Renal tubular acidosis (RTA) is a group of clinical syndromes caused by obstruction of proximal renal tubular reabsorption of HCO3- or dysfunction of distal renal tubular secretion H+, being characterized by hyperchloremic metabolic acidosis with normal anion gap. The clinical manifestations of RTA are complex and diverse, and growth retardation is the most common. RTA can be classified into 4 types according to the location of renal tubular damage and clinical manifestations: type Ⅰ RTA (distal RTA), type Ⅱ RTA (proximal RTA), type Ⅲ RTA (mixed RTA), and type Ⅳ RTA (hyperkalemia RTA). The same gene mutation of RTA can lead to different clinical phenotypes, and different pathogenic genes can also lead to similar clinical phenotypes. The goal of RTA treatment is to correct metabolic acidosis and avoid complications. ADV7103, a novel, extended⁃release drug formulation that combines the advantages of potassium citrate and potassium bicarbonate, is superior to traditional standard treatment in controlling metabolic acidosis. Patients receiving adequate alkali therapy in the early stage generally have a favorable prognosis, but complications may still occur or persist for a long time. This paper mainly reviews the characteristics of different types of RTA, RTA related gene mutations, and treatment and prognosis of RTA, etc., aiming at improving clinicians' understanding of this disease.

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