Page 116 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

106 ELECTROLYTE DISORDERS

disorders of renal tubular function that cause hypokale- produce a variety of steroid hormones, including aldoste-
mia in humans. One of these familial disorders, Bartter rone, deoxycorticosterone, and corticosterone in addi-
syndrome, is especially complex. It can be caused by tion to cortisol. 17,46,115,117,130
mutations in the NKCC2 gene that codes for the luminal Several cats (5 to 20 years of age) with hyperaldos-

þ
Na þ/ -K -2Cl cotransporter found in the thick ascend- teronism have been reported.* Affected cats are
ing limb of Henle’s loop (type I), in the gene for the presented for evaluation of muscle weakness (sometimes
ROMK protein component of renal tubular potassium with ventroflexion of the neck), ataxia, weight loss, poly-
channels (type II), in the CLCNKB gene that codes for uria, polydipsia, and ocular abnormalities (e.g., mydriasis,
the ClC-Kb chloride channel in the basolateral blindness, and retinal detachments) associated with
membranes of tubular cells in the thick ascending limb hypertension. Laboratory features consist of hypokale-
(type III), or in the BSND gene that codes for barttin, mia, hypernatremia, mild metabolic alkalosis, increased
a subunit protein of chloride channels that is required serum creatine kinase activity, dilute urine, extremely
for proper insertion of the channels into the basolateral high serum aldosterone concentrations (usually >1000
membrane (type IV). 94,176 Other rare diseases can arise pmol/L; normal, 194 to 388 pmol/L), and plasma renin
from a loss of function mutation in the NCCT gene for activity that is low or at the low end of the normal
þ

the thiazide-sensitive Na -Cl cotransporter in the lumi- reference range (0.2 to 0.5 ng/L/sec; normal, 0.2 to
nal membranes of the distal convoluted tubule 1.4 ng/L/sec). In two affected cats, urinary FE K was
(Gitelman’s variant of Bartter syndrome) or a gain of more than 50% and consistent with inappropriate
function mutation in the SCNN1 gene for the luminal kaliuresis. 75 In these two cats, chronic renal disease
sodium channel (ENaC) of the principal cells of the also was present and might have contributed to hyperten-
collecting duct (Liddle syndrome). None of these rare sion and increased FE K . Hyperaldosteronism may be
tubular disorders has yet been recognized in veterinary associated with hyperglycemia caused by insulin resis-
medicine. tance, and one affected cat had diabetes mellitus
Mineralocorticoid excess is a relatively uncommon that persisted despite removal of the adrenal tumor. 75
cause of urinary potassium loss and hypokalemia in dogs Aldosterone-producing adrenal tumors in cats often are
and cats. One report described hyperaldosteronism in a 1 to 3 cm in diameter and can be visualized on abdominal
dog thought to be caused by adrenal hyperplasia of the ultrasonography. Cytologic evaluation of fine needle
adrenal zona glomerulosa. 26 Older dogs with hyperaldos- aspirates is consistent with neuroendocrine neoplasia,
teronism as a result of aldosterone-producing adenomas and histologically these tumors are adenomas or
or adenocarcinomas are presented for evaluation of weak- adenocarcinomas. Invasion of the caudal vena cava by
ness and polyuria. 67,102,207 Mild to moderate hyperten- the tumor can result in thromboembolism. 11,75,163
sion may be detected, and hypokalemia, hypernatremia, Removal of adrenal tumors causing hyperaldosteronism
mild metabolic alkalosis, dilute urine, and extremely high can be successful in affected cats, but surgery carries a
serum aldosterone concentrations (>3000 pmol/L; nor- high risk of life-threatening intraoperative or postopera-
mal, 14 to 957 pmol/L) are present on laboratory evalu- tive hemorrhage. 11 Medical treatment with potassium
ation. Dogs with adenomas respond well to surgical supplementation (2 to 6 mEq/day), spironolactone (2
adrenalectomy, but those with adenocarcinomas experi- to 4 mg/kg/day) to antagonize the effects of aldoste-
ence recurrence of clinical signs if metastasis occurs. rone, and amlodipine (0.625 to 1.25 mg/day) to control
One affected dog had polyuria and hyperaldosteronism hypertension and can be used to manage affected cats.
associated with a very small (2 mm) adrenal adenoma that Survival times of 1 to 5 years have been reported for sur-
initially was undetected by computed tomography, and gical or medical management. 11 Concurrent hyperaldos-
the dog responded to treatment with spironolactone. 159 teronism and hyperprogesteronism have been reported in
Ultimately, the tumor was identified and removed, a cat that also had clinical signs of hyperadrenocorticism
and the dog recovered completely. Another dog with and diabetes mellitus. 27 See Chapter 10 for further dis-
an adrenal adenocarcinoma had clinical and laboratory cussion of states of mineralocorticoid excess.
features of mineralocorticoid excess, but serum aldos- Administration of loop or thiazide diuretics may cause
terone concentration was undetectable. 156 Serum hypokalemia as a result of increased flow rate in the distal
desoxycorticosterone concentration was measured and tubules and increased secretion of aldosterone secondary
found to be abnormally high (288 ng/mL; normal, 16 to volume depletion. In one study, dogs with heart failure
to 46 ng/mL). After surgical removal of the tumor, receiving furosemide had significantly lower mean serum
serum potassium concentration normalized, but serum potassium concentrations (mean serum potassium con-
desoxycorticosterone concentration remained high, and centration, 3.9 mEq/L) than did normal dogs (mean
the dog was treated with spironolactone. serum potassium concentration, 4.4 mEq/L) or
Clinical and laboratory features of hyperaldosteronism
also may be observed in dogs with hyperadrenocorticism
caused by adrenal tumors that have been documented to *References 11, 63, 75, 119, 134, 135, 157, 159, 160, 163.