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renal tubular acidosis |
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Renal Tubular Acidosis DefinitionRenal tubular acidosis (RTA) is a condition characterized by too much acid in the body due to a defect in kidney function. DescriptionChemical balance is critical to the body's functioning. Therefore, the body controls its chemicals very strictly. The acid-base balance must be between a pH of 7.35 and 7.45 or trouble will start. Every other chemical in the body is affected by the acid-base balance. The most important chemicals in this system are sodium, chloride, potassium, calcium, ammonium, carbon dioxide, oxygen, and phosphates. The lungs rapidly adjust acid-base balance by the speed of breathing, because carbon dioxide dissolved in water is an acidߞcarbonic acid. Faster breathing eliminates more carbon dioxide, decreases the carbonic acid in the blood and increases the pH. Holding your breath does the opposite. Blood acidity from carbon dioxide controls the rate of breathing, not oxygen. The kidneys also regulate acid-base balance somewhat more slowly than the lungs. They handle all the chemicals, often trading one for another that is more or less acidic. The trading takes place between the blood and the urine, so that extra chemicals end up passing out of the body. If the kidneys do not effectively eliminate acid, it builds up in the blood, leading to a condition called metabolic acidosis. These conditions are called renal tubular acidosis. Causes and symptomsThere are three types of renal tubular acidosis. They include:
Symptoms vary with the underlying mechanism of the defect and the readjustment of chemicals required to compensate for the defect.
DiagnosisRTA is suspected when a person has certain symptoms indicative of the disease or when routine tests show high blood acid levels and low blood potassium levels. From there, more testing of blood and urine chemicals will help determine the type of RTA present. TreatmentThe foundation of treatment for RTA types 1 and 2 is replacement of alkali (base) by drinking a bicarbonate solution daily. Potassium may also have to be replaced, and other chemicals added to maintain balance. In type 4 RTA acidity will normalize if potassium is reduced. This is done by changing the diet and by using diuretic medicines that promote potassium excretion in the urine. PrognosisCareful balancing of body chemicals will usually produce good results. If there is an underlying disease responsible for the kidney malfunction, it may be the determining factor in the prognosis. PreventionRelatives of patients with the possibly hereditary forms of renal tubular acidosis should be tested. ResourcesBooksChesney, Russell W. "Specific Renal Tubular Disorders." In Cecil Textbook of Medicine, edited by J. Claude Bennett and Fred Plum. Philadelphia: W. B. Saunders Co., 1996. Key termsAutoimmune disease — Type of diseases characterized by antibodies that attack the body's own tissues. Fanconi's syndrome — A disorder of the kidneys characterized by glucose in the urine. Lowe's syndrome — A rare inherited disorder that is distinguished by congenital cataracts, glaucoma, and severe mental retardation. Rickets — A deficiency disease that affects the bone development of growing bodies, usually causing soft bones.
renal tubular acidosis (RTA), an abnormal condition associated with persistent dehydration, metabolic acidosis, hypokalemia, hyperchloremia, and nephrocalcinosis. It is caused by the kidney's inability to conserve bicarbonate and to adequately acidify the urine. Some forms of RTA are more prevalent in women, older children, and young adults. Prolonged RTA can cause hypercalciuria and the formation of kidney stones. Prognosis depends on treatment and the extent of renal damage but is usually good. Compare distal renal tubular acidosis, ketoacidosis, metabolic acidosis, proximal renal tubular acidosis, respiratory acidosis. observations Common signs and symptoms of RTA, especially in children, include anorexia, vomiting, constipation, retarded growth, excessive urination, nephrocalcinosis, and rickets. RTA can also cause urinary tract infections and pyelonephritis. Confirming diagnosis of distal RTA is based on laboratory tests that show impaired urine acidification in association with systemic metabolic acidosis. Confirming diagnosis of proximal RTA is based on tests that show bicarbonate wasting as a result of impaired reabsorption. Other significant laboratory findings may include decreased sodium bicarbonate, pH, potassium, and phosphorus; increased serum chloride, alkaline phosphatase, urinary bicarbonate, and potassium; and urine with low specific gravity. interventions Treatment includes the replacement of excessively secreted substances, especially bicarbonate, and may include the administration of sodium bicarbonate tablets, potassium, vitamin D to preserve calcium metabolism, and antibiotics to counter pyelonephritis. Surgery may be required to remove renal calculi. nursing considerations The nurse carefully monitors the results of altered laboratory tests, especially those involving potassium levels and urine pH. The patient's urine is strained to capture any kidney stones for analysis, and the nurse is alert to any signs of hematuria. A patient with a low potassium level is usually advised to eat potassium-rich foods such as bananas, oranges, and baked potatoes. The patient and family are encouraged to seek genetic counseling and RTA screening. acidosis a pathological condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biological activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. It is rare that acidosis occurs in the absence of some underlying disease process. The more obvious signs of severe acidosis are muscle twitching, involuntary movement, cardiac arrhythmias, disorientation and coma. compensated acidosis a condition in which the compensatory mechanisms have returned the pH toward normal. diabetic acidosis a metabolic acidosis produced by accumulation of ketones in uncontrolled diabetes mellitus. hypercapnic acidosis respiratory acidosis. iatrogenic acidosis may result from administration of drugs, such as urinary acidifiers, or anesthetic agents which depress respiration. lactic acidosis the accumulation of lactate in the rumen in ruminants and the stomach of horses, and hence in the blood, as a result of overfeeding with readily fermentable carbohydrate. See also carbohydrate engorgement. metabolic acidosis acidosis resulting from accumulation in the blood of keto acids (derived from fat metabolism) at the expense of bicarbonate, thus diminishing the body's ability to neutralize acids. This type of acidosis can occur when there is an acid gain, as in diabetic ketoacidosis, lactic acidosis, poisoning and failure of the renal tubules to reabsorb bicarbonate. It can also result from bicarbonate loss due to diarrhea or a gastrointestinal fistula. mixed alkalosis and acidosis characterized by low serum chloride, normal or slightly elevated plasma bicarbonate and a very high anion gap. organic acidosis accumulation of organic anions occurs in uremia, diabetic acidosis and lactic acidosis, and ingestion of salicylates, ethylene glycol or methanol. renal tubular acidosis renal tubular malfunction leads to faulty resorption of bicarbonate or excretion of acid and the production of alkaline urine; types I (distal tubular acidosis) and II (proximal tubular acidosis) are identified. respiratory acidosis acidosis resulting from ventilatory impairment and subsequent retention of carbon dioxide. ruminal acidosis acidosis caused by an altered metabolic state, usually lactic acidosis, in the rumen. starvation acidosis a metabolic acidosis due to accumulation of ketones following a severe caloric deficit. uncompensated acidosis a condition in which the compensatory mechanisms have not been applied sufficiently to return the pH of the blood to normal. uremic acidosis see metabolic acidosis (above). renal tubular acidosis Nephrology A condition characterized by functional defects in the distal renal tubules, with inability to form ammonia and exchange hydrogen ions; GFR is normal with persistent metabolic acidosis, hyperchloremia, ↓
urine excretion of acid; the acid pH results in hypercalcemia–kidney stones, excess calcium excretion, and bone demineralization Lab Acid urine, acidosis, ↓ bicarbonate excretion, ↓ ammonium clearance, ↓ K+ clearance,
calcium loss
Renal tubular acidosis
Type I 'Classic' distal RTA, which is due to a selective defect–in secretion of H+–in distal tubule acidification, resulting in a defect in the pH gradient, causing hyperchloremia (with persistent
bicarbonate excretion/↓ reabsorption of bicarbonate), hypokalemia and metabolic acidosis; the urinary pH is inappropriately high (> 6)
Type II Proximal RTA is accompanied by ↓ acidification of the proximal tubule; when the blood pH is ↓, tubular acidification occurs normally; when plasma bicarbonate normalizes, type II RTA wastes bicarbonate, causing metabolic
acidosis, as well as hyperchloremia and hypokalemia, which may be accompanied by Fanconi syndrome with loss of glucose and amino acids, phosphate, calcium, potassium; these Pts are prone to osteopenia, rickets and kidney stones
'Type III' A designation once applied to infants with renal bicarbonate wasting, now considered a type I RTA subtype
Type IV RTA Generalized–nonselective distal RTA, due to aldosterone deficiency or antagonism; hyperchloremia, hyperkalemia, metabolic acidosis, salt wasting
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