Where has all the protein gone? Protein losing nephropathy in dogs and cats
We classically think of two diseases when we think of renal disease - either chronic kidney disease (CKD) which we see commonly, or acute kidney injury (AKI) which requires urgent and often intensive care.
But what other renal diseases are there? How do they differ from CKD, and what do we need to know as nurses, so we can give great care to these patients?
There’s one chronic renal disease we see quite commonly, which differs to our ‘traditional’ CKD quite a bit - protein-losing nephropathy.
These patients can present incredibly unwell, requiring intensive nursing care, and it’s important we know the difference between caring for a PLN patient and caring for a ‘normal’ CKD cat or dog.
Today I’m going to share what PLN is, how it affects our patients, how it is diagnosed and treated, and my top tips for nursing the PLN patient.
(P.S. - If you want to access a library of resources which really help with caring for these guys in the hospital - like fluid therapy calculators, monitoring sheets and nutritional calculators - click here!)
What is PLN?
Protein-losing nephropathy (or PLN) is a disorder of the glomerulus - the ball of capillaries in the renal nephron. Blood flows through the glomerulus under high pressure, causing water and solutes to filter out and eventually become urine. In normal patients, larger molecules such as proteins (albumin & globulin) cannot pass through the glomerulus into the urine, and so remain in the bloodstream.
However, when the glomerulus becomes diseased, it begins to ‘leak’ proteins through its capillary membranes, where they enter the urine. Proteinuria results - this is often very marked; these patients often have a very high urine protein:creatinine ratio.
We can see proteinuria due to other causes, too - so it’s important to know that proteinuria does not always equal PLN:
If patients have high numbers of circulating proteins (multiple myeloma patients, or haemoglobinuria if a blood transfusion is broken down, for example), they can get what we call a pre-glomerular proteinuria (where the proteinuria has come from before the kidney)
Infection, inflammation or neoplasia of the lower urinary tract can cause a post-glomerular proteinuria - where the source of the proteinuria is after the kidney.
PLN is seen when we have glomerular proteinuria - due to disease of the glomerulus itself. There are several causes of protein-losing nephropathy, including:
Glomerulonephritis - acute glomerular/renal inflammation, caused by the immune system
Glomerulopathy - an inherited condition where a collagen deficiency within the glomerulus causes it to lose function
Amyloidosis - the progressive accumulation of an abnormal protein called amyloid, which interferes with glomerular function
Glomerulonephritis can be seen secondary to tick-borne diseases such as Lyme disease and Ehrlichiosis, as well as chronic infections, inflammatory diseases such as pancreatitis or polyarthritis, and endocrinopathies such as Cushing’s disease and diabetes mellitus.
Amyloidosis is commonly seen in Shar Pei dogs and in Abbysinian cats, and inherited glomerulopathies are common in Soft Coated Wheaten Terriers and English Cocker Spaniels.
PLN is seen relatively commonly in dogs, and rarely in cats. Severe or prolonged PLN can lead to the development of chronic kidney disease.
What signs do we see?
In the early stages of the condition, many patients will be asymptomatic. Weight loss and lethargy are usually the first signs seen - the severity of this can vary, from gradual weight loss in patients with moderate proteinuria, to rapid and marked weight loss in patients with severe disease.
Hypertension is also common in PLN patients, so signs of target organ damage - such as visual deficits, retinal haemorrhage or detachment - may also be seen.
Because PLN can cause CKD, we also often see signs associated with this - including PU/PD, anorexia, nausea and vomiting.
As more of the plasma protein albumin is lost in the urine, changes to the patient’s fluid balance will be seen. This occurs because albumin is responsible for maintaining colloidal oncotic pressure - keeping fluid within our blood vessels. When albumin leaves the intravascular space, the vessels don’t have as much oncotic pressure to hold water within the blood. This causes leaking of fluid into tissues and body cavities - resulting in pitting oedema (especially on the ventral abdomen and distal limbs) +/- ascites and/or pleural effusion.
The most severe complication of PLN is thromboembolic disease. This is seen because antithrombin III, a protein which stops blood clots from forming when they shouldn’t, is also lost in the urine. This means our PLN patients are in a hypercoagulable state, and are prone to throwing clots. If one reaches the lungs or brain it is often fatal.
How is it diagnosed?
PLN is diagnosed by documenting proteinuria and identifying the underlying cause where possible. Common tests include:
Urine analysis (including dipstick, SG and sediment examination as active sediment will make accurately assessing proteinuria difficult)
Urine protein:creatinine ratio (to accurately assess proteinuria. A UPC >1 will be seen)
Biochemistry and haematology (to identify any underlying cause for the PLN)
4Dx (to test for tick-borne diseases causing glomerulonephritis)
Thoracic radiographs (to identify any underlying cause for the PLN)
Abdominal ultrasound (to assess the size and structure of the kidneys, and identify any underlying cause for the PLN)
Definitive diagnosis of the underlying disease can be achieved with a renal biopsy. This is performed either surgically or percutaneously with a TruCut needle and samples are examined microscopically, using electron microscopy, and with immunofluorescent staining.
The samples require specialised handling and transport, and are fixed in a variety of reagents, rather than just in formalin (see here for more information).
How are these patients treated?
PLN is treated with a variety of medications, aimed at managing the underlying cause where appropriate, decreasing the proteinuria, preventing thrombus formation, and managing blood pressure. These include:
ACE inhibitors (e.g. benazepril) to decrease proteinuria and delay onset of renal failure
Antihypertensives (e.g. amlodipine) to reduce blood pressure
Diuretics (e.g. spironolactone) to minimise oedema
Anti-thrombotics (e.g. clopidogrel, rivaroxaban) to minimise the risk of clot formation
Immunosuppressants (e.g. cyclosporine, +/- prednisolone) to treat glomerulonephritis - prednisolone should be avoided in dogs unless the underlying cause is steroid-responsive, since prednisolone can cause proteinuria
In addition, supportive care and management of chronic kidney disease is required - with treatments such as intravenous fluid therapy, antiemetics and analgesics.
What about nursing the PLN patient?
There is a lot to think about when nursing the PLN patient:
Nutrition
Nutrition is a vitally important consideration, since the best way to increase albumin levels in most cases is through appropriate nutritional support. A feeding tube - either naso-oesophageal or oesophagostomy tube - should be placed and a nutritional plan made, meeting the patient's RER over an appropriate length of time, depending on their duration of anorexia.
Patients with a voluntary appetite should have volumes consumed recorded, and if they’re consistently eating less than 80-85% of their RER, we should intervene.
The question I’m sure is on your lips is “But Laura, what should we feed?” and it’s actually a lot more simple than you might think - feed them anything they want to eat!
Do not worry about putting them on a renal diet right now. If they end up with CKD and would benefit from that long term, that’s fine - but we can introduce that to them at home, once they’re recovered from hospitalisation and aren’t acutely ill.
Hydration/Fluid Balance
Fluid balance is a big consideration in these patients. Severe hypoalbuminaemia causes fluid shifting and oedema - so careful assessment of the patient’s hydration and perfusion status is needed regularly, to prevent over/underhydration and ensure we’re meeting their fluid needs.
Things to check include:
Skin tent
MM moistness/dryness
CRT
Eye position (sunken or proptosed)
Presence of oedema
Heart rate
MM colour
Pulse quality
Blood pressure
Mentation
Temperature
Vital Parameters
These patients can be quite unstable, particularly if they have an underlying disease causing the PLN (think pancreatitis patients, septic patients etc…), or if they have severe hypertension, oedema or thromboembolic disease.
We want to keep a close eye on the vitals of these patients and re-examine them regularly - including regular assessment of heart rate/rhythm, respiratory rate/pattern/effort, mucous membranes and CRT, pulses, consciousness, blood pressure, urine output etc… The list goes on!
Make sure you’re also including thoracic auscultation in your examinations, too - particularly if you’re worried about fluid overload or pleural effusion.
Pain
Pain assessment should form part of any inpatient nursing plan, but particularly in our medical patients. Inflamed kidneys may be painful, as are conditions such as pancreatitis which can trigger PLN.
These patients should be assessed regularly for signs of pain, ideally using a validated pain scoring system, and appropriate analgesia provided.
Monitoring for Clots
As we said, thrombus formation is a real risk in these patients. The risk to the patient is highest if clots affect the brain or lungs, since this is often fatal - but I’ve also seen lack of limb function when a clot gets lodged in a peripheral vessel (think about our saddle thrombus cats - but affecting one or more limbs, and not just the HLs), and skin/tongue tip necrosis associated with throwing clots.
Make sure you’re checking the neurological and respiratory status of these patients regularly, and noting any abnormalities such as cold(er) extremities, loss of function or sensation of a particular area etc. These could all indicate a clot is affecting that area.
Ongoing Care
These patients, once discharged from their acute illness, often need to come back to see us for regular rechecks. There is no reason why the veterinary nurse can’t play more of a leading role in these, since they are usually for:
Repeat clinical examination
Blood pressure measurement
Bloods to recheck renal parameters and albumin levels
Urine analysis for dipstick, SG, UPC and sediment examination.
We can do so much to support these patients and their families long-term, whilst using our skills and showcasing how amazing veterinary nurses are to the public.
If you want to know more about how the veterinary nurse can support renal patients long-term, I’m showing you how to do just that this spring - make sure you’re on the waiting list to find out more and get early doors access!
So as you can see, there is a lot more to renal diseases than ‘just CKD or AKI’ - and PLN patients can be a bit of a unique challenge, with severe consequences of their disease! In order to nurse them effectively, we need to understand how the disease works and what the consequences are of it in the body - and then base our diagnostic tests, treatments and nursing considerations around that.
Have you seen a PLN patient before? Drop me a DM on Instagram and let me know how you nursed them!
References:
Langston, C. E. 2008. Protein Losing Nephropathy. DVM360, available from: https://www.dvm360.com/view/protein-losing-nephropathy-proceedings
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell, p. 301.
