12 | An introduction to chronic kidney disease in dogs and cats

PodcastRenal
Written By Laura Jones

CKD is one of the most common conditions we see in practice….

 

And whilst we can’t cure it, there’s a lot that we can do to help these patients, to slow the progression of their disease, and buy them as much good-quality life as possible.

In today’s episode of the medical nursing podcast, we’re looking at what chronic kidney disease is, how it occurs, and the treatment and nursing care our CKD patients benefit from.

Let’s begin by looking at what CKD is.

Put simply, it’s defined as renal damage or a progressive, irreversible reduction in renal function which has persisted for at least 3 months.  

What causes CKD?

In most cases, we’re not able to identify the exact cause of the patient’s CKD. Many patients on histology have been found to have chronic tubulointerstitial nephritis (inflammation of the renal tubules in the nephrons) and renal fibrosis.

There are a few theories on what causes this - including

  • Chronic nephrotoxin exposure

  • Hypoxic renal injury (renal ischemia)

  • Obstructive nephropathies (e.g., ureteral obstruction)

  • Chronic pyelonephritis (renal infection)

  • Infections (e.g., retroviral infection; leptospirosis; Lyme disease; leishmania)


Several causes of CKD have been identified in our patients. These include renal dysplasia - a congenital condition where the kidneys don’t form properly in utero; polycystic kidney disease, where cysts form within the renal tissue, growing and interfering with their function, and glomerular diseases, which cause a renal disease known as protein-losing nephropathy.

Renal neoplasias can also cause CKD, and any condition causing an acute kidney injury (eg a urinary obstruction) can also lead to CKD if that renal injury is not addressed promptly.

What about risk factors for CKD?

We know that several factors can increase the risk of a patient developing CKD, and these include breed, age, concurrent diseases, diet, and certain medications, as well as diseases causing AKI.

Shar Peis, English Bull Terriers, Cocker Spaniels, Westies, Persians and Abyssinians are among the breeds at a higher risk of developing CKD.

In terms of age, we know that CKD is a condition primarily affecting older patients, but there are some familial chronic kidney diseases, like renal dysplasia, that affect very young patients.

Next up is concurrent diseases - hypercalcaemia, periodontal disease, cardiac disease, hyperthyroidism, certain infectious diseases and cystitis have all been associated with the development of CKD.

With regard to diet, there is evidence that suggests diets containing higher inorganic phosphate and higher protein levels have been associated with the development of CKD in cats

Lastly, several medications have been associated with CKD. These include NSAIDs, aminoglycoside antibiotics, and certain cytotoxic agents.

What signs do we see in these patients?

Signs can be very varied and initially can be vague and hard to spot, especially in the early stages of the disease. Signs include

  • Polyuria 

  • Polydipsia 

  • Lethargy

  • Weakness

  • Dehydration

  • Anorexia/inappetence

  • Weight loss

  • Poor coat quality

In cases of severe CKD and uremia, vomiting, marked weight loss and anorexia, halitosis (‘uremic breath’) and neurological abnormalities may also be seen. 

In some cases, alterations to calcium and phosphorus balance can lead to secondary renal hyperparathyroidism. Signs of this condition include impaired muscle function and bone resorption in the skull/mandible, leading to softening of these areas.

And how is it diagnosed?

In any patient with, or suspected to have CKD, we’ll be performing a full biochemistry (particularly looking at urea, creatinine, calcium/phosphate and electrolytes, and perhaps SDMA), haematology, urine analysis (including dipstick and SG testing, microscopy, and a protein: creatinine ratio), a, blood pressure assessment and ideally an abdominal ultrasound.

On our biochemistry, BUN and creatinine are usually increased - but they might not always be in the early stages of disease. In patients suspected to have early-stage CKD without azotaemia, we use SDMA to assess their renal function - since SDMA increases at an earlier point in renal disease than creatinine.

Normally, creatinine increases when around 75% of renal function has been lost - compared to SDMA, which increases when between 25 and 40% of renal function has been lost.

Looking at electrolytes, hypokalaemia is quite common in CKD - because it’s excreted in the urine, and these patients are polyuric. They also often have inappetence, and most of our potassium is sourced via food.

Phosphate and calcium are also important parameters to assess in renal patients. Phosphate is commonly increased, and since calcium and phosphate are inversely related, in severe hyperphosphataemia, we can see calcium levels decrease. Phosphate directly affects renal function, which is why restricting dietary phosphate intake is vital to managing CKD long-term.

Other abnormalities we commonly see on diagnostics in CKD patients include:

  • A low urine specific gravity (due to the lack of renal concentrating ability)

  • Proteinuria (as the glomerulus becomes ‘leaky’ and allows larger molecules like proteins to pass through)

  • Hypertension

  • Anaemia (due to a decrease in erythropoietin production in the kidneys)


On diagnostic imaging, we often see smaller, more irregular kidneys with a loss of distinction between the renal cortex and medulla. We can also see abnormalities like nephroliths or ureteroliths, masses, and infarctions, and collect guided samples where needed.

Let’s talk staging…

We need not just to diagnose CKD - but we also need to stage it. Staging is an important part of diagnosis since many of our recommendations are made based on the stage of CKD the patient has.

We stage our patient’s CKD from stage 1-4, based on the degree of their azotaemia - so based on their creatinine results. Stage 1 CKD is non-azotaemic, where our patient has normal creatinine, but another renal abnormality is present - such as a persistently elevated SDMA.

Stage 2 is mild azotaemia. These patients usually have a normal to mildly increased creatinine (up to 250umol/L), but no or very mild clinical signs.

Stage 3 is moderate azotaemia - and these patients have a creatinine of up to 440umol/L. These patients usually have clinical signs present in varying severity - from PUPD to weight loss, anorexia and nausea.

Stage 4 is severe azotaemia. These patients have a creatinine of above 440umol/L and have increasingly severe clinical signs. These patients are at increasing risk of uraemia.

Once we’ve staged our patient, we need to substage them. We do this based on the degree of proteinuria they have (so via their urine protein creatinine ratio) and by the degree of hypertension they have (so via their blood pressure).

Patients are classified as either non-proteinuric, borderline proteinuric or proteinuric depending on their UPC, and as either normotensive, prehypertensive, hypertensive or severely hypertensive depending on their systolic blood pressure.

Staging is important because the treatment we select, advice we give, diets we use and recommendations we make are going to depend on the stage of CKD the patient has.


So we’ve diagnosed and staged our patient. How will we treat and nurse them?

We know that CKD is an irreversible condition, but we can slow the progression of the disease with good long-term management. This is going to not only increase survival time but improve the quality of life in our CKD patients, too.

The way we manage CKD will depend on whether they’re an inpatient or an outpatient.

Caring for the CKD patient in hospital

In the hospital, we aim to provide supportive care - administering fluid therapy to correct dehydration, correcting any acid-base or electrolyte abnormalities, providing nutrition, managing anaemia if present, and providing treatments like antiemetics and appetite stimulants as needed.

Calculating their RER, formulating a nutritional plan, placing a feeding tube, securing vascular access, performing regular hydration assessments, monitoring pain and nausea, monitoring fluid output and adjusting their fluid therapy rate - to name just a few - are all important nursing considerations in hospitalised CKD patients.

And when your patient goes home…

Outside of the clinic, we aim to support the patient’s long-term renal function - managing complications like proteinuria and hypertension, increasing their water intake, and feeding them a diet which will help slow the progression of their CKD.

We can continue to see these patients via renal clinics - which are a fantastic way to provide ongoing nursing support - every few months, to answer queries, examine the patient, and collect samples for staging under the vet’s direction.

The major benefit of this is that it allows us to pick up on subtle changes promptly, and tweak the patient’s management as needed - slowing the progression of their disease and improving their quality of life.

And alongside this, our clients get a first-hand look at how skilled we are as nurses, and just how much we can do!


So that’s an overview of chronic kidney disease in cats and dogs - and the nursing skills these patients benefit from! 

The next time you have a patient with CKD in the clinic - remember there are so many things we can do to help these patients - from day-to-day monitoring to nasal feeding tube placement, getting on top of their hydration and even things like advocating for antiemetics if you’re worried they are still nauseous. 

And our care doesn’t stop when the patient is discharged - so speak to your vet team about how you can help with your CKD patients long-term, too!

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on instagram (@vetinternalmedicinenursing) so I can give you a shout out, and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
Previous

13 | The complete guide to managing acute kidney injury in dogs and cats
Next

11 | Struggling to understand how the kidneys work?