Reabsorption of bicarbonate is typically 80-90% in the proximal tubule and failure of this process leads to decreased systemic buffer and metabolic acidosis. The distal intercalated cells function normally, so the acidemia is less severe than dRTA and the alpha intercalated cells can produce H+ to acidify the urine to a pH of less than 5.3. pRTA also has several causes, and may occasionally be present as a solitary defect, but is usually associated with a more generalized dysfunction of the proximal tubular cells called Fanconi syndrome, in which there is also phosphaturia, glycosuria, aminoaciduria, uricosuria, and tubular proteinuria.The principal feature of Fanconi syndrome is bone demineralization (osteomalacia or rickets) due to phosphate wasting. Type 3: combined proximal and distal
In some patients, RTA shares features of both dRTA and pRTA. This rare pattern was observed in the 1960s and 1970s as a transient phenomenon in infants and children with dRTA (possibly in relation with some exogenous factor such as high salt intake) and is no longer observed. This form of RTA has also been referred to as juvenile RTA.Combined dRTA and pRTA is also observed as the result of inherited carbonic anhydrase II deficiency. Mutations in the gene encoding this enzyme give rise to an autosomal recessive syndrome of osteopetrosis, renal tubular acidosis, cerebral calcification, and mental retardation. It is very rare and cases from all over the world have been reported, of which about 70% are from the Maghreb region of North Africa, possibly due to the high prevalence of consanguinity there.
Types
An overview of types 1, 2, and 4 is presented below (type 3 is usually excluded from modern classifications):

Type 1: distal
Distal RTA (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of H+ secretion into lumen of nephron by the alpha intercalated cells of the medullary collecting duct of the distal nephron.This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Because renal excretion is the primary means of eliminating H+ from the body, there is consequently a tendency towards acidemia. There is an inability to excrete H+ while K+ cannot be reclaimed by the cell, leading to acidemia (as H+ builds up in the body) and hypokalemia (as K+ cannot be reabsorbed by the alpha cell).This leads to the clinical features of dRTA; In other words, the intercalated cells apical H+/K+ antiporter is non-functional, resulting in proton retention and potassium excretion. Since calcium phosphate stones demonstrate a proclivity for deposition at higher pHs (alkaline), the substance of the kidney develops stones bilaterally; this does not occur in the other RTA types. Normal anion gap metabolic acidosis/acidemia
Hypokalemia, Hypocalcemia, Hyperchloremia
Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate).