Proteinuria

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• Definition: an abnormally increased concentration of protein (often albumin) in urine.
• Causes: proteinuria may be preglomerular, glomerular or post glomerular. Glomerular proteinuria is the most important kind. In preglomerular proteinuria, the kidneys are presented with an abnormally increased concentration of small proteins in the blood, which are smaller than the effective the glomerular filtration barrier and exceeds the ability of the renal tubules to reabsorb it. This protein may, for example, be free hemoglobin, myoglobin or, in patients with lymphoma or multiple myeloma, immunoglobulin light chains (Bence-Jones protein). In glomerular proteinuria, the glomeruli are damaged and an abnormally large amount of protein leaks through an excessively permeable glomerular filter into the urinary space. For example, in glomerulonephritis, antigen-antibody complexes may be deposited, or may form, in the glomerular capillary basement membranes, damaging them.  Damage to the filtration barrier leads to glomerular proteinuria, sometimes very severe. Glomerular amyloidosis is another important cause of severe glomerular proteinuria.  In post glomerular proteinuria, tissue damage or inflammation beyond the glomeruli is responsible for the increased urinary protein concentration. For example, bacterial urinary tract infection (upper or lower) can lead to passage of proteinaceous inflammatory exudate in the urine. Damaged renal tubules may fail to reabsorb filtered protein, leading to tubular proteinuria.  Various endocrinopathies, and a variety of other environmental and metabolic factors can lead to benign proteinuria which is usually mild and may be reversible with treatment of the underlying cause.
• Severity: proteinuria may be overt (detectable using conventional urine dipsticks) or less severe. Microalbuminuria is the term used to describe an abnormally large amount of albumin in the urine, but not enough to be detectable using a conventional dipstick. It has recently been suggested that microalbuminuria may be a useful early marker for a wide variety of systemic disease states, particularly inflammatory and neoplastic disorders. Massive (or heavy) proteinuria may lead to the nephrotic syndrome (the combination of heavy proteinuria and consequent hypoalbuminemia, hypercholesterolemia and edema or ascites).
• Signs: preglomerular proteinuria may be associated with discolored urine and clinical signs of the underlying disease. Post glomerular proteinuria is usually associated with abnormally increased frequency of urination, straining, and, again, discolored urine (typically pink or red). Often glomerular proteinuria causes no clinical signs until it is severe. Then it may lead to hypoalbuminemia and sometimes to subcutaneous edema (eg of the distal limbs). Progressive loss of damaged glomeruli may eventually lead to renal failure (with polydipsia/polyuria, inappetence, and vomiting).
• Diagnosis: urine analysis, including sediment examination, urine protein quantitation, serum chemistry profile, histopathologic examination of a kidney biopsy. In preglomerular proteinuria there will be an excessive amount of a protein in the blood. In post glomerular proteinuria there will usually be evidence in the urine sediment of urinary tract inflammation or hemorrhage. In glomerular proteinuria, there will be excessive albumin in the urine, which may be extreme.
• Treatment: categorize the proteinuria and then eliminate the underlying cause, if possible. Glomerular proteinuria may be managed using a renal diet, low-dose aspirin, angiotensin-converting enzyme (ACE) inhibition, ± immunosuppressant / immunomodulator therapy.
• Prognosis: very variable depending upon the underlying cause and the severity. Some cases with glomerular proteinuria progress rapidly despite therapy, others remain stable for prolonged periods. If complicated by thromboembolism (eg pulmonary or caudal aortic) or advanced renal failure, prognosis is poor.

• Cats with preglomerular proteinuria may have pigmenturia (often red or brown because of the presence of hemoglobin or myoglobin ) or other signs related to the underlying cause (eg bone pain, radiographically-evident lucent bone lesions, lymphadenopathy).
• Patients with post glomerular proteinuria may have kidney pain (due to pyelonephritis ), discolored urine , increased frequency of urination, straining to urinate, or other signs of urinary tract inflammation .
• Patients with glomerular proteinuria often have no clinical signs unless urinary protein loss is severe. Non-specific signs of malaise (eg lethargy, depression, weight loss) may develop. Peripheral (eg distal limb) subcutaneous edema will develop if hypoalbuminemia becomes sufficiently severe. Ascites and/or pleural effusion may develop. Polydipsia / polyuria will develop if glomerular injury is sufficiently severe to cause renal insufficiency.
• Signs of an underlying infectious, inflammatory or neoplastic disorder may be evident in patients with glomerulonephritis  (although often not).

• Acute dyspnea or sudden death if pulmonary thromboembolism complicates severe glomerular proteinuria.
• Cold, pulseless, paralyzed hind limbs with nail-bed cyanosis if caudal aortic (saddle) thrombosis develops.
• Signs of uremia if severe renal failure ensues. Signs of uremia include profound depression, anorexia, vomiting, halitosis, weight loss, and oral and gastric mucosal ulceration.
• Acute renal failure may follow anesthesia of a cat with unrecognized severe glomerular proteinuria.

• Any age. 
• Membranous glomerulopathy (syn. membranous glomerulonephropathy, membranous nephropathy), a major cause of glomerular proteinuria in cats, is 6 times more common in males than in females and is more common in young cats (mean 3.6 years; range 1-7 years)
• Cats with familial amyloidosis are usually less than 5 years old when they are first diagnosed. Often they are presented in renal failure, rather than because of heavy proteinuria (this is because amyloid deposits are predominantly in the renal medulla rather than the glomeruli).
• Glomerulonephropathy can develop at any age, but is more frequently diagnosed in middle-aged to older animals. 
• Most of the causes of preglomerular and post glomerular proteinuria are also more common in middle-aged to older animals.

• Renal amyloidosis (not always associated with heavy proteinuria):
  • Abyssinian .
  • Siamese .
  • Oriental shorthair .

• Anesthesia of cats with unrecognized glomerular proteinuria may lead to acute renal failure.
• Arterial thromboembolism may complicate severe glomerular proteinuria. This is because severe glomerular proteinuria leads to a hypercoagulable state. This state results partly from urinary loss of antithrombin-3 and partly because platelet activity may be increased in hypoproteinemic patients.

• For preglomerular proteinuria, intravascular hemolysis (hemoglobinuria), rhabdomyolysis (myoglobinuria), and lymphoid malignancies (Bence-Jones proteinuria) are the most important causes.
• For post glomerular proteinuria, idiopathic cystitis and urolithiasis are important causes. Bacterial urinary tract infections and urinary tract neoplasia are less common.
• The molecular basis of some familial glomerulopathies is beginning to be elucidated.
• Renal amyloidosis in cats is usually caused by accumulation and polymerization of part of the protein serum amyloid A (SAA).  SAA is an acute phase reactant, increasing in inflammatory disease states. It has therefore been conjectured that renal amyloidosis may follow chronic inflammatory disorders. However, there is usually no historical or physical examination evidence of extra-renal inflammation in patients with renal amyloidosis.
• Immune-complex glomerulonephropathy can cause glomerular proteinuria in cats. Unfortunately, it is usually idiopathic, the source of antigens contributing to the glomerular damage remaining uncertain.

Specific causes of glomerulonephropathy include:

• Infections and infestations (eg FeLV, FIV, FIP, abscesses, dirofilariasis, bacterial cholangiohepatitis, mycoplasmal arthritides).
• Non-infectious causes of severe inflammation and tissue damage (eg pancreatitis ).
• Various forms of neoplasia (‘neo-antigens’; lymphoma, leukemia, mast cell tumor).
• Glomerulonephritis may accompany, and presumably have the same underlying cause as, some other immune-mediated disorders, eg
  • Immune-mediated polyarthritis . 
  • Immune-mediated thrombocytopenia .
  • Immune-mediated hemolytic anemia . 
  • Systemic lupus erythematosus (SLE) .
  • Polyarteritis.
  • Familial predisposition to immune complex formation has not been identified in cats.
• True autoimmune response to ‘native’ glomerular antigens (not, as yet, confirmed in cats).

• For preglomerular proteinuria:
  • Disorders associated with intravascular hemolysis (hemoglobinuria).
  • Severe muscle injury, rhabdomyolysis (myoglobinuria).
  • Lymphoid malignancy (eg plasma cell tumor) or another cause of paraproteinemia.
• For glomerular proteinuria:
  • An inflammatory, infectious, or neoplastic source of antigens that can contribute to immune complex formation.
  • A familial predisposition to form immune complexes or deposit amyloid in the glomeruli.
  • Altered (ie increased) intestinal permeability has been postulated to play a role in some canine breeds and may prove to be relevant in cats.
• For post glomerular proteinuria:
  • Factors predisposing to urinary tract inflammation or infection: eg compromised immune function, anatomical defects in the urinary tract, urinary motility disorders, catheterization.
  • Familial tendency to form uroliths.
  • Urinary neoplasia (rare in cats).

• Proteinuria may be preglomerular, glomerular or post glomerular. Glomerular proteinuria is the most important origin of proteinuria.
• In preglomerular proteinuria, the kidneys are presented with an abnormally increased concentration of a small protein in the blood, which are smaller then the effective glomerular filtration barrier and exceeds the ability of the renal tubules to reabsorb it. This protein may, for example, be free hemoglobin, myoglobin or, in patients with lymphoma or multiple myeloma, immunoglobulin light chains (Bence-Jones protein).
• In glomerular proteinuria, the glomeruli are damaged and an abnormally large amount of protein leaks through an excessively permeable glomerular filter into the urinary space. For example, in membranous glomerulopathy, antigen-antibody complexes may be deposited, or may form in situ, in or near the glomerular capillary basement membranes, damaging them. Complement-mediated damage to the filtration barrier leads to glomerular proteinuria, sometimes very severe. Renal amyloidosis is another important cause of glomerular proteinuria. However, in Abyssinian cats amyloid deposition in the renal medulla, rather than in the glomeruli, may cause renal failure with little proteinuria. 
• In post glomerular proteinuria, tissue damage or inflammation beyond the glomeruli is responsible for the excessive urinary protein losses. For example, bacterial urinary tract infection (upper or lower) can lead to passage of proteinaceous inflammatory exudate in the urine. Damaged renal tubules (eg in acute tubular necrosis) may fail to reabsorb filtered protein, leading to tubular proteinuria. 
• Various endocrinopathies, and a variety of other environmental and metabolic factors can lead to benign proteinuria which is usually mild and may be reversible with treatment of the underlying cause.
• In membranous glomerulopathy, the most important cause of glomerular proteinuria in cats:
  • Ag-Ab complexes form in situ or lodge in or near the glomerular capillary basement membranes    complement activation   glomerular injury   leakage of proteins, especially albumin, through the now excessively permeable glomerular filter   proteinuria   (if severe) hypoalbuminemia, weight loss, ascites, peripheral edema and hypercholesterolemia.
  • Glomerular damage   decreased glomerular filtration through affected glomeruli   increased glomerular filtration through other, less damaged nephrons   ‘hyperfiltration’ and glomerulosclerosis of remaining nephrons   (if sufficiently severe) chronic renal failure.
  • Loss of antithrombin III, platelet hyperactivity, and (sometimes) thrombocytosis   hypercoagulable state   thromboembolic disorders (lungs, caudal aorta).

• Hemoglobinuria and myoglobinuria are usually associated with acute, short-lived disorders. Bence-Jones proteinuria may be present for weeks or months before it is detected.
• Post glomerular proteinuria is usually detected fairly quickly because of associated straining, increased frequency of urination, inappropriate urination, and (sometimes) discolored urine.
• The time course of glomerular proteinuria is much more variable. The disease may progress rapidly or remain stable (and sometimes, presumably, undetected) for years.

• Sometimes signs related to the underlying cause of proteinuria are the reason for presentation.
• Sometimes proteinuria is an incidental finding on a routine health screen.
• Otherwise, the presenting problems are very variable and depend on the underlying cause:
  • Pigmenturia, pollakiuria, stranguria, peripheral edema, ascites, pleural effusion, signs of arterial thrombosis.
  • Lethargy, weight loss, polyuria / polydipsia (if renal insufficiency develops).

• If the proteinuria is preglomerular: pigmenturia (maybe).
• If the proteinuria is post glomerular: stranguria, pollakiuria, nocturia, inappropriate urination, discolored urine
• If the proteinuria is glomerular no abnormalities may be reported; or
  • Sometimes the history relates to the underlying cause of glomerular damage.
  • Swollen distal limbs (due to peripheral edema).
  • Abdominal enlargement (if ascites is present).
  • Acute dyspnea (if pulmonary thromboembolism is present).
  • Hindlimb paralysis (if saddle thrombosis is present).
  • Polyuria/polydipsia (if renal insufficiency has developed).
  • Lethargy, weight loss, vomiting/diarrhea (if uremic).

• Pigmenturia (sometimes) if preglomerular.
• Stranguria, pollakiuria, inappropriate urination, discolored urine (if post glomerular).
• Glomerular proteinuria:
  • Often there are no clinical signs.
  • Sometimes there are signs related to the underlying cause of glomerular damage.
  • Weight loss, muscle wasting.
  • Poor haircoat.
  • Pitting, subcutaneous edema of the distal limbs.
  • Ascites (fluid wave on abdominal ballotment).
  • Abnormal kidney size (large or small) or shape.
  • Signs of uremia .
  • Dyspnea without obvious abnormalities on auscultation or radiography (pulmonary thromboembolism).

Urinalysis

• Preferably analyze a sample obtained by cystocentesis  that does not result in complications such as perforation or vagal response.
• Proteinuria  detected on routine dipstick, or another semi-quantitative method.
• If the cause is glomerular, there should be no gross hematuria  or evidence of urinary tract infection (pyuria, bacteriuria, large amounts of cellular debris) on urine sediment examination . If these are present, first investigate and rule out causes of post glomerular proteinuria, rather than investigating glomerular proteinuria. Hyaline casts may be seen on urine sediment examination of animals with glomerular proteinuria.
• Urine protein:creatinine ratio (UPC) should be less than 0.4 in cats. UPC values between 0.4 and 1.0 should be further evaluated for underlying causes. Animals with UPC values over 1.0 should be treated to attempt to reduce proteinuria.

Serum biochemistry

• Hypoalbuminemia  (severe glomerular proteinuria) .
• Hypercholesterolemia  (severe glomerular proteinuria).
• ± Azotemia  (if glomerular damage has led to renal failure).
• Paraproteinemia, eg hypergammaglobulinemia  (preglomerular proteinuria).
• The serum may be discolored by free hemoglobin or myoglobin (preglomerular proteinuria).

Hematology

• Evidence of underlying inflammation, infection or neoplasia in some cases.
• Normocytic, normochromic, non-regenerative anemia in some cases; especially those with chronic inflammation or renal failure.
• Sometimes concurrent immune-mediated thrombocytopenia or anemia is present.

Abdominocentesis

• See technique .
• If any fluid is present, it is usually a transudate (severe glomerular proteinuria).
• FIP exudates in thorax or abdomen are possible as underlying cause of glomerular injury.

Radiography

• Skeletal survey may reveal lucent bone lesions (preglomerular proteinuria due to lymphoid malignancy, eg multiple myeloma ).
• Lymphadenopathy (preglomerular proteinuria due to lymphoid malignancy).
• Urolithiasis, chronic cystitis, bladder neoplasia (post glomerular proteinuria - may require a contrast study to elucidate).
• Look for underlying infectious, inflammatory or neoplastic processes, particularly in the body cavities.
• Poor abdominal contrast, due to ascites, may be present in some patients with severe glomerular proteinuria. Pleural effusion may also be present.
• Kidneys may appear enlarged, small, irregular or (often) normal.

2-D Ultrasonography

• Urolithiasis, chronic cystitis, bladder neoplasia (post glomerular proteinuria).
• Look for an underlying infectious, inflammatory or neoplastic process, particularly in the body cavities.
• Dilated renal pelvis if polydipsic / polyuric.

Histopathology

• Bladder biopsy for investigation of some post glomerular causes of proteinuria.
• Renal biopsy and histopathologic examination required for definitive diagnosis of glomerular diseases. Appropriate samples for light microscopy, electron microscopy and immunofluorescence should be obtained at time of renal biopsy.
• Ultrasound-guided needle biopsy is commonly done, several pieces may need to be taken if a small biopsy needle is used. Consult your pathologist.

Serology

• Can be used to check for selected, potentially underlying, infectious diseases, eg FeLV and FIV testing, toxoplasmosis, cryptococcosis, etc.
• Anti-nuclear antibody test. 
• Coombs test (if suspicious of IMHA). 

Arterial blood pressure measurement

• Systemic arterial hypertension commonly complicates glomerular disease.

• Hypoalbuminemia and hypercholesterolemia support a diagnosis of glomerular, rather than pre- or post glomerular proteinuria.
• Heavy proteinuria ± hyaline casts in the absence of other urine sediment abnormalities, paraproteinemia or pigmenturia strongly supports a diagnosis of glomerular proteinuria.

• Characteristic histopathologic findings on kidney biopsy will determine the cause of glomerular proteinuria.
• For diagnosis of inflammatory bladder disorders and urolithiasis, bladder biopsy, urine bacterial culture and urolith analysis may be needed.
• For diagnosis of neoplastic causes of preglomerular proteinuria, fine needle aspiration biopsy, needle biopsy (eg Trucut®) or surgical biopsy of lesions and histologic examination will be required.

• Very variable, depending on the cause. Findings for pre- and post glomerular causes of proteinuria may include lymphoid malignancy, skeletal muscle injury, and inflammatory or neoplastic lesions in the urinary tract.
• In patients with glomerular proteinuria:
  • Often no gross renal lesions are present.
  • Variable kidney size.
  • Fine stippling of renal cortices may be detected.
  • Chronic cases may have renal fibrosis causing firmness of renal parenchyma, perhaps with some scarring and alteration of the renal contour.
  • Check for evidence of uremia / renal failure (parathyroid gland size, mucosal ulcerations).

• Very variable depending on the cause.
• Cross references: transitional cell carcinoma, multiple myeloma, lymphoma, chronic cystitis, pyelonephritis.
• Membranous glomerulopathy is the most common cause of glomerular proteinuria in cats:
  • Thickening of the glomerular basement membrane. Later, there may be irregular thickening and distortion of the capillary walls and sometimes widening of the mesangium.

• Need to categorize the proteinuria first (preglomerular, glomerular, post glomerular) and then consider differential diagnoses.
• Membranous glomerulopathy / glomerulonephropathy (sporadic or familial).
• Glomerular amyloidosis (proteinuria may be very severe).
• Familial glomerular disease that is not immune complex-mediated or amyloidosis.
• Renal tubular disease (causes proteinuria that is often not as severe as that caused by glomerular disease).
• Bacterial urinary tract infection, lower urinary tract neoplasia (rare in cats), urolithiasis (can cause proteinuria, but sediment usually shows clear evidence of inflammation).
• Genital tract disease (causes proteinuria on free-catch urine samples, but typically not on cystocentesis-derived samples).
• Severe liver disease (causes hypoalbuminemia, but not heavy proteinuria).
• Severe gastrointestinal disease (protein-losing enteropathy typically causes hypoalbuminemia and hypoglobulinemia, but not proteinuria).
• Other causes of abdominal fluid accumulation (abdominal neoplasia, peritonitis , portal hypertension, abdominal hemorrhage).
• Right-sided congestive heart failure (ascites)  or severe heartworm disease (which can also cause glomerulonephritis, to complicate matters).
• Benign proteinuria caused by a wide range of environmental and metabolic factors.

• There are many, diverse causes of preglomerular and post glomerular proteinuria which have equally diverse treatment approaches. Cross references: transitional cell carcinoma, multiple myeloma, lymphoma, chronic cystitis, interstitial cystitis, idiopathic cystitis, pyelonephritis

Standard treatment for glomerular proteinuria

• Detect and eliminate the underlying cause, if at all possible.
• Manage renal failure / renal insufficiency, if it has developed.
• Manage systemic hypertension, if it is complicating the proteinuric state.

Diet

• Feed a moderately protein-restricted, high-quality protein diet (renal diet).
• Restrict phosphorous and sodium intake and supplement n3 fatty acids. (Dietary phosphorous restriction is a critical component of renal diets.)

ACE inhibition

• ACE-inhibitors  help to reduce the degree of proteinuria and slow disease progression. ACE-inhibitors should be implemented in animals with persistent glomerular origin proteinuria wiht UP/C >1. Monitor for developing or worsening azotemia and lower the dose of ACE inhibitor, if azotemia worsens substantially.
• If systemic hypertension is present, and is not controlled by ACE inhibition alone, consider use of other antihypertensive drugs, eg amlodipine  in conjunction with the ACE inhibitor.

Immunomodulation

 Immunosuppressant therapy for protein-losing glomerulopathies is somewhat controversial and there is little evidence to support its use.

• Glucocorticoids are generally not indicated because they can worsen proteinuria and promote thromboembolism. If immune-mediated polyarthritis, thrombocytopenia or hemolytic anemia complicates glomerulonephritis, however, a glucocorticoid may need to be used. Membranous glomerulopathy may respond to glucocorticoid therapy better than other types of glomerulonephropathy but data confirming this benefit is lacking at this time.
• In one study, cyclosporine  was shown not to be effective in treatment of canine glomerulonephritis. No equivalent feline study has been done.

Managing edema or ascites

• Abdominocentesis or thoracocentesis is rarely needed for management of ascites / pleural effusion. Use if respiratory distress or excessive respiratory effort is evident.
• Sodium restriction may help manage edematous states.
• Furosemide  (1-2 mg/kg per os, as needed) is sometimes used to control edema or ascites, but its use may exacerbate hypovolemia and promote azotemia and even uremia. It should be used with caution and careful monitoring, if at all.
• Plasma transfusion, with careful monitoring, may be indicated in severely hypoproteinemic cases.

• Very variable depending on the underlying cause. Cross references:  multiple myeloma, lymphoma, chronic cystitis, interstitial cystitis, idiopathic cystitis, pyelonephritis.
• Heavy proteinuria and azotemia at the time of diagnosis are usually considered negative prognostic indicators. However, some patients with heavy proteinuria presumed to be caused by severe glomerular disease make a full recovery, especially if an underlying cause can be detected and eliminated. Even if the cause 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. Advanced chronic kidney disease is a negative prognostic indicator even if (especially when) the proteinuria resolves.
• The prognosis is generally poor if arterial thromboembolism develops.

• Diminishing proteinuria as assessed by monitoring serial urine protein: creatinine ratios (improvement noted over several weeks).
• Systemic hypertension controlled.
• Alleviation of any concurrent signs such as stranguria, pollakiuria, and discolored urine.

• Incurable underlying cause.
• 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.

• Recent references from PubMed.
• White J D, Norris J M, Bosward K L, Fleay R, Lauer C & Malik R (2008) Persistent haematuria and proteinuria due to glomerular disese in related Abyssinian cats. J Feline Med Surg 10 (3), 219-229 PubMed.
• Whittemore JC, Miyoshi Z, Jensen WA, Radecki SV, Lappin MR. (2007)  Association of microalbuminuria and the urine albumin-to-creatinine ratio with systemic disease in cats.  JAVMA  230, 1165-1169 PubMed.
• Grauer G F (2007) Measurement, interpretation, and implications of proteinuria and albuminuria. Vet Clin North Am Small Anim Pract  37, 283-295 PubMed.
• Elliott J & Syme H M (2006) Proteinuria in chronic kidney disease in cats — prognostic marker or therapeutic target? JVIM 20, 1052-1053 PubMed.
• Welles E G, Whatley E M, Hall A S & Wright J C (2006) Comparison of Multistix PRO dipsticks with other biochemical assays for determining urine protein (UP), urine creatinine (UC) and UP:UC ratio in dogs and cats. Vet Clin Pathol 35, 31-36.
• Kuwahara Y, Ohba Y, Kitoh K, Kuwahara N and Kitagawa H. (2006) Association of laboratory data and death within one month in cats with chronic renal failure. JSAP 47, 446-450.
• Langston C E & Reine N J (2006) Hyperthyroidism and the kidney. Clinical Techniques in Small Animal Practice 21, 17-21.
• Mardell E J & Sparkes A H (2006) Evaluation of a commercial in-house test kit for the semi-quantitative assessment of microalbuminuria in cats. J Feline Med Surg 8, 269-278 PubMed. 
• Syme H M, Markwell P J, Pfeiffer D & Elliott J (2006) Survival of cats with naturally occurring chronic renal failure is related to severity of proteinuria. JVIM 20, 528–535 PubMed.
• White J D, Norris J M, Baral R M & Malik R (2006) Naturally-occurring chronic renal disease in Australian cats: a prospective study of 184 cases. Aus Vet J 84, 188-194 PubMed.
• Lees G E, Brown S A, Elliott J, Grauer G E & Vaden S L (2005) Assessment and management of proteinuria in dogs and cats: 2004 ACVIM Forum Consensus Statement (small animal). JVIM  19, 377-385 PubMed.
• Lees G E (2004) Early diagnosis of renal disease and renal failure. Veterinary Clinics of North America. Small Animal Practice 34, 867-885
• Osborne C A, Bartges J W, Polzin D J, Lulich J P, Johnston G R & Cox V (1996) Percutaneous needle biopsy of the kidney. Indications, applications, technique, and complications. Vet Clin North Am Small Anim Pract 26, 1461-1504
• Arthur J E, Lucke V M, Newby T J (1986) The long term prognosis of feline idiopathic membranous glomerulonephritis. JAAHA 22, 731-737.
• Nash A S, Wright N G, Spencer AJ & Thompson H (1979) Membranous nephropathy in the cat; a clinical and pathological study. Vet Rec 105, 71-77.

• Dr Richard Squires BVSc PhD DVR DipACVIM MRCVS
• Dr Larry G Adams DVM PhD DipACVIM(SAIM)

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