Renal Tubular Acidosis

Below you will find more information about Renal Tubular Acidosis from Medigest. If you believe that you are suffering from any of the symptoms of Renal Tubular Acidosis it is important that you obtain an accurate diagnosis from a medical professional to ensure that you obtain the correct medication or treatment for your condition. There are medical conditions that carry similar symptoms associated with Renal Tubular Acidosis and therefore the information provided by Medigest is offered as a guideline only and should never be used in preference to seeking professional medical advice. The information relating to Renal Tubular Acidosis comes from a third party source and Medigest will not be held liable for any inaccuracies relating to the information shown.


Renal tubular acidosis (RTA) is characterized by the accumulation of acid in the body as a consequence of the failure of the kidney to adequately acidify urine. The term renal tubular acidosis is attributed mostly to defective urinary acidification in otherwise well-functioning kidneys. There are different forms of renal tubular acidosis, each of which has different causes and symptoms.


Treatment depends on the type of renal tubular acidosis present. Patients affected with Types 1 and 2 RTA are usually advised to drink a solution of sodium bicarbonate (commonly known as baking soda) daily to neutralize the acid produced from food. This form of therapy alleviates symptoms and prevents further kidney failure and bone disease. Potassium supplements and other solutions to target RTA are also prescribed. For type 4 RTA patients, the acidosis is often so mild that bicarbonates are not necessary. Elevated levels of potassium in blood can usually be controlled by restricting potassium intake, avoiding dehydration, and substituting or adjusting the dosages of certain drugs.

Symptoms and Signs

The first type of renal tubular acidosis, Distal RTA (dRTA), is the most common form. Symptoms of Type I RTA include normal anion gap metabolic acidosis, urinary stone formation, mild to severe hypokalemia, bone demineralisation (resulting in rickets in children and osteomalacia in adults), and nephrocalcinosis (or deposition of calcium in the substance of the kidney). The second most common type of RTA, proximal RTA (pRTA), is associated with a more generalized malfunction of the proximal tubular cells, but may also occur as a solitary defect. The common feature of pRTA is bone demineralization as a consequence of phosphate wasting. Type 3 RTA is a rare mix of dRTA and pRTA, and pertains to a genetic defect which results in osteopetrosis, distal renal tubular acidosis, proximal renal tubular acidosis, cerebral calcification and subsequent mental impairment. Meanwhile, Type 4 RTA is not actually a tubular disorder at all and does not have a clinical syndrome consistent with other types of renal tubular acidosis. It is, however, associated with a mild metabolic acidosis resulting from a physiological reduction in distal tubular ammonium excretion (secondary to hypoaldosteronism). The most common symptom of Type 4 RTA is hyperkalemia. The metabolic acidosis that results from renal tubular acidosis may be caused either by failure to recover sufficient alkaline (or bicarbonate ions) from the filtrate (blood filtered by the kidneys) in the early portion of the nephron (proximal tubule) or by insufficient secretion of acid (hydrogen ions) into the latter portions of the nephron (distal tubule). Each form of renal tubular acidosis has its own distinct set of potential causes.

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