Secondary Hypoaldosteronism (Hyporeninemic Hypoaldosteronism)

At a Glance

Hyperkalemia and hyperchloremic metabolic acidosis in patients with chronic kidney disease should lead to suspicion of secondary hypoaldosteronism. The juxtaglomerular apparatus in the kidney is the source of production of renin. Consequently, injury to the juxtaglomerular apparatus in kidney disease can impair the production of renin and decrease activation of the renin-angiotensin-aldosterone system. Impaired renin production leads to hypoaldosteronism. (See the chapter on primary hypoaldosteronism.) This disorder is often overlooked because affected patients have kidney disease and other disease processes. Renal injury leading to decreased renin production may be from a variety of causes, including diabetes, obstructive nephropathy, chronic pyelonephritis, analgesic nephropathy, sickle cell disease, and lead nephropathy.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

Electrolyte analysis shows increased potassium, usually with a metabolic acidosis without an increased anion gap. Plasma aldosterone and renin are decreased, although aldosterone release is usually stimulated by hyperkalemia. The plasma aldosterone:renin ratio is often within the normal range (Table 1).

Table 1.

Test Results Indicative of the Disorder

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications - OTC drugs or Herbals - that might affect the lab results?

A number of factors can lead to factitiously high measured serum potassium. Excessive tourniquet time or fist-clenching during specimen collection can lead to increases in serum potassium. Hemolysis of specimens and prolonged storage of serum on the clot can increase serum potassium. High platelet counts increase serum potassium because of release of potassium from platelets during specimen clotting.

Renin production is inhibited by a number of medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), beta blockers, clonidine, and alpha-methyldopa. Renin production is normally suppressed by volume overload and sodium loading and by a recumbent posture. Renin production is increased by volume depletion, upright posture, and diuretics.

This disorder can be exacerbated by a variety of drugs, including NSAIDs, beta-blockers, and potassium-sparing diuretics.

What Lab Results Are Confirmatory?

Measurement of aldosterone and renin in specimens collected in an upright position or after administration of furosemide will usually not show stimulation. Response of aldosterone to adrenocorticotropic hormone (ACTH) stimulation is usually diminished.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

Measurement of serum creatinine or other measures of renal function will show indications of renal injury.