Nephrocalcinosis (deposition of calcium in the substance of the kidney)
Bone demineralisation (causing rickets in children and osteomalacia in adults)
Growth deficiency
Medullary cysts
Sensorineural hearing loss
Hereditary hemolytic anemiaDistal RTA has also been linked to specific genetic mutations that will alter when the disease will present in the patients life. Patients with mutations in ATP6V1B1 and ATP6V0A4 will present with symptoms within the first year of life, while those with mutation of the SLC4A1 have delayed onset around 10 years of age. Electrolyte imbalances remain the same, while in severe cases symptoms can advance to amino aciduria and hyperammonemia. In a large Asian series of Distal renal Tubular Acidosis in Sjogrens Syndrome, late diagnosis is a rule in spite of overt hypokalemic periodic paralysis in a vast majority of themdRTA is the most common form of RTA diagnosed in Western countries, and can be classified as either hereditary (primary) or acquired (secondary). Primary RTA generally results from systemic and autoimmune diseases or drug and toxin exposure in adults, whereas pediatric RTA results from genetic defects in the proteins that facilitate urine acidification at the distal tubule. Hereditary dRTA generally presents as failure to thrive during the first several months of life. Other common clinical manifestations in children include a variety of gastrointestinal and urinary symptoms, including polyuria, polydipsia, constipation, diarrhea, bouts of dehydration, and decreased appetite. Type 2: proximal
Proximal RTA (pRTA) is caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia.
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).