A 47-year-old HIV-positive man is brought to the emergency room because of weakness. The patient has HIV nephropathy and adrenal insufficiency. He takes trimethoprim-sulfamethoxazole for PCP prophylaxis and is on triple-agent antiretroviral treatment. He was recently started on spironolactone for ascites due to alcoholic liver disease. Physical examination reveals normal vital signs, but his muscles are diffusely weak. Frequent extrasystoles are noted. He has mild ascites and 1+ peripheral edema. Laboratory studies show a serum creatinine of 2.5 with a potassium value of 7.3 mEq/L. ECG shows peaking of the T-waves and QRS widening to 0.14.Once the patient is stabilized and the T-waves have normalized, it is important to review the potential causes of his hyperkalemia and to take steps to prevent this from happening again. As you consider the pathophysiology of each confounding factor, which of the following statements is true?
Spironolactone, a potassium sparing diuretic by way of competitive inhibition of aldosterone at the collecting duct of the nephron, can lead to significant hyperkalemia in the setting of chronic kidney disease. Trimethoprim-sulfamethoxazole can also cause hyperkalemia by interfering with potassium exchange in the distal nephron. Heparin, including low-molecular-weight types, directly affects the zona glomerulosa of the kidney, reducing aldosterone production; it can lead to severe hyperkalemia in patients with already damaged kidneys. Adrenal insufficiency also leads to decreased aldosterone synthesis and hyperkalemia. Pseudo-hyperkalemia occurs precisely as described in option c, however, this patient had clinical signs and ECG changes consistent with true hyperkalemia.
Trimethoprim-sulfamethoxazole, which this patient was taking to prevent Pneumocystis infection, causes hypokalemia and therefore deterred this patient from presenting sooner.
Spironolactone, a commonly used diuretic for treating ascites in the setting of cirrhosis, acts as a competitive aldosterone inhibitor at the level of the collecting duct of the nephron, resulting in decreased potassium excretion and hyperkalemia.
This patient most likely had pseudo-hyperkalemia due to the use of a very small needle as well as rough handling of the specimen as it was transported to the laboratory, both of which caused hemolysis and release of potassium into the serum
Once this patient is hospitalized he will likely receive heparin for the prevention of deep venous thrombosis. Heparin should help ameliorate the hyperkalemia in the ensuing days in the hospital.
Kidney