During a follow-up examination two weeks later, the owner reported that the dog was much brighter and was walking normally,
even going for walks. The dog's skin and paws were markedly improved, with minimal pruritus, evidence of coat regrowth, and
resolving deep pyoderma, although superficial pyoderma was still present. The dog's skin was mildly erythematous and somewhat
oily. Evaluation of impression smears revealed no Malassezia organisms. Cytologic examination of skin scrapings revealed large numbers of adult Demodex mites, which were all dead. The only other dermatologic abnormality noted was easily bruised, thin skin. There were larger-than-expected
petechiae, but only in the areas where we performed skin scrapes. Easy bruising after skin scraping is common in dogs with
inflamed skin, especially in those receiving glucocorticoids. We continued oral cephalexin and milbemycin.
At a recheck one month later, the dog's skin was almost normal except for residual hyperpigmentation and mild seborrheic otitis.
Skin scraping results remained positive, but again only dead adult Demodex mites were found. At this time, the owner was optimistic about the dog's recovery and was now willing to investigate the
proteinuria and hypoalbuminemia, so we had the internal medicine service evaluate the dog (see below).
Long-term dermatologic management
During the next four months, the dog's bacterial pyoderma and pododermatitis resolved. Six weeks and 10 weeks after starting
milbemycin therapy, the dog's skin scraping results were negative for Demodex species. Milbemycin therapy was continued for about 14 weeks. Skin scrapings were performed every two or three months, and
the dog experienced a relapse of demodicosis eight months after its initial presentation. We restarted milbemycin at the previous
dosage. This resolved the dog's clinical signs, but skin scraping results remained positive for Demodex mites, so lifelong milbemycin therapy was recommended.
EVALUATION AND TREATMENT OF INTERNAL MEDICINE PROBLEMS
About a month after the adult-onset demodicosis and deep pyoderma were diagnosed, the dog presented to the internal medicine
service for evaluation of proteinuria and hypoalbuminemia. According to the owner, the dog's overall attitude greatly improved
as the pyoderma resolved, but its appetite was still decreased. The polydipsia remained, but the dog was urinating normally.
Physical examination revealed a quiet to depressed dog. Its hydration status, temperature, and pulse and respiratory rates
were normal. There was a generalized thinning of the coat, with evidence of hair regrowth, patchy erythema, and multifocal
crusting. The dog had severe dental tartar, gingivitis, and presumed periodontitis. The dog was somewhat thin, although its
body weight (41 lb) was basically unchanged from the initial evaluation by the dermatology service.
The results of the urinalysis performed at presentation a month earlier ruled out diabetes mellitus, renal insufficiency,
and diabetes insipidus as causes of the PU/PD. There was no glucosuria, and a urine specific gravity of 1.035 in a dehydrated
dog was evidence that the kidneys were capable of producing concentrated urine. Other differential diagnoses for the dog's
PU/PD included iatrogenic or spontaneous hyperadrenocorticism, occult pyelonephritis, hypercalcemia, psychogenic polydipsia,
and liver disease. The differential diagnoses for the proteinuria and historic hypoalbuminemia included glomerulonephritis,
amyloidosis, pyelonephritis, and chronic interstitial nephritis. The urine protein:creatinine ratio of 5.35 was greater than
expected for chronic interstitial nephritis and less than expected for renal amyloidosis.1 Because granular casts, white blood cells, and red blood cells were not present in the urine sediment, pyelonephritis was
unlikely. These observations, along with the history of chronic inflammatory skin disease, made glomerulonephritis the most
likely differential diagnosis. Glucocorticoid use can lead to proteinuria,2 but considering the historical hypoalbuminemia in this dog, it was more likely that glucocorticoid use either predisposed
the dog to glomerulonephritis or exacerbated preexisting glomerulonephritis.3
A complete blood count, serum chemistry profile, and urinalysis were done. A urine bacterial culture and antimicrobial sensitivity
testing were performed after cystocentesis to help rule out pyelonephritis. The urine protein:creatinine ratio was reevaluated
to see if it had improved as a result of therapy for the skin diseases and cessation of exogenous glucocorticoids. A thoracic
radiographic examination was performed to screen for neoplasia, abscesses, or chronic granulomatous diseases. An abdominal
ultrasonographic examination was performed to search for neoplasia, organomegaly, adrenal gland pathology, and urolithiasis,
as well as to evaluate renal architecture. The dog's systolic blood pressure was measured with a Doppler unit, because dogs
with glomerulonephritis have a high incidence of systemic hypertension.4 The results of the diagnostic tests were normal, with a few exceptions. The urine protein:creatinine ratio had markedly
improved to 2.22. The urine specific gravity was 1.030, with 3+ protein and a normal urine sediment. The serum albumin concentration
was still low (2.1 g/dl), with normal concentrations of globulin (3.6 g/dl; normal = 2.6 to 4.4 g/dl) and total protein (5.7
g/dl). The cholesterol concentration was elevated (344 mg/dl; normal = 111 to 290 mg/dl). The dog's systolic blood pressure
was normal at 130 mm Hg. Seven readings were recorded; the highest and lowest were excluded, and the remaining five were averaged.
Further diagnostic testing was recommended for the following week.
An ACTH stimulation test was performed to rule out hyperadrenocorticism, and a bile acid tolerance test was performed to rule
out hepatic dysfunction as possible causes for the PU/PD. The dog had not received glucocorticoids for about a month, which
is an adequate time to allow for a meaningful interpretation of the ACTH stimulation test. Because infectious diseases are
known to cause glomerulonephritis, serologic testing for infectious diseases common to the dog's geographic area (e.g. ehrlichiosis, leptospirosis, Lyme disease) was performed. The findings from these tests were normal.
A thyroid panel was performed to rule out concurrent hypothyroidism as a cause for the dog's continued depression and dermatologic
disease. Although this could have been performed on initial evaluation by the dermatology service, interpretation of thyroid
testing at that time would have been more difficult because of nonthyroidal illness and glucocorticoid administration.
The thyroid panel revealed a slightly low total T4 concentration (13 nmol/L; normal = 15 to 67 nmol/L), a normal free T4 concentration by dialysis (18 pmol/L; normal = 6 to 42 pmol/L), and an elevated canine TSH concentration (77 mU/L; normal
= 0 to 37 mU/L). There was no increase in antibodies against T4, T3, or thyroglobulin. These discordant findings were consistent with sick euthyroid syndrome.5 Early hypothyroidism or a spuriously normal free T4 result was another possibility. Repeat thyroid testing over time was advised, particularly if the skin disease did not respond
to appropriate therapy.