History:

“Walter” is a 6-year-old MC Labrador Retriever that presented for a 4-week history of progressive lethargy and anorexia. He was seen by his regular veterinarian 2 weeks prior to presentation and treated conservatively. No improvement was seen. He presented to his regular veterinarian who obtained blood work at that time. Blood work revealed marked azotemia ( BUN- 71, Creatine- 4.3), hypoalbumenima (2.3) and elevations in both phosphorus and potassium. No urinalysis was obtained. The CBC was unremarkable and he tested positive for Lyme on a Snap test.
There were no previous known health issues. The owner reported that “Walter” did vomit twice over the past 2 weeks, and also thought he was drinking more than normal.

Physical exam:

Walter was quiet, alert and responsive- his muzzle was edematous; He was thin and mildly dehydrated. The rest of the exam was unremarkable.

Diagnosis:

Blood was obtained for a blood gas, tick serology and Leptospirosis titers. The blood gas was unremarkable. Lyme IgG antibody was positive (1:512) and Leptospirosis titers were negative. Urine was collected and submitted for urinalysis, culture and a urine P:C. The urine specific gravity was low ( 1.010). There was proteinuria (2000), in an otherwise benign urine sediment. The urine P:C ratio was 8.5. Blood pressure on presentation was 220 and was repeatable. Thoracic and abdominal radiographs were unremarkable. Abdominal ultrasound revealed kidneys that were at the upper limits of a normal size with hyperechoic cortices and faint renal pelvic distension (left greater than right). The pancreas was visible, possibly secondary to abdominal effusion. The renal changes were felt to be non-specific. Differentials included nephritis ( Glomerulonephritis or leptospirosis), amyloidosis or other renal diseases. The liver was small. “Walter” was started on fluids at rate of 1.5 times maintenance, pepcid, and antibiotics. Ampicillin was instituted to treat for Lyme and other potential infectious agents. He was started on Norvasc and enalapril for his persistent hypertension. “ Walter” initially responded to therapy, however then slowly declined. His blood work showed a steady decline in albumin, platelet count , and red blood cell count. There was an initial improvement in renal values, however they never returned to normal. Walter started to develop hind limb edema and the facial edema worsened. He stopped eating and became more lethargic and depressed. Fluid therapy was decreased to maintenance and then later stopped due to his worsening edema. Walter continued to decline and the owners elected euthanasia.

Summary:

There are two major protein losing renal disorders in dogs and cats: immune complex glomerulonephritis and renal amyloidosis. Glomerulonephritis is generally considered to be the more common occurring glomerular disease in dogs and is usually the result of immunologic glomerular injury. It typically causes significant protein loss through the glomerulus, resulting in the nephrotic syndrome. Renal proteinuria, hypoalbuminemia, hypercholesterolemia and peripheral edema or body cavity effusion characterize nephrotic syndrome. In addition, it often causes chronic renal failure due to progressive loss of functional nephrons.
Clinical signs of dogs with glomerulopathies vary. They may be free of clinical signs, may have non-specific signs of disease ( weight loss, lethargy) or may present with signs consistent with chronic renal failure or uremia ( polyuric, polydipsia, anorexia, vomiting, and malodorous breath). Owners may report specific signs related to an underlying inflammatory, infectious or neoplastic condition. Signs of fluid retention ( ascites, peripheral edema) or thromboembolism ( e.g. dyspnea, loss of limb function) may be the reason for presentation. Many dogs may look normal on physical examination where others may have evidence of predisposing inflammatory, infectious or neoplastic processes. Other dogs may have non-specific evidence of systemic disease ( poor body condition and/or coat). In advanced disease states, there may be oral ulcerations and pale mucous membranes. Peripheral edema and abdominal enlargement have been noted as well.
Proteinuria is the hallmark of glomerular disease. A UP:C greater than 1, which is free of inflammation or blood, is considered abnormal. . Isosthenuria is a variable finding in dogs with glomerulopathies. Casts can be common in dogs with glomerular disease- casts are most often hyaline but can be granular, waxy or fatty. Other clinicopathologic findings may include hypoproteinemia due to hypoalbuminemia, hypercholesterolemia, azotemia, hyperphosphatemia and nonregenerative anemia. Abnormalities found in the hemogram may reflect underlying infectious, inflammatory or neoplastic disease. Thrombocytosis is common. The kidneys may look normal or irregular (big or small) on radiographs. Similar changes in shape and size can be seen on ultrasound however increased echogenicity of the cortex and loss of corticomedullary distinction may be noted. Occasionally the renal pelvis may be dilated. Hypertension is a common finding. A thorough screening is recommended for underlying infectious, inflammatory or neoplastic conditions ( i.e. thoracic films, tick and leptosporsis titers, renal biopsy etc) In many of these patients, an underlying cause is not found. Some of the more common infectious agents that can cause a protein losing kidney disease are Brucellosis, Ehrlichiosis, Leptospirosis, Borelliosis, chronic bacterial infections, and heartworm disease. Non-infectious causes include inflammatory bowel disease, systemic lupus, hyperadrenocorticism, and lymphosarcoma.

Treatment:

The goals of treatment with glomerular diseases are to treat potentially underlying disease processes and to reduce proteinuria and manage uremia and other complications associated with renal failure. The use of angiotensin-converting enzyme inhibitors ( ACE inhibitors) to reduce proteinuria in dogs with glomerulopathies is recommended. Typically, enalapril ( 0.5mg/kg PO) is given once daily. Adequate blood pressure control of hypertensive dogs may also lead to reduction in protenuria and slow the progression of the disease. Additional anti-hypertensive agents ( amlodipine) may be necessary. Low dose aspirin therapy may be administered to prevent thromboembolism and may have the added benefit of attenuating progressive glomerular injury through inhibition of platelet cyclooxygenase.
The use of immunosuppressive drugs is generally limited to dogs that have developed glomerulonephritis secondary to a steroid responsive disease, such as systemic lupus. Corticosteriods may exacerbate proteinuria and cause additional glomerular lesions. Dietary protein restriction may be useful in the management of dogs. Fluid therapy should be used if dogs are showing signs of dehydration or are uremic. Fluid therapy in dogs with nephrotic syndrome is difficult to manage, as they are prone to developing or worsening peripheral edema, ascites, pleural effusion and pulmonary edema. Close monitoring and measuring body weight frequently is recommended during fluid administration.
The prognosis is often guarded. It is best based on a combination of factors; severity of renal dysfunction, assessment of renal histology ( if possible) and response to therapy. Patients should be monitored very closely, both clinically and with frequent blood work, urine P: C and blood pressure checks.