![]() In particular, the distal form (type 1) is associated with diminished H(+)-ATPase activity, impairing the ability to maximally acidify the urine. Sjögren Syndrome, renal tubular acidosis, severe hypokalaemia, nephrocalcinosis INTRODUCTIONĪ renal tubular acidosis (RTA) may be suspected in the presence of metabolic acidosis and hypokalaemia, secondary to high urinary excretion of potassium as a natural renal buffering mechanism. These can be avoided if there is a prompt diagnosis leading to potassium supplementation, alkali replacement therapy and immunomodulation. Severe hypokalaemia, nephrolithiasis, nephrocalcinosis, and chronic renal failure are among SS-associated type 1 renal tubular acidosis (RTA1) complications. ![]() The renal tubular acidosis in the presence of SS is usually due to auto-immune lymphocytic tubular infiltration.Sjögren Syndrome (SS) can lead to cutaneous involvement (hypergammaglobulinemic vasculitis) and also kidney SS-involvement characterized by renal tubular acidosis. ![]() A significant clinical improvement was achieved following adequate treatment.Ĭonclusion: Extra-glandular involvement in SS is usually due to autoimmune lymphocytic infiltration and severe complications can be avoided if there is a prompt diagnosis. Results: Additional evaluation confirmed primary SS with type 1 renal tubular acidosis (RTA1) and gammaglobulin-mediated vasculitis. ![]() Materials and methods: A case of a 32-year-old woman presenting with flaccid tetraparesis, in the setting of severe hypokalaemia, is described. Objectives: To highlight systemic involvement features in Sjögren Syndrome (SS). ![]()
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