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Glomerulonephritis 391
• Urinalysis: proteinuria, variable urine ○ Arthrocentesis, echocardiography, bone edema, in which case colloidal support may
marrow aspirate, thoracic radiographs
concentration, sometimes hematuria ○ Adrenocorticotropic hormone stimulation be necessary. Use cautiously.
VetBooks.ir urine concentration and urine sediment or low-dose dexamethasone suppression ○ Dextrans: use with caution because of Diseases and Disorders
○ Proteinuria must be interpreted in light of
○ Hetastarch 10-20 mL/kg/day IV
reported link to renal failure.
exam.
test
○ Dipstick measure of proteinuria should
like immunoreactivity
be confirmed by sulfosalicylic acid (SSA) ○ Species-specific pancreatic lipase, trypsin- ○ Large volumes of species-specific plasma or
human albumin: expensive and short-lived
test or quantitative measures (e.g., UPC effect (ongoing renal loss)
ratio [p. 1391]). TREATMENT • Immunosuppressive treatment may be useful
○ Significant proteinuria often precedes loss in up to 48% of protein-losing nephropathy
of urine concentrating ability or azotemia. Treatment Overview cases (e.g., glucocorticoids, mycophenolate
• Urine culture: indicated in all cases Treatment mainly consists of medications [p. 60])
• Thoracic radiographs: evidence of underly- to decrease the degree of proteinuria. When ○ Immunosuppression is best reserved for
ing disease (neoplasia, chronic infectious appropriate, medications for the management of animals with biopsy-confirmed immune-
or inflammatory disease) or pulmonary hypertension and thromboembolic disease are mediated GN after the most likely
thromboembolism occasionally identified used. If the patient is in renal failure, supportive underlying infectious causes have been
• Abdominal radiographs: often unremarkable. management is advised. A step-by-step approach ruled out. It can also be considered in
Kidneys may be small. May identify evidence to treatment is shown on p. 1420. rapidly progressing disease where biopsy
of underlying disease (neoplasia, chronic is not indicated due to advanced state
infectious or inflammatory disease). Acute and Chronic Treatment of disease.
• Abdominal ultrasound: hyperechoic, • Address underlying disease conditions directly. • Clinical signs of uremia and electrolyte and
small kidneys, decreased corticomedullary • If respirations are compromised by large- acid-base disorders are addressed as for overt
distinction, evidence of underlying disease volume pleural effusion or severe ascites, CKD (pp. 169 and 516).
(neoplasia, chronic infectious or inflamma- centesis is indicated. Diuretic drugs are • Dietary therapy: supplementation of poly-
tory disease), or unremarkable largely ineffective for rapid mobilization of unsaturated fatty acids and dietary protein
body cavity fluid (p. 1164). restriction (i.e., renal diet)
Advanced or Confirmatory Testing • Oxygen support may be required for animals
• UPC ratio with pulmonary thromboembolism (pp. 842 Drug Interactions
○ Concurrent culture and sensitivity results and 1146). • ACE inhibitors may cause hypotension when
must be negative to rule out bacterial • Proteinuria reduction by angiotensin- combined with diuretics or other vasodila-
infection as cause of elevated ratio. converting enzyme (ACE) inhibitor treat- tors (rare but greater risk in hypovolemic/
○ Normal for dogs < 0.5; cats < 0.4. Most ment: for dogs, enalapril 0.5 mg/kg PO q inappetent patient).
animals with GN (or amyloidosis) have 12-24h or benazepril 0.5 mg/kg PO q 24h, • ACE inhibitors may reduce proteinuria and
ratios > 2. up to a maximum of 2 mg/kg/day ameliorate hypertension but may worsen
• Microalbuminuria testing • If proteinuria persists (UPC > 1) despite ACE azotemia, requiring monitoring of blood
○ Does not provide additional benefit inhibitor use, consider angiotensin II receptor urea nitrogen (BUN) and creatinine during
in animals with elevated UPC. These antagonists (e.g., telmisartan 1 mg/kg PO q therapy.
assays detect very small quantities of 24 hours; can increase to maximum daily dose • Nonsteroidal antiinflammatory agents may
urine albumin that would be missed on of 5 mg/kg) and/or aldosterone antagonist reduce efficacy of ACE inhibitors (avoid use).
routine dipstick and are redundant when (spironolactone 1-2 mg/kg PO q 12h)
proteinuria has been identified. ○ If UPC remains > 1 or is not reduced Possible Complications
• Renal biopsy is the only definitive means by one-half after single-agent ACE • Third-space retention of fluids
of diagnosis of GN, allowing morphologic inhibitor or angiotensin II receptor • Cachexia
classification of disease and identifying type blocker (ARB), consider cautious use of • Worsening renal azotemia as a result of ACE
and location of immunoglobulin. Cortical combined therapy. In humans but not inhibitor use (uncommon)
tissue is examined by light microscopy, dogs, combined therapy has been linked • Hypotension secondary to ACE inhibitor
immunofluorescence, and electron to higher incidences of kidney failure. and calcium channel blocker
microscopy. Contact the International • If hypertension persists despite ACE inhibi- • Worsening of renal azotemia with dextran
Veterinary Renal Pathology Service at The tor use, calcium channel blockers may be use
Ohio State University (Dr. Rachel Cianciolo’s indicated (amlodipine 0.05-0.5 mg/kg PO • Thromboembolic disease as a result of low
lab) or Texas A&M University (Drs. George q 24h [dogs]; 0.625 mg/CAT PO q 12-24h). antithrombin and/or protein C levels
Lees and Mary Nabity’s lab). • Anticoagulant therapy can reduce the risk • Bleeding tendency from aspirin, warfarin use
• Determining serum antithrombin concentra- of thromboembolic disease. Unfractionated • Gastrointestinal ulceration as a result of
tions may help quantify risk of thrombo- heparin is not effective because of loss of azotemia or aspirin therapy
embolic disease (<80% suggests increased antithrombin. • Hyperkalemia due to ACE inhibitors and/
risk). ○ Aspirin 0.5 mg/kg PO q 24h to q 12h or aldosterone antagonists
• A variety of other tests may be indicated (dog) or clopidogrel 2 mg/kg PO q 24h
in a search for an underlying cause of GN. (dog) Recommended Monitoring
The choice of tests depends on history and ○ Warfarin initial dose is 0.1-0.2 mg/kg PO Stable animals are monitored every 3-4 months.
physical exam, results of initial evaluation q 24h. Rechecks should be more frequent if treatment
(CBC, serum biochemistry profile, imaging ■ Prothrombin time (PT) should be changes are made or when indicated by chang-
studies), geographic region, and environmen- monitored and dose adjusted until PT ing clinical signs.
tal exposures. Common examples include = 1.5 to 2.5 times upper limit of normal • Physical exam
○ Serologic tests for heartworm, bor- range. Not generally recommended • UPC (ideally, pooled samples)
reliosis, feline leukemia virus, feline unless benefit outweighs risk (e.g., • Serum BUN/creatinine/phosphorus/potassium/
immunodeficiency virus, Ehrlichia canis, prior embolic event while on aspirin) albumin
coccidioidomycosis • Uremic animals may require fluid therapy • Blood pressure
○ Antinuclear antibody test (p. 169). Hypoalbuminemia may result in • Urinalysis/culture
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