Renal Tubular Acidosis and Management Strategies: A Narrative Review

Abstract

Renal tubular acidosis (RTA) occurs when the kidneys are unable to maintain normal acid−base homeostasis because of tubular defects in acid excretion or bicarbonate ion reabsorption. Using illustrative clinical cases, this review describes the main types of RTA observed in clinical practice and provides an overview of their diagnosis and treatment. The three major forms of RTA are distal RTA (type 1; characterized by impaired acid excretion), proximal RTA (type 2; caused by defects in reabsorption of filtered bicarbonate), and hyperkalemic RTA (type 4; caused by abnormal excretion of acid and potassium in the collecting duct). Type 3 RTA is a rare form of the disease with features of both distal and proximal RTA. Accurate diagnosis of RTA plays an important role in optimal patient management. The diagnosis of distal versus proximal RTA involves assessment of urinary acid and bicarbonate secretion, while in hyperkalemic RTA, selective aldosterone deficiency or resistance to its effects is confirmed after exclusion of other causes of hyperkalemia. Treatment options include alkali therapy in patients with distal or proximal RTA and lowering of serum potassium concentrations through dietary modification and potential new pharmacotherapies in patients with hyperkalemic RTA including newer potassium binders.

Utilization of Nursing Defect Management Evaluation and Deep Learning in Nursing Process Reengineering Optimization

“…Nursing defect management has an important environment in nursing safety management. Nursing defects are reported in time, which can find problems in nursing work environment for managers to avoid similar problems [10]. The adverse events that have occurred are scientifically handled, and the root causes of the system are corrected to avoid the recurrence of defects.…”

Review of the Pathophysiologic and Clinical Aspects of Hypokalemia in Children and Young Adults: an Update

“…Potassium balance plays a crucial role in the regulation of acid-base homeostasis. During metabolic acidosis, there is an exchange of K + for the extracellular H + , thereby providing a basis for the PT cell to generate NH 3 , and thereafter causes urinary excretion of net ammonium acids [ 57 •]. Close to 100% of the filtered potassium is reabsorbed by PT and the TALH [ 56 ].…”

“…The early section of the principal cell (DCT1) has apical NCCT, and the later part has ENaC (DCT2) [ 39 ••, 60 ]. Type A intercalated cells (IC) on the CCD has a luminal proton pump and H + -K + -ATPase, and type B IC has apical Cl − /HC03 − exchanger (Pendrin) [ 39 ••, 57 •, 62 ]. Sodium uptake by ENaC generates a lumen-negative PD, which in turn increases a basal amount of K + recycle by the apical ROMK (Kir1.1) of the DCT2 [ 39 ••, 57 •].…”

“…Type A intercalated cells (IC) on the CCD has a luminal proton pump and H + -K + -ATPase, and type B IC has apical Cl − /HC03 − exchanger (Pendrin) [ 39 ••, 57 •, 62 ]. Sodium uptake by ENaC generates a lumen-negative PD, which in turn increases a basal amount of K + recycle by the apical ROMK (Kir1.1) of the DCT2 [ 39 ••, 57 •]. An apical Maxi-K with a larger capacitance is recruited to handle greater demand for K + secretion (as in hyperkalemia and/or higher tubular flow) [ 39 ••, 61 ].…”

“…A lower sodium delivery to DCT2 reduces the expression of ENaC, reduces K secretion, and therefore corrects the potassium deficiency [ 63 ]. CCD contributes to acid-base regulation such that negative lumen created by ENaC through Na + absorption enhances H + secretion by type A IC [ 39 ••, 57 •, 62 ].…”