Feline nephrotic syndrome

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Nephrotic syndrome is characterized by the combination of protein in the urine, low protein level in the blood, high cholesterol and abnormal fluid accumulation in any part of the body (oedema). Dogs are affected more commonly than cats. The average age of onset varies, but middle-aged dogs are most commonly affected. Several breeds are felt to be at higher risk than average.

The glomeruli of the kidneys are the parts that normally filter the blood. They consist of capillaries that are fenestrated (leaky, due to little holes called fenestrae or windows) and that allow fluid, salts, and other small solutes to flow through, but normally not proteins. In nephrotic syndrome, the glomeruli become damaged due to inflammation and hyalinisation so that small proteins, such as albumins immunoglobulins and anti-thrombin can pass through the kidneys into urine. Albumin is the major protein in the blood which maintains colloid osmotic pressure- this prevents leakage of blood from vessels into tissue. However, experiments show that the edema formation in nephrotic syndrome is more so due to microvascular damage and intense salt and water retention by the damaged kidneys (due to increased angiotensin secretion). The mechanism is very complex and still not fully understood. In response to leakage of albumin, the liver begins to make more of all its proteins, and levels of large proteins (such as alpha 2-macroglobulin and lipoproteins) increase. The excess lipoproteins end up in the urine filtrate, which is then rebsorbed by the tubular cells, which end up shedding and forming oval fat bodies or fatty casts.

Common causes of nephrotic syndrome in cats include: 

1) Glomerulonephritis (GN)

This is an inflammation of the kidney – specifically in the area referred to as the glomerulus. Familial (appearing in multiple members of the same family) GN has been reported in cats. Acquired GN is uncommon. In most reports of GN in the cat, no predisposing factors have been found and the disease has been classified as idiopathic. Young adult male cats typically are affected and there is no breed predisposition. The clinical presentation falls into two categories: classical nephrotic syndrome characterized by subcutaneous oedema, ascites, proteinuria, hypercholesterolemia, and hypoalbuminemia without marked azotemia, and chronic renal failure with azotemia. Laboratory abnormalities in cats with GN include proteinuria, hypoalbuminemia, hypercholesterolemia, and non-regenerative anaemia. The presence of azotemia and hyperphosphatemia is variable. Histologically, the lesions are those of membranous nephropathy with IgG and complement deposition. An attempt should be made to diagnose and treat any underlying disease process that might have resulted in the development of GN. Cats with oedema and ascites but without azotemia may be treated with furosemide (2–4 mg/kg q24h) and prednisolone (2–4 mg/kg q24h). These cats also should be fed a high protein, low sodium diet. Cats with azotemia and end-stage renal disease due to GN should be treated for chronic renal failure. The prognosis for cats with GN is variable. The disease is slowly progressive although remissions have been described. Cats with end-stage renal disease secondary to GN have the shortest survival times (a few weeks to a few months). Non-azotemic cats presented with the nephrotic syndrome do better and survive several months to several years.

2) Amyloidosis

This is the deposition in organs and tissues of a protein called amyloid that compromise normal function. Familial amyloidosis has been reported in the Oriental shorthair, Abyssinian and Siamese. Acquired amyloidosis is uncommon. The type, number, and severity of clinical signs associated with the nephrotic syndrome are variable. Signs may be associated with an underlying disease process, such as with infection and immune disease.

Clinical symptoms

Oedema or ascites (fluid in the abdominal cavity), acute dyspnea (difficulty breathing) or panting, anorexia, weight loss, lethargy, loss of vision

Diagnosis

Diagnosis is based on clinical symptoms and confirmed  by the demonstration of large amounts of albumin in the urine. Confirmation can only be accurately confirmed with biopsy of kidney tissue. Other tests include: Complete blood count (CBC), Biochemical profile, Urinalysis, Urine Protein:Creatinine Ratio, Bacterial urine culture, Chest and abdominal X-rays, Abdominal ultrasound +/- kidney biopsy, Blood pressure

Treatment

It is most important to determine whether the patient’s condition warrants admission to the hospital for treatment, or treatment at home as an outpatient. Treatment may include: