Mineralocorticoid deficiency

Mineralocorticoids promote sodium and water retention and potassium excretion to regulate intravascular volume and serum potassium concentrations, respectively.¹ The clinical signs associated with mineralocorticoid deficiency can range from mild to severe.⁸ Dogs with mineralocorticoid deficiency may have a history of weakness, lethargy, polyuria and polydipsia, tremors, or collapse.^1,8 Most of these clinical signs are the result of hypovolemia, hypotension, or hyperkalemia. Hyponatremia may alter resting membrane potentials of skeletal muscle, leading to tremors.¹ Physical examination findings may include weakness, mild to severe dehydration, hypothermia, weak pulses, and bradycardia.^4,8

The classic serum chemistry profile abnormalities associated with mineralocorticoid deficiency are hyponatremia and hyperkalemia since mineralocorticoids regulate sodium reabsorption and potassium excretion in the renal tubules (Table 2). Hyponatremia can be exacerbated by hypovolemia-induced vasopressin release and free water retention.¹ A sodium to potassium ratio < 27:1 is consistent with mineralocorticoid deficiency; however, many diseases can decrease the sodium to potassium ratio in dogs. Thus, a low sodium to potassium ratio is not specific for hypoadrenocorticism or mineralocorticoid deficiency.¹⁴

Glucocorticoid and mineralocorticoid deficiency

Dogs with concurrent glucocorticoid and mineralocorticoid deficiency may have a combination of any of the previously mentioned clinical signs (Table 1), physical examination findings, and clinicopathologic abnormalities (Table 2). Other abnormalities include hypochloremia, azotemia, metabolic acidosis, hypercalcemia, and increased alanine aminotransferase and aspartate aminotransferase activities.^4,7,8,15 Hypovolemia and consequential hypoperfusion of the kidneys or liver may result in prerenal azotemia or increased alanine aminotransferase and aspartate aminotransferase activities, respectively.^1,8 The hyponatremia may lead to medullary washout and dilute urine, often in the face of dehydration.⁸

Take care when categorizing azotemia in patients with mineralocorticoid deficiency since many dogs will have isosthenuria or minimally concentrated urine in the face of prerenal azotemia. Lactic acid production and decreased renal hydrogen ion secretion contribute to metabolic acidemia.⁴ Hypercalcemia may develop because of decreased renal excretion of calcium and hemoconcentration, but the exact pathogenesis is unknown.¹⁵

OTHER CLINICAL FINDINGS

Several imaging and electrocardiographic findings may be recognized in dogs with hypoadrenocorticism. However, not all dogs with hypoadrenocorticism will have these diagnostic findings.

Imaging

Radiographic changes may include microcardia, a narrowed caudal vena cava or descending aorta, hypoperfused lung fields, and microhepatia. These findings are secondary to hypovolemia.^3,16,17 Rarely, megaesophagus is recognized.^6,16 Bilateral atrophy of the adrenal glands may be noted on ultrasonographic evaluation.¹⁷

Electrocardiogram

Atrial standstill, ventricular premature contractions, atrial fibrillation, or atrioventricular block may be documented in patients with hyperkalemia when the serum potassium concentration is > 7 mmol/L.^2,3 In severe cases, ventricular fibrillation or asystole may develop.¹⁸