ISSN 2398-2969      

Nephrotic syndrome

icanis

Introduction

  • Cause: glomerulonephritis or amyloidosis.
  • Signs: weight loss, lethargy, dyspnea, peripheral edema.
  • Diagnosis: proteinuria, edema (subcutaneous, ascites), hypoalbuminemia, hypercholesterolemia.
  • Treatment: symptomatic.
  • Prognosis: good to poor.

Pathogenesis

Etiology

Predisposing factors

General
  • Breed.
  • Inflammatory/infectious process.

Pathophysiology

  • Immune complexes or amyloid are deposited on glomerular basement membrane → loss of normal glomerular basement membrane → proteinuria → loss of intravascular oncotic pressure → edema and hypercholesterolemia (in response to decreased oncotic pressure).
  • Chronic renal protein loss → inflammatory cells and mediators in glomerulus → renal failure.
  • Chronic renal loss of antithrombin III, increased synthesis of fibrinogen and increased platelet adhesiveness → hypercoagulable state.
  • Proteinuria → hypovolemia → activates renin-angiotensin-aldosterone system, may → hypertension.

Timecourse

  • A few recover or the disease may be controlled for months-years.
  • Rapid progression if renal failure.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rasedee A et al (1996) Naturally occurring canine nephrotic syndrome is a potentially hypercoaguable state. Acta Vet Scand 27 (3), 369-377 PubMed.
  • Vilfranca M et al (1993) A canine nephropathy resembling minimal change nephrotic syndrome in man. J Comp Pathol 109 (3), 271-280 PubMed.

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