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The term renal tubular acidosis (RTA) is applied to a group of transport defects in the reabsorption of bicarbonate (HCO3_), the excretion of hydrogen ion (H_), or both. This condition was first described in 1935, confirmed as a renal tubular disorder in 1946, and designated "renal tubular acidosis" in 1951. The RTA syndromes are characterized by a relatively normal GFR and a metabolic acidosis accompanied by hyperchloremia and a normal plasma anion gap.
RTA is classified into 4 major forms: distal, proximal, hyperkalemic and combined RTA. Distal RTA is associated with reduced urinary acid secretion, proximal RTA ( pRTA ) is characterized by impaired bicarbonate (HCO3_) reabsorption, hyperkalemic RTA is an acid-base disturbance generated by aldosterone deficiency or resistance and combined RTA is due to carbonic anhydrase II deficiency. Electrolyte and acid-base disturbances are key components of each disorder .
Patients with pRTA present with growth failure in the 1st yr of life. Additional symptoms can include polyuria, dehydration (from sodium loss), anorexia, vomiting, constipation, and hypotonia. Patients with primary Fanconi syndrome have additional symptoms, secondary to phosphate wasting, such as rickets. Hypokalemia and related symptoms are also restricted to cases with the Fanconi syndrome.
Distal RTA shares features with those of pRTA, including non-anion gap metabolic acidosis and growth failure; distinguishing features of distal RTA include nephrocalcinosis and hypercalciuria Combined proximal and distal RTA is a type observed as the result of inherited carbonic anhydrase II deficiency in different organs and systems.
Patients with type IV RTA can present with growth failure in the first few years of life. Polyuria and dehydration (from salt wasting) are common. Laboratory tests reveal a hyperkalemic non-anion gap metabolic acidosis. Urine may be alkaline or acidic. Elevated urinary sodium levels with inappropriately low urinary potassium levels reflect the absence of aldosterone effect .
The first step in the evaluation of a patient with suspected RTA is to confirm the presence of a normal anion gap metabolic acidosis, identify electrolyte abnormalities, assess renal function, and rule out other causes of bicarbonate loss such as diarrhea .
The mainstay of therapy in all forms of RTA is bicarbonate replacement. Patients with pRTA often require large quantities of bicarbonate, up to 20 mEq/kg/24 hr. The base requirement for distal RTAs is generally in the range of 2-4 mEq/kg/24 hr, although patients' requirements can vary. Patients with type IV RTA can require chronic treatment for hyperkalemia with sodium potassium exchange resin .
Renal Tubule Acidosis
Arterial blood gases, Blood anion gap, serum electrolytes, renal function test, urine analysis
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Published on BioPortfolio: 2017-08-31T20:23:22-0400
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The reuptake of water, ELECTROLYTES, and other substances by the KIDNEY to the blood supply.
The amount of the RENAL BLOOD FLOW that is going to the functional renal tissue, i.e., parts of the KIDNEY that are involved in production of URINE.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
The presence of an increased amount of blood in a body part or an organ leading to congestion or engorgement of blood vessels. Hyperemia can be due to increase of blood flow into the area (active or arterial), or due to obstruction of outflow of blood from the area (passive or venous).
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