Page 708 - Small Animal Internal Medicine, 6th Edition
P. 708

680    PART V   Urinary Tract Disorders


            neoplasms, but there is no discernible associated inflamma-  femoral artery embolism), or sudden blindness may occur
            tory or neoplastic disease in up to 50% of dogs with reactive   because of retinal detachment resulting from systemic
  VetBooks.ir  systemic amyloidosis.                             hypertension.
                                                                   Physical examination findings usually are related to the
              The cause of species differences in the tissue tropisms of
            reactive amyloid deposits is unknown. In the dog, amyloid
                                                                 poor hair coat, dehydration, oral ulceration, small irregu-
            AA deposits are most common in the kidney, and clinical   presence of CKD and uremia (e.g., poor body condition,
            signs are caused by renal failure and uremia. The spleen,   lar kidneys). Other physical examination findings may be
            liver, adrenal glands, and gastrointestinal tract also may be   related to the presence of underlying infectious, inflamma-
            involved,  but  associated  clinical  signs  are  rare.  In  the  cat,   tory, or neoplastic diseases. Affected Shar Pei dogs may have
            there is widespread deposition of amyloid deposits, but clini-  a previous history of so-called Shar Pei fever, episodic joint
            cal signs are due to renal failure and uremia. The Shar Pei   swelling usually involving the tibiotarsal joints, and high
            dog, Siamese cat, and Oriental Shorthair cat can be excep-  fever  that  resolves  within  a  few  days,  regardless  of  treat-
            tions to these general rules. Severe liver deposition of amyloid   ment. Some physical examination findings may be related
            can cause rupture of the liver and acute hemoabdomen in   to severe protein loss (e.g., ascites, edema, poor body condi-
            these breeds. Within the kidney itself, the distribution of   tion and hair coat). Retinal hemorrhages, vascular tortuos-
            amyloid deposits varies among species. For example, amy-  ity, and retinal detachment may occur because of systemic
            loidosis is primarily a glomerular disease in the dog, whereas   hypertension.
            amyloid deposits may have a predominant medullary distri-
            bution in the cat.                                   Laboratory Findings
                                                                 A careful search for known associated diseases (see Box 40.1)
                                                                 is a crucial part of the diagnostic evaluation, despite the fact
            CLINICAL FINDINGS                                    that the glomerular disease ultimately is idiopathic in most
                                                                 cases. Marked persistent proteinuria with inactive urine
            Most  animals  with  glomerular  disease  are  middle-aged  or   sediment is the hallmark of glomerular disease. Increased
            older at presentation. There is no sex predilection in dogs,   numbers of hyaline casts and occasionally lipid droplets may
            but approximately 75% of cats with GN are males. Any breed   be observed in the urine sediment of animals with nephrotic
            can be affected by glomerular disease, but familial forms of   range proteinuria. Isosthenuria (urine specific gravity,
            membranoproliferative GN  have been  reported  in soft-  1.007-1.015) may be observed if 67% or more of the nephron
            coated Wheaten Terriers (associated with mutations in the   population has become nonfunctional, and earlier loss of
            slit diaphragm proteins, nephrin, and Neph3/filtrin), Brit-  concentrating ability may occur in animals with medullary
            tany Spaniels (associated with hereditary deficiency of the   deposition of amyloid (e.g., Abyssinian cats, Shar Pei dogs).
            third  component  of  complement),  and Bernese  Mountain   Glomerulonephritis or amyloidosis can lead to chronic
            dogs (often associated with positive serology for  Borrelia   renal failure with the expected biochemical abnormalities
            burgdorferi). Hereditary defects of GBM type IV collagen   (e.g., azotemia, hyperphosphatemia, metabolic acidosis).
            occur as an autosomal recessive trait in English Cocker   Hypoalbuminemia occurs in many dogs with glomerular
            Spaniels and as an X-linked dominant trait in male Samo-  disease (up to 75% of dogs with amyloidosis and 60% of dogs
            yeds. Basement membrane defects are also suspected to   with GN). Hypercholesterolemia occurs in most dogs with
            occur in Doberman Pinschers and Bull Terriers. Familial   glomerular disease (up to 60% of dogs with GN and 90% of
            renal amyloidosis occurs in young Abyssinian, Siamese, and   dogs with amyloidosis) but tends to be a nonspecific finding
            Oriental Shorthair cats and in Shar Pei dogs. Familial amy-  in cats with renal disease. Hypercholesterolemia may be
            loidosis also has been reported in Beagles and English   caused in part by increased hepatic synthesis of cholesterol-
            Foxhounds.                                           rich lipoproteins secondary to chronic hypoalbuminemia.
                                                                   The UPC ratio avoids the confounding effect of total urine
            History and Physical Examination Findings            solute concentration (i.e., specific gravity) on the qualitative
            There are several possible clinical presentations of dogs and   assessment of proteinuria. It correlates well with 24-hour
            cats with glomerular disease. Clinical signs may be related   urinary protein loss but is much easier to measure—that is,
            to the presence of CKD if more than 75% of the nephron   it does not require a 24-hour urine sample. The magnitude
            population has become nonfunctional (e.g., anorexia, weight   of increase in UPC is roughly correlated with the nature of
            loss, lethargy, polyuria, polydipsia, vomiting). This presenta-  glomerular disease. UPCs are highest in dogs with glomeru-
            tion is common. Signs may be related to an underlying infec-  lar amyloidosis (often >10) and lowest in those with intersti-
            tious, inflammatory, or neoplastic disease, or proteinuria   tial renal disease (usually <10). Animals with GN have very
            may be an incidental finding detected during diagnostic   variable UPC (normal to >30). The presence of hematuria or
            evaluation of another medical problem. Clinical signs occa-  pyuria potentially can make the UPC difficult to interpret; it
            sionally may be related to classical nephrotic syndrome (e.g.,   may cause a false-positive result. Normal UPC is < 0.5 in
            ascites, subcutaneous edema). Signs may be related to   dogs and < 0.4 in cats. In one study of dogs, results of UPC
            thromboembolism (e.g., sudden onset of dyspnea with pul-  obtained on three separate urine samples correlated well
            monary embolism, sudden onset of paraparesis with iliac, or   with a single determination made from a pooled sample of
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