The renal handling of electrolytes also influences acid-base balance. 

Aluminium hydroxide reacts with HCl to form aluminium chloride this in turn reacts with intestinal secretions to produce insoluble salts, especially phosphate. The chloride is released and reabsorbed so systemic acid-base balance is not altered. It tends to constipate. Sufficient aluminium may be absorbed from the intestine to create a risk of encephalopathy in patients with chronic renal failure. Hypophosphataemia and hypophosphaturia may result from impaired absorption due to phosphate binding. 

The electrolytes and acid-base balance should be restored in careful coordination with the renal function. In hyponatraemia, either the fluid intake should be reduced to 700-1,000 ml/day, or a combination of a hypertonic salt solution (3%) and a loop diuretic should be administered intravenously, (s. p. 308) Likewise, an attempt can be made using a combination of diuretics and urea diuresis. Generally, sodium and water intake should be restricted. It is imperative to achieve an even volumetric balance, possibly supported by the cautious intake of fluid. 

Factors that regulate distal tubular secretion of are intalce of Na" and K, plasma concentration of mineralocor-ticoids, and acid-base balance. Because renal conservation mechanisms are slow to respond, depletion can be an early consequence of restricted intake or losses of K by extrarenal routes. Diminished glomerular filtration rate is typical of renal failure, and the consequent decrease in distal tubular flow rate is an important factor in the retention of K seen in chronic renal failure. Renal tubular acidosis and metaboUc and respiratory acidoses and alkaloses also affect renal regulation of excretion. These topics are discussed in much greater detail in Chapters 45 and 46. 

Renal Mechanisms in the Regulation of Acid-Base Balance... 

Continuous renal replacement therapy (CRRT) is used for the management of fluid overload and the removal of uremic toxins in patients with ARF and other conditions." The several forms of CRRT are extensively described in Chap. 42. Which of these therapies will be optimal for a given patient is dependent on several factors, including bleeding risk, degree of hypercatabolism, acid-base balance, and experience of the health care provider. 

Dow SW, Fettman MJ, Smith KR, et al. 1990. Effects of dietary acidification and potassium depletion on acid-base balance, mineral metabolism and renal function in adult cats. J Nutr 120(6) 569-578. 

Note that haemodialysis and peritoneal dialysis may relieve many of the symptoms of chronic renal failure and rectify abnormal fluid and electrolyte and acid-base balance. These treatments do not. however, reverse the other metabtilic, endocrine or haematological consequences of chronic renal failure. 

Respiratory alkalosis is much less common than acidosis but can occur when respiration is stimulated or is no longer subjcci to feedback control (Fig. 4). Usually these are acute conditions, and there is no renal compensation. The treatment is to inhibit or remove the cause of the hyperventilation, and the acid-base balance should return to normal. Examples are ... 

Phenacetin has analgesic and antipyretic but no antiinflammatory properties. Phenacetin and its deethylated metabolite, acetaminophen, are superior to aspirin in that they do not cause hypoprothrombinemia, GI irritation, or disturbances of acid-base balance. The serious, but rare, side effects of phenacetin are methemoglobinemia, hemolytic anemia, fatal hepatic necrosis, and hypoglycemic coma. Both interstitial nephritis and renal papillary necrosis can be caused by phenacetin and acetaminophen. The less toxic acetaminophen should be used only in patients who cannot tolerate aspirin or in whom aspirin is contraindicated (see also Table 3). 

This major extracellular anion plays an important role together with sodium in maintaining osmolality and acid-base balance, and in the central nervous system (e.g., where chloride facilitates the effects of some inhibitory compounds such as gamma aminobutyrate in neurons). After passing freely through the renal glomeruli, chloride is passively reabsorbed in the proximal convoluted tubules and actively reabsorbed in the loop of Henle by an active chloride pump. It is also reabsorbed with sodium in the distal tubules. In most situations, plasma sodium and chloride tend to parallel each other. 

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. 

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-... 

Firstly, the influence of main dietary representants, the carbohydrates, the fats, and the proteins on the acid—base balance should be mentioned. In addition, the function of the biosynthesized uric acid on the alkali reserve will be discussed in some detail. Subsequently, some quantitative aspects of uric acid synthesis, turnover, and renal and extrarenal excretion in healthy persons and gouty patients will be dealt with, followed by the detailed description of a special mechanism, preserving the serum bicarbonate by mobilization of bone phosphates. Finally, some clinical observations, supporting our concep- tion of the interrelation between hyperproduced uric acid and acid-base balance, will be discussed briefly. 

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