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 : ususally no clinical signs until advanced. Proteinuria leads to hypoalbuminemia and sometimes to ascites or edema. Severe glomerular damage leads to loss of nephrons and eventually to renal failure (causing polydipsia/polyuria, inappetence, vomiting).
  • Diagnosis : urine analysis, serum chemistry profile, histopathologic examination of kidney biopsy.
  • Treatment : detect and eliminate the underlying source of antigen, if possible. Special diet, angiotensin-converting enzyme (ACE) inhibition, +/- low-dose aspirin (with great care), +/- immunosuppressant/immunomodulator therapy.
  • Prognosis : variable. Some cases progress rapidly despite therapy, others remain stable for prolonged periods. Many undetected cases probably go on to develop renal failure and are diagnosed at that stage. If complicated by thromboembolism, eg pulmonary or caudal aortic, prognosis is poor.

Diagnosis

Clinical signs

  • Often there are no clinical signs.
  • Sometimes signs are related to the underlying source of antigens.
  • Weight loss, muscle wasting.
  • Poor hair coat.
  • Ascites.
  • Abnormal kidney size (large or small), shape (lumpy), or texture (swollen, turgid).
  • Signs of uremia    .
  • Dyspnea, cyanosis (if complicated by pulmonary thromboembolism).
  • Hindlimb paralysis, cyanosis, absence of femoral pulses (if complicated by aortic 'saddle' thrombosis).
  • Hyphema or retinal detachment in some cats (if GN complicated by severe systemic hypertension    ).

Diagnosis

Differential diagnosis

  • Glomerular disease that is not GN, eg familial renal amyloidosis     in Abyssinian cats.
  • Bacterial urinary tract infection (can cause proteinuria, but sediment usually shows evidence of inflammation).
  • Severe liver disease (causes hypoalbuminemia, but not heavy proteinuria).
  • Severe gastrointestinal disease (- protein losing enteropathy     typically causes hypoalbuminemia and hypoglobulinemia, not just hypoalbuminemia).
  • In patients with acites, other causes of abdominal fluid accumulation (abdominal neoplasia, peritonitis    , portal hypertension    , abdominal hemorrhage).
  • Hyperthyroidism     often causes mild proteinuria.

Outcomes

Prognosis

  • Variable. Depends on response to therapy. 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 recivery, especially if an underlying source of antigen is detected and eliminated. Even if the source of antigen is not found, some animals respond well to therapy and may remain stable for years. Many 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

  • Improvement in clinical demeanor.
  • Diminishing proteinuria as assessed by monitoring serial urine protein creatinine ratios (improvement typically over days to weeks).
  • Control of systemic hypertension.

Reasons for treatment failure

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