Case 25

Presentation: 

A six month old, intact, male, mix breed dog (pothound) was presented to AcaseAweek Clinic with a history of anorexia, weight loss and lethargy. The dog has an indoor/outdoor lifestyle, is fed puppy Science Diet, is up to date on its vaccinations and is treated for ectoparasites with Adam’s spray. The owner was away during the summer and upon return found ticks on the dog. There are four other dogs in the household, one of them is showing similar clinical signs and happens to be this patient’s brother. 

Physical examination revealed that the patient was mildly depressed, alert and responsive, had a temperature of 100.4ºF, heart rate was 100bpm, respiratory rate was 12bpm and weighted 18.2 kg.

Ears, eyes, nose, throat: mild black, thick, tarry exudate on both ears. No ocular or nasal discharge observed.

Mucus membranes: grey, pale and slightly yellow (icterus). CRT<2>

Lymph nodes: generalized lymphadenopathy.

Laboratory tests:

Snap test: Ehrlichia, Heartworm, Anaplasma and Lyme disease negative.

CBC: unremarkable, except for mild eosinophilia.

Chemistry profile:

• AP 1259 U/L (46-337)
• ALT 673 U/L (8-75)
• Glob: 4.1 g/dL (2.3-3.8)
• TBIL: 1.3 g/dL (0.0-0.8)

Urinalysis- unremarkable.

What is your tentative diagnosis? Give list of differentials.

What diagnostic test(s) will you perform to confirm your diagnosis?

How will you treat and manage this case?

Solution to this case

Solution for case 24

Click here to see this case

Tentative diagnosis: Azotemia due to chronic renal failure (CRF).

Further diagnostic tests:
* Abdominal radiography/ultrasound to demonstrate decreased size of kidneys.

* Urine creatinine:protein ratio.

* Renal biopsy (not commonly performed).

* Blood pressure to demonstrate hypertension.

Isosthenuria is a common finding in chronic renal failure when two thirds of the functioning nephrons are lost.

Azotemia is seen when at least three fourths of the functioning nephrons are lost. Azotemia presents with increased BUN, creatinine, GI, and neurological clinical signs. This patient’s presentation would suggest that she has lost at least three fourths of her functioning nephrons.

Predisposing factors for CRF are age, chronic obstruction, infection, heart failure, and tubular disease. A urine sample taken from this patient, via a cystocentesis, ruled out bacterial infection. Patient’s heart sounded normal on auscultation. The renal failure was attributed to her age.

Management of chronic renal failure is a multifactor process. Most importantly hydration and electrolytes must be maintained with in normal limits. An appropriate renal diet will be low in protein, phosphorous, and sodium. Some other factors which must be addressed in the management of chronic renal failure include anemia, proteinuria, and gastrointestinal processes.

Anemia is due to decreased production of erythropoietin by renal peritubular cells. The anemia could also be from blood loss via GI ulcers, or iatrogenic from blood draws. The anemia is non-regenerative normochromic normocytic.

Treatment of anemia with erythropoietin (EPO) is indicated when the PCV falls below 18% and the patient is showing clinical signs of anemia/hypoxia. Caution must be used with EPO since it is of human origin. Dogs can produce antibodies against it. In severe anemia requiring immediate relief of clinical signs a blood transfusion can be done.

Proteinurea is seen because glomeruli have been damaged enough to allow loss of protein and anti-thrombin III. This decreases oncotic pressure, leading to edema. The loss of anti-thrombin III causes coagulation issues. Many of these patients have pulmonary thromboembolism as a complication.

These patients can be treated with angiotensin converting enzyme inhibitors which decreases the pressure in the glomeruli by dilating the efferent renal artery. This decrease in pressure helps prevent loss of proteins into the urine. Canine patients with CRF and proteinuria tend to have a decreased survival.

GI ulcers and nausea and vomiting are the common clinical signs seen. Uremic toxins activate the chemoreceptor trigger zone which leads to the nausea and vomiting. These uremic toxins also increase gastrin production which increases hydrochloric acid production in the stomach, leading to GI ulcers.

These complications are treated by decreasing the uremic toxins via hydration; protecting the stomach by decreasing acid production, and controlling the nausea and vomiting by blocking the chemoreceptor trigger zone. Acid production can be decreased using histamine blockers or proton pump inhibitors. Sucralfate can be used to protect/coat ulcers. The nausea can be controlled with medication targeted at dopamine antagonism, serotonin, or neurokinin.

Treatment:

Hospitalize patient
– NPO
– Fluid diuresis to decrease azotemia
* * Maintenance: 60ml/kg/24 hours = 2100ml
* * Deficit (5%) = 1715ml
* * Total fluid/day = 3850ml (160ml/hr)
– Decrease gastric acid and control N/V
* * Famotidine 20mg Q12 hours
* * Anti-emetic - Cerenia (maropitant citrate)
– Re-evaluate
* * BUN, Creatinine, Phosphorus every 48 hours
* * PCV and TP daily

The patient remained azotemic.
– After 3 days, fluids increased to 250ml/hr during the day and 160ml/hr during the evening.
– NPO
– Continue H2 blocker and Cerenia
– Continue to monitor BUN, SCr, TP, PCV, Phosphorus
The patient did not improve and was euthanized on consultation with owner.

See following Links for more info on CRF:

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/130603.htm

http://courses.vetmed.wsu.edu/vm552/urogenital/crf.htm

http://www.marvistavet.com/html/body_chronic_renal_failure.html

http://www.felinecrf.com/what0.htm