Causes of drug-induced hyperkalemia in CKD are mostly due to reni

Causes of drug-induced hyperkalemia in CKD are mostly due to renin–angiotensin–aldosterone inhibitors such

as ACE inhibitors, ARBs, and spironolactone, or excessive intake of potassium-containing foods. Other causes include the administration of β-blockers, digitalis, NSAIDs, nafamostat mesilate, trimethoprim, or pentamidine. CKD patients caused by diabetic nephropathy may be associated with hyporeninemic hypoaldosteronism, which may cause hyperkalemia despite relatively well-preserved kidney function, namely, type IV renal tubular acidosis. Metabolic acidosis As kidney RXDX-101 function declines, renal excretion of acids decreases and blood bicarbonate consumption is increased, click here resulting in decreased serum bicarbonate concentration. In

CKD stages 3–5, therefore, normal anion gap hyperchloremic metabolic acidosis occurs. The presence of metabolic acidosis is suspected if [Na–Cl-12] is less than 20. Further kidney function decline leads to decrease of endogenous inorganic acid salt excretion, such as sulfuric acid and phosphoric acid, resulting in aggravation of metabolic acidosis (coexistence of increased anion gap metabolic acidosis). Management of such a case requires a consultation to nephrologists. Practical management of hyperkalemia AZD6244 Modification of diet: potassium-rich food is avoided as possible. An appropriate amount of fruit should be taken. Cooked vegetables are preferred to uncooked vegetables. Vegetables should be placed in a large volume of boiling water which helps potassium Sirolimus emanate from vegetables. Vegetables prepared in this way are used for daily cooking. If hypertension or edema exists, a small dose of loop diuretics is administered. Note: diuretics administered in the evening may increase nocturnal urinary frequency. An example: 20–40 mg of

furosemide at one time or divided into two times after breakfast and lunch. 30–60 mg of azosemide at one time or divided into two times Anion exchange resin is prescribed. Since this agent tends to cause constipation, it is started with a small dose and its dose is adjusted depending on serum K levels. An instance: 5–15 g of Kalimate, one time or divided into two or three times, suspended in 50 mL water, oral intake 5–15 g of Kayexalate, one time or divided into two or three times suspended in 50 mL water, oral intake 5–15 g of Argamate, one time or divided into two or three times If metabolic acidosis presents, it is corrected. An instance: 1.5–3 g of sodium bicarbonate, divided into three times”
“Patients with CKD develop mineral metabolism disorder, which is called CKD mineral and bone disorder (CKD-MBD), including not only bone disorder, but also systemic disease affecting life expectancy through vascular calcification. Development of CKD-MBD is caused by complicated mechanisms such as secondary hyperparathyroidism and impaired mineralization and matrix formation of the bone.

Comments are closed.