Glomerulonephritis

GN

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Introduction

  • Cause : deposition or in situ formation of antigen-antibody complexes in the basement membranes of glomerular capillaries in the kidneys.
  • Signs : often no clinical signs until very advanced. Proteinuria leads to hypoalbuminemia and sometimes to subcutaneous edema, eg of the distal limbs. Severe glomerular loss may eventually lead to signs of acute or chronic renal failure, eg polydipsia/polyuria, inappetence, vomiting.
  • Diagnosis : urine analysis, serum chemistry profile, histopathologic examination of a kidney biopsy.
  • Treatment : detect and eliminate the underlying source of antigen, if at all possible. Special diet, low-dose aspirin, angiotensin-converting enzyme (ACE) inhibition, +/- immunosuppressant/immunomodulator therapy.
  • Prognosis : very variable. Some cases progress rapidly despite therapy, others remain stable for prolonged periods. If complicated by thromboembolism (eg pulmonary or caudal aortic), prognosis is poor.

Diagnosis

Clinical signs

  • Often there are no clinical signs.
  • Sometimes there are signs related to the underlying source of antigens.
  • Weight loss, muscle wasting.
  • Poor haircoat.
  • Pitting, subcutaneous edema of the distal limbs.
  • Ascites (fluid thrill on abdominal palpation).
  • Abnormal kidney size (large or small) or shape.
  • Signs of uremia .
  • Dyspnea without obvious abnormalities on auscultation (thromboembolism).

Differential diagnosis

  • Familial glomerular disease that is not GN.
  • Renal amyloidosis (proteinuria may be more severe than in glomerulonephritis).
  • Bacterial urinary tract infection (can cause proteinuria [Urinalysis: protein] , but sediment usually shows evidence of inflammation ).
  • Severe liver disease (causes hypoalbuminemia [Blood biochemistry: albumin] , but not heavy proteinuria).
  • Hyperadrenocorticism (hypercoagulable state, proteinuria due to systemic hypertension and/or urinary tract infection, with a non-active or active urinary sediment examination respectively).

Outcomes

Prognosis

  • Very variable. Especially heavy proteinuria and presence of azotemia at the time of diagnosis of GN are usually considered negative prognostic indicators. However, some patients with heavy proteinuria make a full recovery, especially if an underlying source of antigens is detected and eliminated. Even if the source of antigens is not found, some animals respond to therapy and may remain stable for years. Some cases eventually progress to chronic renal failure and need to be managed for that.
  • The prognosis is generally poor if thromboembolism develops.

Expected response to treatment

  • Diminishing proteinuria as assessed by monitoring serial urine protein creatinine ratios (improvement noted over several weeks).
  • Systemic hypertension controlled.

Reasons for treatment failure

  • Progression to chronic renal failure and uremia.
  • Progressive or uncontrolled proteinuria, hypoalbuminemia → intractable edema, ascites or fatal thromboembolism.
  • Uncontrolled hypertension → fatal cerebral vascular accident or other complications.
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