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• W2888504014 endingPage "350" @default.
• W2888504014 startingPage "334" @default.
• W2888504014 abstract "Renal tubular acidosis (RTA) represents a group of diseases characterized by (1) a normal anion gap metabolic acidosis; (2) abnormalities in renal HCO3− absorption or new renal HCO3− generation; (3) changes in renal NH4+, Ca2+, K+, and H2O homeostasis; and (4) extrarenal manifestations that provide etiologic diagnostic clues. The focus of this review is to give a general overview of the pathogenesis of the various clinical syndromes causing RTA with a particular emphasis on type I (hypokalemic distal RTA) and type II (proximal) RTA while reviewing their pathogenesis from a physiological “bottom-up” approach. In addition, the factors involved in the generation of metabolic acidosis in both type I and II RTA are reviewed highlighting the importance of altered renal ammonia production/partitioning and new HCO3− generation. Our understanding of the underlying tubular transport and extrarenal abnormalities has significantly improved since the first recognition of RTA as a clinical entity because of significant advances in clinical acid-base chemistry, whole tubule and single-cell H+/base transport, and the molecular characterization of the various transporters and channels that are functionally affected in patients with RTA. Despite these advances, additional studies are needed to address the underlying mechanisms involved in hypokalemia, altered ammonia production/partitioning, hypercalciuria, nephrocalcinosis, cystic abnormalities, and CKD progression in these patients. Renal tubular acidosis (RTA) represents a group of diseases characterized by (1) a normal anion gap metabolic acidosis; (2) abnormalities in renal HCO3− absorption or new renal HCO3− generation; (3) changes in renal NH4+, Ca2+, K+, and H2O homeostasis; and (4) extrarenal manifestations that provide etiologic diagnostic clues. The focus of this review is to give a general overview of the pathogenesis of the various clinical syndromes causing RTA with a particular emphasis on type I (hypokalemic distal RTA) and type II (proximal) RTA while reviewing their pathogenesis from a physiological “bottom-up” approach. In addition, the factors involved in the generation of metabolic acidosis in both type I and II RTA are reviewed highlighting the importance of altered renal ammonia production/partitioning and new HCO3− generation. Our understanding of the underlying tubular transport and extrarenal abnormalities has significantly improved since the first recognition of RTA as a clinical entity because of significant advances in clinical acid-base chemistry, whole tubule and single-cell H+/base transport, and the molecular characterization of the various transporters and channels that are functionally affected in patients with RTA. Despite these advances, additional studies are needed to address the underlying mechanisms involved in hypokalemia, altered ammonia production/partitioning, hypercalciuria, nephrocalcinosis, cystic abnormalities, and CKD progression in these patients. Clinical Summary•Patients with renal tubular acidosis have a normal anion gap metabolic acidosis due to H+/base transport defects in the proximal tubule and collecting duct.•Clinicians should be aware of the associated abnormalities in renal monovalent cation (Na+, K+, NH4+), divalent cation (Ca2+), and water transport.•Extrarenal manifestions often provide important additional diagnostic clues. •Patients with renal tubular acidosis have a normal anion gap metabolic acidosis due to H+/base transport defects in the proximal tubule and collecting duct.•Clinicians should be aware of the associated abnormalities in renal monovalent cation (Na+, K+, NH4+), divalent cation (Ca2+), and water transport.•Extrarenal manifestions often provide important additional diagnostic clues." @default.
• W2888504014 created "2018-08-31" @default.
• W2888504014 creator A5048085772 @default.
• W2888504014 date "2018-07-01" @default.
• W2888504014 modified "2023-10-18" @default.
• W2888504014 title "Renal Tubular Acidosis: H+/Base and Ammonia Transport Abnormalities and Clinical Syndromes" @default.
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