Final answer:
Renal loss from hypoaldosteronism, diuretic therapy, or a tubular defect can lead to hyperkalemia, which is an excessive level of potassium in the blood. Aldosterone plays a key role in the excretion of potassium, and its deficiency or impaired function leads to decreased K+ secretion and higher blood levels of K+.
Step-by-step explanation:
Renal loss due to hypoaldosteronism, diuretic therapy, or a tubular defect can lead to hyperkalemia, which is high levels of potassium (K+) in the blood. Various conditions can cause such renal loss, which includes renal failure, severe dehydration, Addison's disease, and certain effects of diuretic use. Hyperkalemia occurs because aldosterone helps in Na+ reabsorption and K+ secretion in the kidneys; deficiency of aldosterone or its effects leads to less secretion of K+ and more K+ retention in blood.
Conversely, excessive reabsorption of Na+ due to an increase in aldosterone and water reabsorption, or conditions such as Cushing's syndrome and prolonged cortisone or ACTH treatment, can lead to hypernatremia. Underproduction of ADH can impact aldosterone release and impair kidney function, causing electrolyte imbalance and improper kidney functioning.