Overview of Hyperkalemic Renal Tubular Acidosis
Hyperkalemic renal tubular acidosis, also known as type IV renal tubular acidosis, is a condition characterized by dysfunction of the cation-exchange segment of the distal renal tubule, which is responsible for the secretion of potassium and hydrogen, as well as a lack of aldosterone or a low response to aldosterone. It refers to the acidosis caused by potassium and hydrogen secretion in the “cation exchange segment” of the distal renal tubule, and at the same time, aldosterone deficiency or low response to aldosterone. It is common in middle-aged and old-aged people, and clinically characterized by hyperchloremic metabolic acidosis and hyperkalemia, and the severity of acidosis and hyperkalemia is often disproportionate to the degree of renal insufficiency. In addition to treating the cause of the disease, lowering blood potassium is the main purpose of treatment.
Causes
1. Aldosterone deficiency
It is the most common cause in adult patients, often secondary to diabetic nephropathy, tubulointerstitial nephropathy, renal calcification and other diseases. Some patients with mild to moderate renal failure may also inspire aldosterone reduction and develop this disease, characterized by acidosis and hyperkalemia disproportionate to the decrease in glomerular filtration rate (GFR).
2. Aldosterone resistance
Various endocrine disorders are characterized by a state of resistance to the corresponding enzyme. The childhood form has renal sodium loss and a decreased distal tubular response to aldosterone.
3. voltage-dependent renal tubular acidosis (RTA)
Loss of negative voltage difference in the collecting tubular lumen reduces H+ and K+ secretion.
Symptoms
The manifestations are hyperchloremic acidosis and persistent hyperkalemia, but the electrocardiogram is mostly devoid of hyperkalemia, and the severity of hyperkalemia and acidosis is not commensurate with the degree of renal insufficiency. Urine pH often remains below 5.5, but total urinary acid excretion remains markedly reduced. Salt loss of varying degrees and associated symptoms may also be present.
Examination
1. Blood tests
Elevated blood chloride, hyperkalemia, acidosis.
2. Urinalysis
Urine pH is often below 5.5, and renal reabsorption of HCO3- is decreased (15%) when plasma HCO3- concentration is normal.
Diagnosis
Clinically confirmed renal tubular acidosis, presence of chronic kidney disease or adrenal disorders, persistent hyperkalemia, high suspicion of hyperkalemic renal tubular acidosis.
Treatment
1. Treatment of etiology
Actively treat the primary disease, prohibit drugs that inhibit the production of aldosterone and hinder the action of aldosterone.
2. Symptomatic treatment
(1) Correcting acidosis: taking sodium bicarbonate, correcting acidosis can help reduce hyperkalemia.
(2) Reduce hyperkalemia: low-potassium diet, oral ion-exchange resin, and oral diuretic furosemide. When severe hyperkalemia (>6.5 mmol/L) occurs, dialysis treatment should be carried out promptly.
(3) Adrenocorticotropic hormone therapy: oral fludrocortisone, renal tubular antialdosterone child-type patients should be supplemented with sodium salt or sodium bicarbonate, limiting the intake of potassium or taking polysulfonated styrene to reduce the blood potassium; adult-type should limit the intake of sodium and add thirophenol diuretics.