Protein-losing nephropathy: the technician's role quiz

Protein-losing nephropathy: the technician's role

NATIONAL HARBOR, MD – Protein-losing nephropathy (PLN) is a term that describes diseases of the glomerulus, a complex filtration bed that allows water and solutes to pass. When damage to the glomerulus occurs, larger molecules, i.e. albumin and ATIII, can pass, causing damage that may be transient, or persistent and progressive, explained Dawn Terrill, CVT, VTS (SAIM), speaking at the American College of Veterinary Internal Medicine Forum.
Glomerulonephritis is the most common cause of PLN and is due to immune complex deposition in the glomeruli, which triggers inflammation along filtration membranes. Amyloidosis is due to a pathologic deposition of polymerized proteins called amyloids, in the kidneys.
Both glomerulonephritis and amyloidosis are triggered by inflammation elsewhere in the body, with the kidneys acting as an innocent bystander. Proteinuria can be the first sign of kidney damage; it occurs earlier than changes in urine specific gravity or bloodwork.
Ms. Terrill stressed that persistent proteinuria with an inactive urine sediment equals renal disease, even if all other values are normal.1


Causes of PLN include infection, inflammation, corticosteroid excesses from Cushing’s disease or long-term steroid use, and less commonly, neoplasia. Most commonly, PLN is idiopathic, with no known cause, noted Ms. Terrill. There are also some familial causes such as Shar-Pei amyloidosis and the hereditary PLN and protein-losing enteropathy (PLE) in soft-coated wheaten terriers.

Clinical signs

If diagnosed early, there are usually no clinical signs. Polyuria and polydipsia are very common, and often the first signs owners note. Decreased appetite and vomiting may occur as the disease progresses. If nephrotic syndrome develops, peripheral edema will be noted. Nephrotic syndrome occurs in advanced PLN, and is characterized by proteinuria, hypoalbuminemia, hypocholesteremia, and peripheral edema. Ms. Terrill said that the prognosis for nephrotic syndrome is very guarded.


A minimal database should consist of a CBC, chemistry panel, urinalysis, plus or minus urine culture and urine protein creatinine ratio (UPC). A three-day urine collection by the client prior to their appointment is recommended. It is also recommended to mix 2 mls of urine from each sample and submit the 6 mls. A study performed in 2010 notes that this helps alleviate the day-to-day variance that can occur from a single sample.2
If infection is suspected, a urine culture should be done first. A urinalysis with reflex UPC is not recommended as the veterinarian knows the patient better and they, not the lab, should be the ones to determine if a UPC is run or not.
Ms. Terrill stressed the importance of doing a urinalysis with every annual screening. This may give insight into early renal disease due to the proteinuria or a decreased urine specific gravity. Albumin and creatinine values may be normal until very late stages of renal disease. In one study, 19% of apparently healthy elderly dogs had persistent proteinuria, which is associated with risk of death and progression of chronic kidney disease.3
In addition to the minimal database, testing for tick-borne diseases and leptospirosis should be performed, as both cause inflammation and damage to the kidney. To look for sources of inflammation, thoracic radiographs and abdominal ultrasound are recommended; ultrasound also allows the veterinarian to assess kidney structure.

Importance of doing blood pressure

Systemic hypertension (> 160 mmHg) has been reported in 80% of dogs with glomerular disease.4 Increased proteinuria is associated with an increase in systemic hypertension.5 Blood pressure should be taken yearly on young healthy dogs and at every visit for at-risk patients, such as those with heart disease, renal disease, hyperthyroidism, and those on hypertensive medications.
Ms. Terrill said that when taking blood pressures, the technician should be consistent and use the same size cuff and same leg on the patient each time. The leg should be level with the heart and the patient should be in lateral recumbency whenever possible. Three to five measurements should be taken and averaged. The patient’s demeanour should be noted and all vitals should be recorded in the patient’s record.6 A Doppler unit provides a good quality, low cost method of obtaining blood pressure. It is accurate in small animals, and the pulse rate and quality are easily assessed. 

General treatment

The PLN patient should be transitioned to a prescription renal diet to decrease stress on the kidneys. Ace inhibitors are used to help control hypertension within the kidney. Enalapril is started at a low dose and slowly increased to a maintenance dose. Creatinine is checked after each increase to be certain the blood flow within the kidney is not being reduced too much, which would adversely affect the glomerular filtration rate (GFR).  Anticoagulants, i.e. low dose aspirin or clopidogrel, are used to help prevent clotting. Omega 3 fatty acids help reduce inflammation in the kidneys and elsewhere in the body. Antihypertensive medications are used as needed to control systemic hypertension. Anti-nausea medications, appetite stimulants, and gastroprotectants are used as needed to keep the patient eating.
The goals of treatment are to reduce proteinuria, thereby slowing the destruction of renal cells; reduce inflammation that can lead to further renal damage; control systemic hypertension which can lead to further proteinuria, as well as damage to other target organs; prevent nausea; reduce risk of clotting that can lead to pulmonary thromboembolism; and improve the animal’s overall quality of life.

Patient information

The history that is obtained from the client will help the veterinarian provide better care for the patient. Travel history may impact testing, as different areas of the country have different diseases that may cause inflammation that can lead to PLN. Polyuria and polydipsia are often the first clinical signs a client will see in a dog suspected of PLN. Changes in appetite or weight, or any GI upset, such as vomiting or diarrhea, should be noted.
Owners should be instructed to bring all medications that the pet is on to the appointment, including supplements. A diet history should also be obtained, including brand(s) of food being eaten, dry and/or canned, human food and treats, and the amounts fed and how often.

Client communications

Client communications are an essential part of the technician’s job. To help clients and patients, technicians should explain the disease in terms the client can understand, by using drawings, pictures, or analogies. Teaching medical terms and providing handouts for the client to read, and explaining the purpose of each medication prescribed, will be helpful in improving compliance, as owners will understand the importance of each medication to the treatment of PLN.
It is also important to explain the purpose of the lab work being performed. This helps educate the owner and improve compliance. Also, it is important to discuss how prescription renal diets will improve the patient’s quality of life and slow the progression of renal disease.7 Ms. Terril suggested formulating a diet plan for each patient, providing handouts with information on prescription renal diets and how to make the transition, as well as kcal/cup and kcal/can of each diet. Finally, she said, provide support via weekly phone updates.


Protein losing nephropathy is a manageable, but progressive disease. Technicians can educate their clients by providing diet information, medical therapy, regular exams, and follow-up blood work. CVT


1.         Lees, GE, et al. 2004 ACVIM Forum Consensus Statement (Small Animal). J Vet Intern Med 2005;19:377-385.

2.         LeVine, DN, et al. Vet Clin Path 2010; 39:53-56.

3.         Marynissen, SJJ, et al. Journal Vet Intern Med 2017;31:93-101.

4.         Textbook of Vet IM, Vol 2, Chap 325, pg 1971.

5.         Textbook of Vet IM, Vol 2, Chap 157, pg 660.

6.         ACVIM Consensus Statement. J of Vet Intern Med 2007;21:542-558.

7.         Jacob, F, et al. Journal Am Vet Med Assoc 2002;220: 1163-1170.