renal tubular acidosis


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Renal Tubular Acidosis

 

Definition

Renal tubular acidosis (RTA) is a condition characterized by too much acid in the body due to a defect in kidney function.

Description

Chemical 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 symptoms

There are three types of renal tubular acidosis. They include:
  • Distal renal tubular acidosis (type 1) may be a hereditary condition or may be triggered by an autoimmune disease, lithium therapy, kidney transplantation, or chronic obstruction.
  • Proximal renal tubular acidosis (type 2) is caused by hereditary diseases, such as Fanconi's syndrome, fructose intolerance, and Lowe's syndrome. It can also develop with vitamin D deficiency, kidney transplantation, heavy metal poisoning, and treatment with certain drugs.
  • Type 4 renal tubular acidosis is not hereditary, but is associated with diabetes mellitus, sickle cell anemia, an autoimmune disease, or an obstructed urinary tract.
Symptoms vary with the underlying mechanism of the defect and the readjustment of chemicals required to compensate for the defect.
  • Distal RTA results in high blood acidity and low blood potassium levels. Symptoms include mild dehydration; muscle weakness or paralysis (due to potassium deficiency); kidney stones (due to excess calcium in the urine); and bone fragility and pain.
  • Proximal RTA also results in high blood acidity and low blood potassium levels. Symptoms include mild dehydration.
  • Type 4 RTA is characterized by high blood acidity and high blood potassium levels; it rarely causes symptoms unless potassium levels rise so high as to cause heart arrhythmias or muscle paralysis.

Diagnosis

RTA 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.

Treatment

The 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.

Prognosis

Careful 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.

Prevention

Relatives of patients with the possibly hereditary forms of renal tubular acidosis should be tested.

Resources

Books

Chesney, 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 terms

Autoimmune 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.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

acidosis

 [as″ĭ-do´sis]
1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH.
2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidot´ic.

Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma.

In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, respiratory disorders, or liver disease.
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.
hyperchloremic acidosis renal tubular acidosis.
lactic acidosis a metabolic acidosis occurring as a result of excess lactic acid in the blood, due to conditions causing impaired cell respiration. It occurs most commonly in disorders in which oxygen is inadequately delivered to tissues, such as shock, septicemia, or extreme hypoxemia, but it can also result from exogenous or endogenous metabolic defects. Initially manifesting as hyperventilation, it progresses to mental confusion and coma.
metabolic acidosis any of the types of acidosis resulting from accumulation in the blood of keto acids (derived from fat metabolism) at the expense of bicarbonate; this diminishes the body's ability to neutralize acids. This type is contrasted with respiratory acidosis. It occurs when there is either an acid gain (as in diabetic ketoacidosis, lactic acidosis, poisoning, or failure of the renal tubules to reabsorb bicarbonate) or a bicarbonate loss (as in diarrhea or a gastrointestinal fistula).

The symptoms of metabolic acidosis include weakness, malaise, and headache. As the acid level goes up these symptoms progress to stupor, unconsciousness, coma, and death. The breath may have a fruity odor owing to the presence of acetone, and the patient may experience vomiting and diarrhea. Loss of fluids can deplete body fluid content and aggravate the acidosis. Hyperventilation may occur as a result of stimulation of the hypothalamus. blood gas analysis will reveal a lowered pH and an elevated PaCO2. (See accompanying table.)
Treatment and Patient Care. Treatment of metabolic acidosis is primarily concerned with control of the underlying causes. Diabetic ketoacidosis may be corrected by the administration of insulin and fluids. In acute renal failure the patient requires dialysis, and in chronic uremic acidosis the condition is controlled by restricting sodium intake and buffering with bicarbonate. The patient's vital signs should be checked frequently to assess the progress of compensation. A rising pulse rate and a drop in blood pressure frequently occur as a result of hypovolemia in the diabetic-acidotic patient, and cardiac arrhythmias can be caused by increased calcium levels in the blood. A careful recording of intake and output provides a means of determining the kidneys' ability to regulate the acid-base balance. Safety measures to avoid injury during involuntary muscular contractions should be carried out. (See also convulsions.) Nursing measures to relieve discomfort from vomiting and to avoid the hazards of aspiration of vomitus are required. Education of the patient and family in the prevention of acute episodes of metabolic acidosis, particularly diabetic ketoacidosis, is of primary importance.
renal tubular acidosis (RTA) a metabolic acidosis resulting from impairment of the reabsorption of bicarbonate by the renal tubules, characterized by low plasma bicarbonate and high plasma chloride; the urine is alkaline.
respiratory acidosis acidosis resulting from ventilatory impairment and subsequent retention of carbon dioxide, in contrast to metabolic acidosis. The respiratory system has an important role in maintaining acid-base balance. In response to an increase in the hydrogen ion concentration in body fluids, the respiratory rate increases, causing more carbon dioxide to be released from the lung. When either an acute obstruction of the airways or a chronic condition involving the organs of respiration causes interference with the exhalation of the carbon dioxide produced by metabolic activity, carbon dioxide accumulates in the blood and unites with water to form carbonic acid.

Acute respiratory acidosis occurs when there is a relatively sudden malfunction of respiratory activities, as in upper airway obstruction, acute infections and inflammation of the lung and bronchial tissues, and pulmonary edema. In acute respiratory acidosis the compensatory chemical buffer systems are of limited benefit in restoring the acid-base balance because they depend on normal blood circulation and tissue perfusion for optimal effect. The physiologic regulators, the lungs and kidneys, are of little help because the lungs are malfunctioning and the kidneys require more time to compensate than the acute condition permits.

Chronic respiratory acidosis results from gradual and irreversible loss of ventilatory function, as in chronic obstructive pulmonary disease (COPD). Although the patient in this condition does have an increased retention of CO2, there is time for the kidneys to compensate by retaining bicarbonate and thereby maintaining a pH within tolerable limits. If, however, even a minor respiratory infection develops, the patient is subject to a rapidly developing state of acute acidosis because the lungs cannot be depended upon to remove more than a minimal amount of CO2.
Treatment and Patient Care. The initial treatment for acute respiratory acidosis is to establish an airway immediately and maintain adequate ventilation and hydration. Acute cases may require the use of an endotracheal tube or tracheostomy tube. Some form of intermittent positive pressure breathing is applied through a machine-driven ventilator, essentially to force adequate O2 delivery and concomitant CO2 removal from the lungs, thereby avoiding further rises in CO2 levels to the point that CO2 narcosis will develop. Beyond a certain point the respiratory center may cease responding to the higher CO2 levels, and breathing will stop abruptly. Drugs that further depress the respiratory center (narcotics, hypnotics, and tranquilizers) must be avoided. Patients in the acute stage are watched for cessation of breathing and cardiac arrest. cardiopulmonary resuscitation may be required to revive the patient.

It is recommended that oxygen administration be limited in patients with chronic obstructive pulmonary disease (COPD). In COPD the stimulus to breathe is a hypoxic state, therefore administration of high concentrations of O2 will remove this needed stimulus. The rate of oxygen flow should be closely correlated with blood gas studies. In patients with acute lung diseases the stimulus to breathe is still dependent on CO2 concentrations, so that O2 can be supplied without fear of inhibiting the stimulus to breathe.

Measures that facilitate breathing are essential to patient care during respiratory acidosis. Frequent turning, coughing, and deep breathing exercises to encourage oxygen–carbon dioxide exchange are beneficial, as is suctioning when needed to remove secretions obstructing the airway. postural drainage, unless contraindicated by the patient's condition, may be effective in promoting adequate ventilation.
starvation acidosis a metabolic acidosis due to accumulation of ketones following a severe caloric deficit.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

re·nal tu·bu·lar ac·i·do·sis (RTA),

a clinical syndrome characterized by decreased ability to acidify urine, and by low plasma bicarbonate and high plasma chloride concentrations, often with hypokalemia; often complicated by osteomalacia, nephrocalcinosis, or renal calculi.
See also: primary renal tubular acidosis, secondary renal tubular acidosis.
Farlex Partner Medical Dictionary © Farlex 2012

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
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

re·nal tu·bu·lar ac·id·o·sis

(rē'năl tū'byū-lăr as'i-dō'sis)
A clinical syndrome characterized by decreased ability to acidify urine, and by low plasma bicarbonate and high plasma chloride concentrations, often with hypokalemia.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
References in periodicals archive ?
Distal renal tubular acidosis was present in six (6%) patients while four (5%) had no identifiable cause of calculus disease.
Hess, "Prevalence and densitometric characteristics of incomplete distal renal tubular acidosis in men with recurrent calcium nephrolithiasis," Urological Research, vol.
Arruda, "Hyperkalemic renal tubular acidosis: Effect of furosemide in humans and in rats," Kidney International, vol.
Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosis. J Am Soc Nephrol 1992;3:264-71.
Celik, "A primary Sjogren's syndrome patient with distal renal tubular acidosis, who presented with symptoms of hypokalemic periodic paralysis: report of a case study and review of the literature," Rheumatology International, vol.
His renal tubular acidosis remains and it will only be a matter of time before he needs another op.
Differential diagnosis included secretory form of CDD with secondary lactic acidosis and renal tubular acidosis. Evaluation of CDD included negative stool white blood cells, blood, urine, cerebrospinal fluid and stool cultures as well as virology on multiple occasions.
Type 1 or distal renal tubular acidosis (dRTA) is an uncommon condition in adults, usually associated with autoimmune disorders (1).
(6) A positive urine AG (in the range of 20 - 30 mmol/l) indicates that impaired secretion of H+ ions, as found in distal renal tubular acidosis, plays a role in the evolution of the acidosis.