Case Study: Feline Chronic Renal Disease vs Hyperaldosteronism


Katherine Arnell, DVM

Melvin, a 9 year old male neutered DSH, presented to the Veterinary Specialty Hospital for
evaluation of an acute onset of ataxia and cervical ventroflexion. He is strictly indoors with no
history of toxin exposure, no travel history, and no significant prior medical history.

On presentation, Melvin was bright, alert and hydrated with mild cervical ventroflexion. His signs
quickly progressed to marked cervical ventroflexion, generalized weakness, reluctance to walk, and
a plantigrade stance with prolonged standing. The remainder of his neurologic examination was

Melvin’s neurologic signs are consistent with neuromuscular disease. Differentials for generalized
neuromuscular disease include hypokalemic myopathy, myasthenia gravis, infectious or
inflammatory myopathy, toxin, and less likely a vascular event. Differentials for hypokalemia
include hyperaldosteronism, chronic renal disease, metabolic alkalosis, dietary deficiency,
concurrent insulin therapy, and use of medications such as penicillins, amphotericin B, and loop

A complete blood count was unremarkable. A chemistry panel showed hypokalemia (3.2 mmol/L),
mild azotemia (BUN 59 mg/dL and creatinine 2.9 mg/dL), hypercalcemia (11.1 mg/dL), and
hypophosphatemia (1.7 mg/dL). A urinalysis showed a USG of 1.026 with 4+ blood, few epithelial
cells, and few calcium oxalate crystals. The urine potassium concentration was elevated (69.7
mmol/L). A systolic blood pressure was mildly elevated (170 mmHg), however subsequent
measurements were normal. Abdominal ultrasound exam revealed moderate bilateral chronic
renal changes and multifocal hyperechoic splenic nodules most consistent with benign

Due to the possibility for hyperaldosteronism as a cause for Melvin’s hypokalemia, an aldosterone
level was submitted and was elevated at 1,043 pmol/L (reference range 194-388 pmol/L).

Melvin was treated with intravenous fluids containing potassium chloride and potassium
phosphate supplementation. Overnight, he remained stable, but his neurologic status did not
improve. Despite fluid therapy, his potassium level decreased to 2.3 mmol/L. His intravenous
potassium supplementation was increased and oral potassium gluconate was started. His
phosphorous level increased to 8.6 mg/dL, and potassium phosphate supplementation was
subsequently discontinued. Serial blood work showed marked improvement in acid-base balance
and potassium levels, with normalization of his potassium level and renal values within 72
hours. His intravenous fluids with potassium chloride supplementation were tapered and he
continued to do well. His cervical ventroflexion resolved and his overall strength improved. He
was then discharged with instructions to continue oral potassium gluconate BID and switch to a
renal diet. He was rechecked three days later, and was clinically doing well at that time. Recheck
blood work showed normokalemia (3.95 mmol/L). He was rechecked two weeks later, and was
continuing to do well. Recheck blood work showed normokalemia (4.2 mmol/L), mildly elevated
BUN (51 mg/dL), and normal creatinine (1.6 mg/dL). A repeat aldosterone concentration was
below the reference range at 67 pmol/L.

Hypokalemia is typically defined as a serum potassium concentration below 3.6
mmol/L. Treatment depends on the severity of hypokalemia and associated clinical signs including
polyuria, polydipsia, ileus, and muscular weakness. Potassium can be supplemented both
intravenously and orally, and frequent measurement of potassium concentration is essential to
assess response to therapy and avoid iatrogenic hyperkalemia. The primary cause for the
hypokalemia should also be identified and treated appropriately.
Hyperaldosteronism generally reflects the appropriate physiologic response to counteract
hyponatremia, hyperkalemia, and hypotension. In Melvin’s case, we did not know initially if the
hyperaldosteronism was secondary to an aldosterone-secreting adenocortical adrenal tumor
(Conn’s syndrome) or secondary to renal disease given his azotemia. There was no evidence of an
adrenal tumor noted on his abdominal ultrasound exam, although changes are not always
apparent. Cats with adrenal tumors will have aldosterone concentrations ranging from 800-14,000
pmol/L and most have concentrations greater than 1000 pmol/L. Cats with renal disease can have
aldosterone concentrations ranging from 130-1,670 pmol/L. These cats will typically have bilateral
micronodular hyperplasia of the zona glomerulosa of the adrenal cortex and have
ultrasonographically normal adrenal glands.

Due to the overlap of aldosterone concentration ranges between these two diseases,
interpretation of concentrations can be challenging and other clinical parameters must also be
evaluated, including electrolytes, blood pressure, and ultrasound examination of the adrenal
glands. In Melvin’s case, we rechecked an aldosterone level approximately two weeks later and it
was below the reference range.
This finding in combination with his normal adrenal ultrasound, normal blood pressure, and
improved azotemia would suggest chronic renal disease as the cause of his previously documented
Melvin is continuing to do very well clinically and loves his new renal diet. We are gradually
tapering his potassium gluconate supplementation and his renal values remain stable.


Download the PDF for this case study here: Feline_Chronic_Kidney_Disease

0 replies

Leave a Reply

Want to join the discussion?
Feel free to contribute!

Leave a Reply

Your email address will not be published. Required fields are marked *