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830.e2 Protein-Losing Nephropathy

Protein-Losing Nephropathy Client Education
Sheet
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BASIC INFORMATION
• Tubular dysfunction
○ Basenji (1-5 years) • Dyspnea (if severely uremic, after thrombo-
embolic event, or effusion present)
Definition • Membranous nephropathy • Blindness (if hypertensive)
Protein-losing nephropathy (PLN) is any ○ Doberman pinscher, possibly (3-4 years)
condition in which glomerular damage leads to • Juvenile renal disease (renal dysplasia) PHYSICAL EXAM FINDINGS
biologically significant loss of plasma proteins. ○ Many dog breeds Often unremarkable, although Shar-pei dogs may
Subsequent nephron loss may lead to chronic or have fever, tibiotarsal joint pain, and joint effusion.
acute kidney failure. It is commonly recognized RISK FACTORS Other findings may suggest an underlying disease
in dogs but less so in cats. • Corticosteroid excess (iatrogenic, hyperad- process. In addition to findings mentioned under
renocorticism) History/Chief Complaint, signs may include
Synonyms • Systemic hypertension • Dehydration
PLN, proteinuric kidney disease • Diabetes mellitus • Poor haircoat
• Chronic infections (bacterial, rickettsial, • Pallor
Epidemiology protozoal, fungal, viral, parasitic) • Oral ulceration
SPECIES, AGE, SEX • Chronic inflammatory disease, including • Lipid corneal deposits
• Familial nephropathy immune-mediated disease • Retinal hemorrhage/detachment
○ Dogs > cats • Neoplasia • Kidneys may be normal sized, small, or large
○ Age at onset of illness varies with breed. • Some drugs or toxins (e.g., pamidronate; (rare).
○ Sex predisposition: see Genetics, Breed tyrosine kinase inhibitor Palladia)
Predisposition Etiology and Pathophysiology
• Glomerulosclerosis CONTAGION AND ZOONOSIS • Familial nephropathy
○ Either sex Some infectious causes of GN are zoonotic. ○ Diverse group of hereditary renal diseases
○ Incidence increases with age; average of ○ Defects vary with individual diseases and
8 years GEOGRAPHY AND SEASONALITY include familial amyloidosis, failure of
• Membranous nephropathy Some infectious causes of GN are geographically tubular protein resorption, and defects
○ Either sex and/or seasonally limited. in type IV collagen in the glomerular
○ Most common PLN in the cat basement membrane.
○ Mean age: cats 3-4 years; dogs 7 years ASSOCIATED DISORDERS ○ In some cases, nephropathy is associated
• Minimal change nephropathy • Nephrotic syndrome with other conditions (e.g., food sensitivity
○ Uncommonly described in dogs and • Chronic kidney disease [soft-coated wheaten terrier], complement
cats • Systemic hypertension deficiency [Brittany spaniel]).
• Glomerulonephritis (GN) • Hyperlipidemia ○ Juvenile renal dysplasia may also be
• Amyloidosis • Thromboembolic disease, including pulmo- accompanied by proteinuria.
• Drug- or toxin-induced damage nary thromboembolism • Glomerulosclerosis
○ Results from hyperfiltration in dogs with
GENETICS, BREED PREDISPOSITION Clinical Presentation typical chronic kidney disease, often as an
Familial nephropathy: typical age of onset DISEASE FORMS/SUBTYPES end-stage lesion
in parentheses and pattern of inheritance if • GN ○ Reported in dogs with familial
known • Amyloidosis nephropathy, systemic hypertension,
• Glomerular disease • Familial nephropathy diabetes mellitus, hyperadrenocorticism,
○ Bernese mountain dog (2-5 years), • Glomerulosclerosis and postradiation therapy. Many other
suspected autosomal recessive • Membranous nephropathy causes are described in people.
○ Brittany spaniel (4-9 years), autosomal • Minimal change disease ○ Sclerosis ultimately leads to altered intra-
recessive • Other rare forms described (e.g., crescentic, glomerular hemodynamics and progressive
○ Rottweiler (<1 year) IgA nephropathy) renal failure.
○ Soft-coated wheaten terrier (2-11 years) • Membranous nephropathy
○ Beagle (2-8 years) HISTORY, CHIEF COMPLAINT ○ Immune complex deposition in the
• Amyloidosis Clinical signs are often absent before glomerular basement membrane without
○ Beagle (5-11 years) development of azotemia or severe hypo- evidence of inflammation
○ English foxhound (5-8 years) albuminemia. Shar-pei dogs may present ○ Primary (most common) and secondary
○ Shar-pei (1-6 years) for lameness and/or fever. When signs are forms can be distinguished by the location
○ Abyssinian cat (1-5 years), autosomal present, they may be due to kidney failure, of the immune complex deposition.
dominant with incomplete penetrance nephrotic syndrome, or an underlying disease • Minimal change nephropathy
○ Oriental shorthair cat (<5 years) process. ○ Loss of anionic charge in glomerulus leads
○ Siamese (<5 years) • Lethargy to selective albumin loss.
• Basement membrane abnormality • Anorexia ○ Because electron microscopy is required
○ Bull terrier (1-10 years), autosomal • Weight loss for diagnosis, it may be underreported in
dominant • Polyuria and polydipsia (PU/PD) veterinary medicine.
○ Doberman pinscher (<1-6 years) • Vomiting (if uremic) • Glomerulonephritis
○ English cocker spaniel (<2 years), auto- • Halitosis (if uremic) • Amyloidosis
somal recessive • Pendulous abdomen (ascites; if • Drugs and toxins cause glomerular damage by
○ Samoyed (<1 year), X-linked dominant hypoalbuminemic) multiple mechanisms (e.g., podocyte damage,
(males affected) • Subcutaneous edema (if hypoalbuminemic) glomerulosclerosis).

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