A physiology-based approach to a patient with hyperkalemic renal tubular acidosis

Abstract

Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe a 54-year-old liver transplant patient that was admitted with flaccid muscle weakness associated with plasma potassium level of 9.25 mEq/L. Additional investigation revealed type 4 renal tubular acidosis and marked hypomagnesemia with high fractional excretion of magnesium. Relevant past medical history included a recent diagnosis of Paracoccidioidomycosis, a systemic fungal infection that is endemic in some parts of South America, and his outpatient medications contained trimethoprim-sulfamethoxazole, tacrolimus, and propranolol. In the present acid-base and electrolyte case study, we discuss a clinical approach for the diagnosis of hyperkalemic renal tubular acidosis and review the pathophysiology of this disorder.

Renal calcification in children with renal tubular acidosis: What a paediatrician ‎should ‎know‎

“…As aldosterone also regulates potassium levels in the body by enhancing its excretion in the urine, the reduced aldosterone activity in type 4 RTA leads to impaired potassium secretion, resulting in hyperkalemia. Patients with type 4 RTA can present with muscle weakness, arrhythmia, or even cardiac arrest due to hyperkalemia[ 9 , 51 ].…”

“…This can cause issues such as impaired growth and development, muscle wasting, bone demineralization (osteoporosis), and an increased risk of kidney stone formation. RTA can also disrupt electrolyte balance, leading to abnormalities like hypokalemia or hyperkalemia[ 9 ]. Hypokalemia can result in muscle weakness, fatigue, and cardiac arrhythmias, while hyperkalemia can be life-threatening and cause cardiac abnormalities.…”

Review: Management of Hyperkalemia in Kidney Transplant Recipients

“…[11] These mechanisms include impaired function of the sodiumchloride cotransporter (NCC) in the distal convoluted tubule as well as downregulation of mineralocorticoid expression via RAAS suppression leading to hyperkalemic type 4 renal tubular acidosis. [12] In addition, supratherapeutic CNI concentrations can result in afferent renal arteriolar vasoconstriction and acute kidney injury resulting in impaired potassium elimination. [13][14][15] These mechanisms offer insight into unique treatment options for hyperkalemia.…”