History
Renal tubular acidosis (RTA) type IV generally is asymptomatic unless severe hyperkalemia leads to muscle weakness or life-threatening arrhythmia (see Hyperkalemia). [17] Acidosis usually is mild and asymptomatic. The condition is usually discovered during routine laboratory evaluations.
Because several commonly used drugs may unmask RTA type IV, hyperkalemia commonly is discovered during follow-up testing of a patient started on one of those agents. These drugs include medications affecting the renin-angiotensin-aldosterone axis (see Causes). Hyperkalemia with moderate doses of such agents may suggest a forme fruste of RTA type IV.
If the patient is newly discovered to have hyperkalemia and mild-to-moderate renal failure, focus the history on the causes of renal disease. In particular, consider long-term analgesic use, exposure to lead (industrial or from moonshine liquor), and obstructive symptoms. Other illnesses (eg, diabetes, sickle cell anemia, and systemic lupus erythematosus [SLE]) would likely have become apparent earlier.
Other important historical data consist of dietary intake (including pica, fad diets, and use of salt substitutes) and current use of medications (ie, over-the-counter [OTC] and prescription drugs).
Physical Examination
The underlying renal disease and any associated illnesses (eg, SLE or sickle cell disease) dominate the physical findings. Except for arrhythmia and muscle weakness in severe cases, hyperkalemia produces no physical signs.
Mild acidosis may be present, but associated physical signs (eg, Kussmaul respiration) usually are absent. However, some cases of symptomatic acidosis with dyspnea have been described. Patients demonstrate no signs of adrenal insufficiency, because glucocorticoid excretion is intact by definition. Patients usually are hypertensive, in association with their underlying renal disease. Assessment of patient volume status is important because therapy commonly includes the use of diuretics.
Adrenal insufficiency is part of the differential diagnosis and manifests with findings (such as fever, orthostatic changes, hyperpigmentation, and signs of illnesses [eg, SLE]) that, when resulting in treatment with long-term corticosteroids, can lead to secondary hypoadrenalism.
-
Renin-antiotensin-aldosterone system.
