Chronic kidney disease (CKD) is a relatively common disorder in cats and dogs, especially pervasive in geriatric felines. Although this renal disorder is non-curative and progresses over time, several therapeutic interventions can be initiated to slow your pet’s disease progression and improve his or her lifespan and quality of life.

The Meowing Vet provides pet owners with a comprehensive understanding of chronic kidney disease and renal failure in dogs and cats. Join us as we explain the classic clinical signs and health consequences of CKD and how it is diagnosed, staged, and managed.

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The Basics: Kidneys & Kidney Disease

The body has two kidneys, a left and a right one that are positioned near the back just above the pelvis. The kidneys are connected to a large blood supply, and these organs are vital to the health of the remainder of the body; humans and animals need at least one functional kidney in order to survive. A long, thin tube called a ureter branches off the bottom aspect of each kidney and enters the bladder, transporting urine (the product of the kidneys via a processing action known as micturation). The bladder stores urine and in turn is connected to a short, wider tube called the urethra, which allows urine to pass out of the animal. The kidneys and ureters comprise the upper urinary tract while the bladder and urethra make up the lower urinary tract.

The inner aspect of each kidney is comprised of many functional units called nephrons. The two main components of each nephron are the glomeruli (plural for glomerulus) and renal tubules. The glomeruli primarily function to filter the body of toxins and cellular metabolic waste, scrubbing the blood to remove these harmful products where they can be removed from the body in urine. The rate at which the glomeruli filter the bloodstream is termed glomerular filtration rate (GFR); a decreased GFR (as occurs with chronic kidney disease) means that the kidneys are behind in their duties to remove toxins from the blood. The tubules, on the other hand, work to balance the body’s fluid levels, electrolyte balance, and acid-base status (i.e. blood pH). The tubules act like a door, selectively opening to allow excess water, electrolytes (like sodium and potassium), and hydrogen atoms (which control the blood’s pH) to exit into urine where they can be removed; conversely, the tubules can also close, keeping these molecules (along with important blood proteins and glucose) inside the bloodstream. Disease of the glomeruli is termed glomerulonephritis while damage to the renal tubules results in tubulointerstitial nephritis. Other functions of the kidneys include: producing the hormone erythropoietin (EPO), which plays an important role in red blood cell production; and converting vitamin D to its active form in the body.

When the kidneys are not functioning normally, there is some degree of renal insufficiency. (By the way, the term “renal” simply means something relating to the kidneys.) Multiple factors may cause damage or injury to the kidneys, resulting in various degrees of renal insufficiency. If the problem arises within hours to days, this is termed acute kidney disease (AKD), or more recently renamed acute kidney injury (AKI). AKD may result from a plethora of reasons: infection, toxins, or poor blood perfusion to the kidneys due to a drastic and sudden dip in blood pressure, blood loss due to trauma, or certain anesthetic events. AKD is typically characterized by anuria (or the absence of urine production), high potassium levels in the blood, and enlarged and painful kidneys. (We’ll discuss how chronic kidney disease differs from acute kidney disease as this article continues.)

Certain causes of acute kidney disease can be treated, resulting in a complete cure. Others result in such severe and sudden renal damage that death from acute renal failure may occur. In the middle of these extremes lies those causes of AKD that cannot be cured yet do not result in the immediate death of the animal. These cases go on to progress to chronic kidney disease (CKD). In addition to complications from AKD, CKD may also stem from other disorders affecting the kidneys. Both kidneys are typically affected. Such disorders include congenital anomalies (i.e. those present since birth), hereditary renal problems, chronic infection or inflammation, prolonged exposure to certain chemicals toxic to the kidneys (i.e. nephrotoxins), and cancer.

According to Xavier Roura of the International Renal Interest Society (IRIS), “The prevalence of CKD has been estimated to be 0.5-1.0% in dogs and 1.0-3.0% in cats, but it increases with age, especially in cats. It has been estimated that as many as 30-50% of cats 15 years of age or older have CKD. Nephron damage associated with CKD is usually irreversible and often progressive.”

CKD can advance to chronic renal failure (or CRF; also called chronic kidney failure). This occurs at stages 2 and higher of CKD (see staging criteria below) when azotemia develops (high BUN and high creatinine noted on bloodwork) and the kidneys have poor urine concentrating ability (resulting in dilute urine, observed as a low USG on urinalysis).

Unfortunately, CKD is non-curative and will continue to progress and worsen over time until the kidneys ultimately fail completely. This end stage occurs due to irreversible scarring (or fibrosis) of the kidneys, in which chronic injury has eventually caused the functional aspects of the kidneys (namely, the nephrons) to be replaced with non-functional scar tissue.

 

Causes of Chronic Kidney Disease & Predisposed Pet Breeds

CKD may arise from a variety of different causes, ranging from incurable acute kidney disease (AKD), to complications spawned from infection and inflammation, to genetic disorders. Both dogs and cats may be affected, of any breed and age. While some animals may be born with congenital conditions lending themselves to kidney disease, the majority of CKD cases occur in older pets, and age is certainly a contributing risk factor of CKD development. Geriatric felines are especially notorious for developing kidney disease, with a large proportion being affected to various degrees with advancing years.

The most common causes of CKD include (but are not limited to):

• Congenital or familial/genetic causes of CKD (and their corresponding predisposed dog and cat breeds):
  • Renal amyloidosis (an accumulation of amyloid, an abnormal protein that can become lodged in the kidney, causing injury): Abyssinian cat, Beagle, English foxhound, Shar Pei
  • Unilateral renal agenesis (being born with only one rather than both kidneys): Beagle
  • Polycystic kidney disease (a condition in which large fluid-filled sacs form in the kidneys, causing renal dysfunction): Persian cat, Domestic Longhair Cat (DLH), Cairn terrier
  • Renal dysplasia (being born with abnormal nephrons): Lhasa apso, Shih Tzu, and many other canine breeds
  • Cystinuria (the genetic metabolic disorder of having abnormally high levels of the amino acid cysteine in the urinary tract): Newfoundland
  • Fanconi syndrome (abnormalities in the renal tubules): Basenji
• Infectious or inflammatory causes of CKD:
  • Glomerular disease (a.k.a. glomerulonephritis): may be an autoimmune disorder (such as systemic lupus erythematosis, SLE), or an immune-mediated response may be triggered by an infection (for example, following Lyme disease); glomerulonephritis is especially problematic in dogs
  • Tubular disease (a.k.a. tubulointersititial nephritis): – examples include:
    • Leptospirosis
    • Feline Infectious Peritonitis (FIP)
    • Pyelonephritis: i.e. kidney infection, which can sometimes stem from an untreated lower urinary tract infection (UTI) of the bladder; an overall uncommon cause of CKD
• Kidney cancer: (example: renal lymphoma) – overall, a rare cause of CKD
• Prolonged urinary tract obstruction: results in hydronephrosis (swelling of the kidneys) due to the buildup of urine; typically results in acute renal failure, but if the patient survives, he or she can develop chronic renal disease – examples include:
  • Urinary stones (uroliths) blocking the flow of urine out of the body (particularly stones of the kidneys or ureters)
  • Bladder cancer (transitional cell carcinoma, TCC) blocking the outflow of urine
  • Obstructive Feline Lower Urinary Tract Disease (FLUTD)
• Nephrotoxins: usually results in acute renal failure, but if the patient survives, he or she can develop chronic kidney disease – examples include:
  • Ingestion of grapes, raisins, sultanas, currants
  • Exposure to lilies (felines)
  • Antifreeze (ethylene glycol) ingestion
  • Vitamin D-containing rodenticide (rat poison) toxicity
  • Consumption of contaminated jerky pet treats from China
  • Certain drugs: for example, an overdose of a non-steroidal anti-inflammatory drug (NSAID), of which cats are especially sensitive; use of the antibiotic amikacin
• Idiopathic (of unknown origin): The most common cause of CKD is idiopathic, meaning the inciting cause cannot be determined. Idiopathic glomerulonephritis is most common in dogs while idiopathic tubulointerstitial nephritis may occur in either dogs or cats.

 

Clinical Signs of CKD

At the very earliest start of kidney disease, clinical signs may not have develop yet, so there may be no outward indication that your pet has an emerging kidney problem. However, once the number of damaged nephrons increases, the following clinical signs will appear.  Signs may also have an insidious onset, meaning they first occur subtly and gradually. At first, only a few signs may occur, but as the kidney disease progresses, subsequent signs will develop over time. Such clinical signs of CKD include:

• Excessive urination and increased water consumption (polyuria and polydipsia, or PU/PD, respectively): Because the kidneys are not working normally, they allow more water than they should to leak out of the bloodstream and be pooled into urine (polyuria, PU). To compensate for this increased fluid loss, your pet is triggered to drink more water (polydipsia, PD). If your pet is peeing large streams frequently (and perhaps having accidents of large puddles in the house more than usual), and if you’re having to refill your pet’s water bowl more often, it’s time to schedule a veterinary appointment because your pet likely has PU/PD. (Polyuria is not to be confused with pollakiuria. With polyuria, your pet will urinate large volumes of urine at a time. With pollakiuria, your pet may urinate frequently but will only produce small amounts at a time. Pollakiuria is common with urinary tract infections, or UTIs.)
• Decreased energy (lethargy, depression)
• Weight loss
• Poor appetite (inappetance, anorexia)
• Vomiting and nausea: Ugh! CKD patients often feel like s**t!!! We all know how awful the feeling of nausea is. Can you imaging being nauseous 24-7 for months to years at a time?! It breaks my heart that so many CKD patients struggle with chronic nausea and vomiting, severely impacting their quality of life. Why does this occur with CKD? It’s partially due to the buildup of toxins in the bloodstream that the damaged kidneys can’t remove, including gastrin. Gastrin is a hormone that triggers the production of digestive stomach juices when your pet has a meal. Gastrin circulates in the bloodstream before it is normally removed from the body by the kidneys when a meal has been digested. We know now that patients with kidney disorders do not adequately remove such waste products from the blood. Therefore, gastrin can build up in the bloodstream, promoting increased production of gastric acid that irritates the lining of the stomach (gastritis) and can lead to stomach ulcers and hemorrhage in severe cases.
• Diarrhea or constipation: In addition to vomiting, some renal patients may also have diarrhea while others struggle with constipation (secondary to dehydration, which causes the stools to be hard). Constipation is especially common in felines with CKD.
• Oral ulcerations: Toxins accumulate in the bloodstream of dogs and cats with renal disease because they are not effectively filtered out by the injured kidneys. This toxic buildup can cause painful, red oral ulcers to form on the tongue, mouth, and back of the throat. These ulcers need to be treated since they will dissuade your pet from eating and drinking.
• Uremic odor: Since toxic waste is not removed from the bloodstream in CKD patients, certain toxins (such as blood urea nitrogen, or BUN) can start to cause your pet to have a urine-like odor permeating from his or her skin and fur. This is not because your pet urinated on itself; this occurs because toxins (such as elevated BUN, also known as uremia) try to escape through your pet’s pores.
• Weakness and pale gums: These signs are indications of anemia (decreased red blood cell count), as can occur with CKD. If anemia becomes severe enough, your pet may experience difficulty breathing (dyspnea) due to impairment of the body to oxygenate adequately secondary to a low red blood cell count.
• Fluid accumulation in the abdomen (ascites) and limbs (peripheral edema): Blood proteins are typically kept inside the bloodstream by that “selective door” effect of normally functioning kidneys. With CKD, however, the kidneys can’t hold that “door” closed as well, so things leak out; this includes some blood proteins. Certain blood proteins (such as albumin) are important in maintaining oncotic pressure in the bloodstream (in a nutshell, the presence of these proteins inside blood vessels helps attract water molecules, keeping them inside the bloodstream). If blood proteins are lost in urine (proteinuria), the oncotic pressure of the bloodstream decreases, so water molecules seep out of the blood vessels. Fluid may enter certain body cavities, such as the abdomen, causing an accumulation of fluid in the belly (a.k.a. ascites). Fluid may also migrate out into the limbs, causing peripheral edema. This tends to occur with more severe CKD, especially of glomerular origin.
• Blood clots: Other effects of proteins lost in the urine may be an increased risk of blood clot formation. Why? Some blood proteins are anti-thrombotic proteins (such as antithrombin), which help prevent unnecessary blood clot formation in the body. If these types of proteins are lost in urine, the body becomes hypercoagulable, meaning it has a propensity to develop more blood clots. This blood clots can cause severe problems if they form or migrate in the brain (increasing the risk of stroke), heart, lungs, spine, or limbs.
• Multi-organ injury: Other organs besides the kidneys can become impaired with CKD secondary to inadequate hydration, metastatic calcification, hypertension (which can lead to sudden blindness and heart disease), and blood clot formation.
• Seizures: Seizures may occur when less than 5% of the kidneys’ remaining nephrons are functioning – at the very end stage of the kidney disease process.

 

Diagnosing CKD

Diagnosis renal disease is typically quite straightforward. However, sometimes detecting the underlying trigger of the kidney damage is a bit trickier and may never be determined in some cases (i.e. those regarded as idiopathic). CKD is diagnosed via the following exam findings and laboratory test results:

• Clinical signs: Based on the presence of the aforementioned clinical signs that you describe to your vet, CKD will be high on the list of diagnostic possibilities.
• Physical examination: I can’t convey enough how vital a good physical exam performed by your vet can be to reveal your dog or cat’s overall health status. Your vet will note the same clinical signs that you have likely detected at home: lethargy, weight loss, a uremic odor, possible oral ulcerations, pale gums, potential abnormal fluid accumulation, and secondary effects of hypertension. Additionally, your vet will also be highly suspicious of CKD if he or she observes the following exam irregularities:
  • Dehydration: Your pet’s hydration status is assessed on physical exam via the mucous membranes and skin turgor. Your vet will feel the mucus membranes of the gums: normally, they should be moist; with dehydration, they will feel dry and tacky. Your vet will also gently pull up on a bit of skin between your pet’s shoulder blades to assess hydration (i.e. the skin turgor test). If the skin immediately bounces back to its original position, this is a sign of a well-hydrated animal; if, however, the skin is delayed in returning to its previous position or if it remains tented up altogether, the pet is dehydrated. Additionally, the corneas of the eye may also be dry in severely dehydrated animals.
  • Irregular kidney palpation: Kidneys are more easily palpable in cats (meaning, they’re easy to feel by your vet during a physical exam) while normal kidneys may be difficult to feel in most dogs (though sometimes the left kidney may be palpable). With CKD, the kidneys feel small, firm, and otherwise abnormal (like they have lumps and bumps on the surface). Though most patients with CKD have kidneys which are smaller than normal, certain causes of CKD may result in larger kidneys (termed renomegaly); these include polycystic kidney disease, FIP, renal lymphoma, and hydronephrosis secondary to a urinary tract obstruction.
• Bloodwork: As discussed, CKD can cause dehydration as well as electrolyte imbalance and other anomalies in the bloodstream. The most classic bloodwork findings associated with CKD include renal azotemia (high BUN and creatinine), low potassium, high phosphorus, and anemia (among other findings). (Other specialized blood tests such as SDMA may also be used to help identify dogs and cats at-risk for CKD sooner, i.e. before clinical signs develop and kidney injury progresses.)
  • Renal azotemia (elevated BUN & creatinine): 75% of the kidneys’ nephrons must be damaged prior to the development of renal azotemia, measured as increased blood urea nitrogen (BUN; a waste product primarily made of digested dietary proteins by the gut) and increased serum creatinine concentration. (Elevated BUN is also termed uremia.) Creatinine is a waste product produced by skeletal muscle cells and is typically removed from the bloodstream and dumped into urine for excretion when the kidneys are functioning normally. Once azotemia is noted (in an otherwise hydrated animal), then that pet’s kidneys are only functioning at 25% or less. The measurement of creatinine concentration in the blood is an important prognostic indicator for CKD (read more below under “Staging”).
  • Low potassium (hypokalemia): Potassium (K+) is a vital electrolyte that participates in nerve and muscle impulses throughout the body. Unfortunately, potassium is often decreased with CKD cases, especially in cats, due to reduced dietary consumption (remember, CKD patients often lose their appetite) as well as increased loss of potassium in urine due to leaky kidneys. Low potassium can cause patients to be very weak, so supplementation is key.
  • High phosphorus (hyperphosphatemia): Excess levels of the mineral phosphorus (P) is normally excreted from the body by the kidneys. However, with decreased glomerular filtration rate (GFR) secondary to CKD, the body is a bit slow in ridding itself of extra phosphorus, causing its level to rise in the bloodstream. Hyperphosphatemia can be problematic for two reasons:
    • 1) It contributes to decreased calcium concentration in the bloodstream via a complex endocrine disorder called renal secondary hyperparathyroidism. This hormonal disorder involves parathyroid hormone (PTH), released by the body’s parathyroid glands, to regulate vitamin D, calcium, and phosphorus levels. The main goals of PTH are to lower phosphorus and increase calcium. High phosphorus levels infringe on this mode of action, preventing calcium levels from rising sufficiently.
    • 2) Excess phosphorus can bind with calcium in body, forming mineralizations (or calcifications) that can lodge in different organs in the body (i.e. metastatic mineralization), causing organ dysfunction. If mineral plaques form in an already damaged kidney, this can worsen pre-existing CKD.
  • +/- Low calcium (hypocalcemia): Mild hypocalcemia may be noted in some, but not all, CKD patients; its presence tends to be a feature of more severe CKD cases. We previously explained how one of the roles of the kidneys is to convert vitamin D to its active form. Vitamin D, along with calcium and phosphorus, aids in the development of a healthy skeleton. These molecules are regulated by parathyroid hormone (PTH), as explained above. Calcium levels decline when active vitamin D levels are low (due to decreased renal production) and phosphorus levels are high (due to decreased renal clearance). Furthermore, calcium tends to follow the blood protein albumin, so if albumin leaks out of a damaged kidney (see below), so will its buddy, calcium.
  • +/- Low blood proteins (hypoproteinemia): Damaged kidneys become leaky, allowing important things like blood proteins to sometimes slip out of the bloodstream (especially the small protein, albumin, leading to hypoalbuminemia). This loss will be reflected on bloodwork via a decreased plasma protein (PP) level on CBC and a low measurement of total protein (TP) and albumin on blood chemistry tests.
  • High cholesterol (hypercholesterolemia): Like phosphorus, cholesterol is also normally excreted from the body via the kidneys, so decreased GFR due to CKD can cause elevations in the bloodstream.
  • Metabolic acidosis: As explained prior, the kidneys are important in regulating the acid-base status of the blood, ensuring that it is at a proper pH. Damaged kidneys do not adequately remove excess hydrogen (H+) ions from the blood nor do they hold in bicarbonate (HCO3), resulting in overly acidic blood. This acidic state can interfere with cellular activity and blood cell functions. Acidosis will appear on blood chemistry as low TCO2.
  • Low red blood cells (anemia of chronic disease): Another important role of healthy kidneys is producing erythropoietin (EPO), a hormone that promotes red blood cell (RBC) production. Red blood cells are important for transporting oxygen and other nutrients to all other cells in the body while also removing their waste byproducts. With CKD, EPO production decreases; subsequently, so does red blood cell production, resulting in anemia. Anemia will be detected on bloodwork as a decreased PCV, HCT, or RBC measurement on CBC. The red blood cells that are present will be normocytic (of normal size), normochromic (of normal color when stained), and non-regenerative.
• Urinalysis (UA): Since the kidneys are involved in creating urine, no diagnosis of CKD would be complete without a urinalysis! With early kidney disease, changes on urinalysis can be perceived prior to changes on bloodwork. UA changes occur when only two-thirds (66%) of nephrons are lost while renal azotemia is not detected until three-fourths (75%) of nephrons are damaged.
  • Dilute urine: When a pet without kidney disease becomes dehydrated, the body tries to conserve what little water content it has left, so the kidneys retain water in the blood; this results in urine that is more concentrated, being darker than normal and resulting in an elevated urine specific gravity (USG, a urinalysis test used to determine how concentrated or dilute a patient’s urine is). This fails to occur with kidney disease. With CKD your pet’s urine likely be paler than usual due to being more dilute. This happens because the diseased kidneys cannot remove toxins, salts, and other products from the blood and effectively concentrate them into urine. The urine also contains more water content because the kidneys have lost much of their ability to keep water inside the bloodstream, so more leaks out into urine, diluting the urine further while also dehydrating the patient. Despite being dehydrated, the urine specific gravity will not reflect this since the urine is counter-intuitively dilute with CKD. Instead, the USG will be lower than expected, or isosthenuric (USG will be between 1.008-1.012 in CKD patients). 66% of the kidneys’ nephrons must be damaged before isosthenuria is noted on urinalysis. Once urine becomes this dilute in a patient with CKD, the kidneys are only functioning at 33% efficiency or less.
  • Proteinuria: High levels of protein should not normally be found in urine (proteinuria), especially if it is dilute. Damage to the kidneys, primarily the glomeruli, may cause them to become leaky, thereby allowing important blood proteins (such as albumin) to escape the bloodstream and be removed from the body in urine. This can lead to low blood protein concentration, which can disrupt the oncotic pressure of the blood and allow free fluid to seep out into the rest of the body (causing ascites and peripheral edema, as previously discussed). Other proteins such as anti-thrombotic proteins may also be lost in the urine, impairing your pet’s ability to prevent blood clots. Furthermore, larger proteins trying to escape glomeruli that has already sustained injury can further damage the kidneys, causing a cyclical effect of worsening kidney function and proteinuria. Therefore, detecting proteinuria and trying to treat it is vital for your pet’s overall prognostic outcome. If proteinuria is discovered on a basic UA, a specialized test called the UPC ratio should be performed (see below).
• Urine protein : creatinine ratio (UPC ratio): As stated, the presence or absence of proteinuria serves as a prognostic indicator of the severity of your pet’s CKD and can be used to help determine your pet’s projected lifespan. If proteinuria is detected on a routine urinalysis, a specialized test called the urine protein : creatinine ratio test (or UPC ratio) will be performed. The purpose of this test is to detect if protein found in urine is actually due to kidney leakage secondary to renal damage (i.e. proteinuria of renal origin versus other sources of urinary protein). UPC is especially helpful in assessing function of the glomeruli in glomerulonephritis cases.
• Urine culture: Even if the routine urinalysis did not suggest the presence of a urinary tract infection (UTI), a urine culture (seeing if microorganisms grow from a urine sample) is still important to perform as it will ensure that a subtle UTI is neither contributing to the kidney disease nor complicating its treatment.
• Imaging via abdominal radiographs (X-rays) and/or ultrasound: The size and shape of the kidneys can be better visualized via X-rays or ultrasound, supporting a diagnosis of CKD. Furthermore, these imaging tools are also used to identify any stones (uroliths) which may be hiding out in the urinary tract or any evidence of pyelonephritis (kidney infection) – both of which could be treated and greatly improve the health of the kidneys.
• Renal biopsy?: A biopsy of the kidneys is rarely performed anymore since it is invasive and will not yield much more information than can already be gained through other less invasive diagnostic tests.
• Blood pressure measurement: Between 50-90% of canine and feline CKD patients have high blood pressure (hypertension). Hypertension may become more severe with glomerular diseases causing the CKD. Hypertension occurs secondary to CKD due to activation of the renin-angiotensin-aldosterone system (RAAS). This is an endocrine system of feedback hormones that control the body’s fluid balance. The RAAS cascade is activated during dehydration, prompting the conservation of sodium and limited water reserves in the bloodstream in order to increase blood pressure. RAAS also triggers vasoconstriction, tightening and narrowing of the blood vessels to also help boost blood pressure. As CKD and dehydration worsens, the RAAS can get a little out of hand, doing more harm than good by elevating the systemic blood pressure too high, resulting in hypertension. Uncontrolled hypertension can have multi-systemic health effects, known as end-organ damage. Such consequences of hypertension include sudden blindness due to retinal damage, cardiovascular disease, and a swifter progression of the CKD to renal failure. Hypertension can also worsen proteinuria by “forcing” more proteins out of the bloodstream and through the kidneys, damaging more glomeruli in the process. Therefore, your vet will wish to measure your dog or cat’s systolic blood pressure and keep tabs on it with subsequent re-checks. Hypertension should always be treated with appropriate dietary modifications and medications (see below under “Therapy”). Such treatments will also help improve proteinuria as well.

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Curious what your pet’s bloodwork and urinalysis results mean? Read The Meowing Vet’s previous articles on routine labwork results:

• Interpreting Your Pet’s Bloodwork Results

• Understanding Your Pet’s Urinalysis Results

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Staging CKD

Chronic kidney disease is staged in order to help your vet determine the degree of renal damage that your pet has already sustained, providing insight for tailoring a therapeutic plan for your individual dog or cat as well as determining your pet’s projected prognosis. Determining your pet’s stage of CKD is based upon guidelines by the International Renal Interest Society (IRIS), thus you may hear your vet refer to “IRIS staging.” Staging is primarily based on your pet’s blood serum creatinine concentration (when your pet is well hydrated). A normal serum creatinine is between 0.8-2.1 mg/dL on most laboratory reference ranges. As explained,  creatinine levels increase higher and higher as fewer and fewer nephrons are functioning. (An exception to this rule may occur in underweight animals with muscle wasting. Since creatinine is a waste byproduct of skeletal muscle metabolism, creatinine levels may not significantly rise if the patient has poor muscle mass. Therefore, staging may be a bit more difficult in these animals.)

PLEASE NOTE: The following tables are best viewed on larger mobile devices or on desktop browsers.

Stages range from 1 to 4 with stage 1 being less mild and stage 4 being most severe. Chronic renal failure (CRF) occurs at stages 2 and up.

Serum creatinine concentration (mg/dL)	Stage 1: non-azotemic CKD	Stage 2: mild renal azotemia	Stage 3: moderate renal azotemia	Stage 4: severe renal azotemia
Dog	<1.4	1.4-2.0	2.1-5.0	>5.0
Cat	<1.6	1.6-2.8	2.9-5.0	>5.0

These stages may be further classified by the detection of: 1) protein in the urine (proteinuria) via the UPC ratio test (see details above); and 2) high blood pressure (systemic hypertension). The presence of either proteinuria or hypertension carries a worse prognosis for the CKD patient.

Urine protein : creatinine ratio (UPC ratio)	Classification
<0.2 (normal)	Non-proteinuric
Dogs: 0.2-0.5 Cats: 0.2-0.4	Borderline proteinuric
Dogs: >0.5 Cats: >0.4	Proteinuric

 

Systolic blood pressure (mmHg)	Diastolic blood pressure (mmHg)	Category	Risk Level
<150	<95	Normal	Minimal
150-159	95-99	Mild hypertension	Low
160-179	100-119	Moderate hypertension	Moderate
≥180	≥120	Severe hypertension	High

Further species-specific details can be found in the canine and feline CKD staging algorithms by IRIS on their website.

 

Therapy for CKD

As explained, chronic kidney disease is quite sadly incurable. Therefore, management is regarded as “therapy” rather than “treatment.” These therapeutic modalities are aimed not only at slowing the rate of progression of the kidney disease but also at alleviating the side effects and clinical signs of CKD. Sometimes, a CKD patient presents in a critical state, requiring hospitalization for re-hydration and electrolyte correction. Once stabilized, some or all of the therapies discussed below will be initiated at home in order to achieve the following goals.

Goals of Therapy

• Stages 1 & 2: Diagnose and treat the inciting disease which may be worsening the renal disease (ex. treat a urinary tract infection, remove obstructive urinary stones, etc.). Unfortunately, the primary trigger is rarely identified at such an early stage of kidney disease.
• Stages 2 & 3: Slow down progression of the kidney disease via renoprotective agents (i.e. things that protect the kidneys; for example: eating a prescription renal diet, controlling high phosphorus levels, managing high blood pressure and controlling proteinuria, etc.).
• Stages 3 & 4: Palliative care, meaning not much is likely to help slow down the disease process at this stage. Instead, the goal is to alleviate the secondary effects of CKD which can make pets feel ill and to attempt to make the dog or cat feel better (for example, stimulating the appetite, controlling nausea and vomiting, treating severe anemia, etc.). Prescription renal diets may still be used at these advanced stages. Hospice care is to be considered at end-stage kidney failure.

Therapy Considerations

• Maintain adequate hydration status: Due to your pet’s impaired ability to retain fluids in the bloodstream, your dog or cat with CKD is at risk of dehydration, which can worsen kidney function and contribute to a progression in disease severity. Therefore, ensure that your pet has access to fresh water AT ALL TIMES! You can also encourage some finicky cats to drink with use of a water fountain for pets. Despite drinking large amounts of water, some patients still cannot keep up with the amount of fluids lost in their urine. These dogs and cats will benefit from periodic subcutaneous fluid administration (i.e. sub-Q fluids, or specially balanced fluids placed under the skin). Our pets have looser skin than we humans do, providing perfect pockets to hold fluids. Your vet may recommend that you bring your pet to the clinic regularly for sub-Q fluid administration or may show you how to administer fluids to your pet at home if you’re comfortable. A specially formulated fluid solution, often lactated ringer’s solution (or LRS), is used. Following sub-Q fluid administration, typically delivered between your pet’s shoulder blades, a bulge of fluid will sit on top of your pet’s back at first, causing your dog or cat to resemble a cute little camel with a hump. Gradually, the fluids will be absorbed into the bloodstream to re-hydrate your pet, and the lump will dissipate. (Alternatively, a gastrostomy tube may be placed in some pets to provide another route to easily administer fluids.)
• Avoid nephrotoxic drugs: If your pet is on certain medications such as a non-steroidal anti-inflammatory drug (NSAID) like carprofen (Rimadyl®), deracoxib (Deramaxx®), or meloxicam (Metacam®), your vet may recommend to discontinue use in order to preserve remaining renal function. Side effects of chronic use of NSAIDs, especially at high doses, include kidney function impairment. However, these medications may be vital to the quality of life of some patients, such as those with severe pain from osteoarthritis. In such circumstances, a compromise must be met between keeping the pet comfortable while also protecting the kidneys, so the NSAID may be used at a lower dose or swapped for a different analgesic (pain relief) medication. High doses of glucocorticoid steroids (such as prednisone or prednisolone) may also need to be stopped (if at all possible) or decreased as these medications can also have renal side effects.
• Proper nutrition: Regardless of which disease your dog or cat may have or not, a healthy diet is essential to the overall well-being of your pet. Special nutritional considerations must be managed with chronic kidney disease in order to slow down progression of renal damage. The dietary goals of CKD therapy include: 1) feeding a diet lower in protein amount but with better quality protein (this will decrease BUN production during digestion); 2) reducing the amount of phosphorus in the diet; 3) reducing the amount of sodium in the diet (in order to block the RAAS cascade); 4) feeding a diet high in omega-3 fatty acids (which will reduce inflammation to help protect remaining nephrons); and 5) feeding an alkalinizing diet (to combat metabolic acidosis and, thus, raise blood pH to a normal level).
  • Prescription diet: Feeding your pet a prescription renal diet is the #1 recognized way to improve your pet’s survival when battling CKD (stages 2 and 3). These diets are specially formulated to meet the strict nutritional needs that a dog or cat with kidney disease requires.  Examples of such diets include: Hill’s® Prescription Diet® k/d®, Purina® Pro Plan Veterinary Diets® NF Kidney Formula®, and Royal Canin Veterinary Diet® Renal™ Support formulas. If your pet likes canned wet food, choose that option if possible, since the additional moisture in the wet diet will aid in keeping your pet hydrated.
    • Alternatively, astutely formulated homemade diets may be considered, but only by explicitly following your veterinarian or veterinary nutritionist’s strict guidelines to ensure that they’re appropriate for a renal diet.
    • However, if your pet absolutely will not eat a renoprotective diet, anything he or she will eat is important in order to provide some nutrition.
  • Nutritional supplements: In addition to an appropriate probiotic supplement (read more below under “Enteric Dialysis”), providing your pet with an omega-3 fatty acid supplement can be helpful. Such a supplement should be of a marine/fish (not vegetarian) source and be high in levels of EPA and DHA. Click here to learn more about the health benefits of omega-3 fatty acids and for product examples.
• Appetite stimulants: If your pet’s appetite has still not returned to normal, an appetite stimulant may be considered to give your pet the munchies. Examples include mirtazapine, cyproheptadine, and capromorelin (Entyce® by Aratana Therapeutics). If your pet still won’t eat, a feeding tube may be considered as a last resort.
• Treat nausea and vomiting: Nausea is a dreadful side effect of CKD. To combat it, antacids can be taken as often as daily. These medications reduce stomach acid stimulated by increased gastrin levels. Examples include either H2 blockers (such as famotidine) or proton pump inhibitors (PPIs, such as omeprazole). For more severe nausea and vomiting, other occasional anti-emetic medications such as oral or injectable maropitant (Cerenia® by Zoetis) may be prescribed.
• Correct potassium level: Low serum potassium concentration (hypokalemia) is a common consequence of CKD due to decreased dietary intake and increased excretion in the urine. Hypokalemia causes your pet to feel weak. Potassium may be supplemented at home via oral potassium citrate or potassium gluconate.  Product examples include Tumil-K® by Virbac or Renal K+™ by Vetoquinol. For severe cases, your vet may recommend hospitalization to administer potassium chloride intravenously (IV).
• Correct acid-base anomalies: If your pet’s blood is deemed severely acidic as observed on bloodwork findings, your vet may administer either sodium bicarbonate or potassium citrate to alkalinize the blood.
• Prevent high phosphorus levels: High phosphorus levels in the bloodstream (hyperphosphatemia) can lead to metastatic calcification and renal secondary hyperparathyroidism, as explained. Reducing phosphorus in the diet is a key goal in dietary management of CKD. However, as CKD advances (stages 3 & 4), medications that bind excess phosphorus may also be needed. Such products include calcium carbonate (such as TUMS® or Epakitin® by Vetoquinol), calcium acetate, or aluminum hydroxide. These medications must be given concurrently with a meal in order to be effective. Most animals do not like these medications placed directly in their food; instead, you can allow your pet to eat and then administer these medications directly by mouth immediately thereafter. Epakitin® by Vetoquinol tends to be more palatable than other products. If hyperphosphatemia is severe enough to induce renal secondary hyperparathyroidism, chances are that calcium levels are pretty low. In these cases, the medication calcitriol may be necessary in order to raise serum calcium concentration.
• Treat high blood pressure: To prevent end-organ damage, hypertension should be well controlled. Anti-hypertensive medications such as calcium-channel blockers (ex. amlodipine) are useful in cats while angiotensin-converting enzyme (ACE) inhibitors such as benazapril or enalapril are useful in both cats and dogs. Moreover, ACE inhibitors are of special aid in reducing blood pressure as well as proteinuria in cases of glomerulonephritis, thereby preventing further glomerular damage. Dietary restriction of sodium is also important in reducing blood pressure.
• Treat anemia: Once anemia (low red blood cell count) is severe enough (usually when the hematocrit, or HCT, is <20%), your vet will recommend treating it. Anemia does not tend to result in clinical signs of illness until stages 3 or 4 CKD. Blood transfusions or erythropoietin (EPO) administration may be considered. However, EPO supplementation is not only expensive, but it is also risky, potentially causing seizures, hypertension, and more severe anemia (due to an auto-immune reaction to its administration). Therefore, EPO should only be given when very necessary.
• Dialysis: Dialysis (more specifically, hemodialysis) is the medical procedure of running a patient’s blood through a filtration machine that acts as an artificial kidney as it removes toxins to purify the bloodstream. Though a mainstay of chronic kidney disease therapy in human patients, dialysis is not readily available for most veterinary patients with CKD. Some specialty veterinary facilities, however, may have dialysis capabilities for dogs and cats.
  • “Enteric Dialysis” (meaning removal of toxins through the gastrointestinal system): This therapy is readily available however. Azodyl™ is an oral probiotic supplement by Vetoquinol that adds healthy probiotics (good bacteria) to the gut, creating a concentration gradient that pulls uremic (BUN) toxins out of the bloodstream and into the GI tract to be removed via defecation instead of urination. This product’s action at effectively reducing uremia may be of questionable efficacy in some patients, but it may be worth considering.
• Kidney transplant: Kidney transplantation is much more common in human medicine with end-stage CKD patients than it is in veterinary medicine. This procedure is extremely uncommon (and very pricey) in the veterinary world. Such an operation also has ethical uncertainties, especially in regards to the donor animal. With that said, a successful kidney transplant was performed in a cat in early 2018 at the Ryan Veterinary Hospital of the University of Pennsylvania School of Veterinary Medicine (USA). The cat who was selected to donate one of its kidneys was adopted by the same owner of the recipient feline. Perhaps scientific and medical advancements will one day make dialysis and organ transplants (include renal) more common in animals.

 

The Importance of Re-Checks

There is no denying the fact that having a pet with chronic kidney disease is both time-consuming and financially taxing. Due to the progressive and non-curative nature of this disease, you will be visiting your vet quite frequently to track how rapidly your pet’s kidneys are failing and how best to keep your pet comfortable. Besides euthanasia when the time is right, there is no other option since declining all treatments is a cruel way of allowing your pet to suffer unnecessarily. Therefore, regular re-checks are important.

Until your pet has stabilized (eating and drinking and no longer losing weight), your vet may wish to see your pet every few weeks and even weekly in some cases. Cases that suddenly worsen (we call these “acute on chronic” cases) may require hospitalization or more frequent re-checks. However, once your pet is stable, your vet will recommend a re-check every 3-6 months. These visits will allow your vet to perform a physical exam and lab tests to monitor body weight, hydration, red blood cell count, electrolytes, proteinuria, and blood pressure. As much as these frequent re-checks may add to your already hectic schedule, I strongly encourage you to follow your vet’s instructions and show up at your re-check appointments for the welfare of your pet. The sooner that your vet sees something going awry in your pet’s health, the sooner an interventional therapy can be started, improving your dog or cat’s odds of survival.

 

Prognosis of CKD

As much as we all wish it were otherwise, CKD is irreversible and incurable, and despite the best efforts of both pet owners and veterinarians, our beloved dogs and cats will eventually succumb to kidney failure. However, by carefully following the recommended therapies described above, we can hopefully expand the life expectancy of our pets with CKD. But, what I feel is even more important that increasing the quantity of a patient’s life, is improving the quality of the life of our wonderful furry companions. With end-stage kidney failure comes a high degree of suffering towards the end of our pet’s life – despite our best medical efforts.

As difficult as it is to think about, our role as both pet guardian and vet are to prevent animal suffering. I recommend to owners of pets with a chronic, terminal illness to track their pets’ well-being with a quality of life checklist. Once there are more bad days than good days, I strongly recommend euthanasia to prevent further undue suffering in the face of an illness that has no cure. As a pet owner first and foremost myself, I truly understand how difficult and gut-wrenching this decision can be. Owners are often unsure of when to grant their pets the greatest kindness of peace by letting them go. I think back to the words of Dr. Jessica Vogelsang: “It’s better to be a week too early than a minute too late.” If in doubt, speak with your personal veterinarian, who can help guide you through end-of-life care for your pet.

Different causes of chronic kidney disease carry different prognostic outlooks. Since idiopathic CKD is the most common type, we will go over the statistics looking at the average expected lifespan of these CKD cases – more specifically, idiopathic chronic renal failure (CRF, stages 2 and up).

Dogs with chronic renal failure do not tend to live as long as their feline counterparts. However, like in cats, a prescription renal diet increases survival time. Dogs with idiopathic CRF not eating a renoprotective diet live an average of a mere 6 months versus 19 months when they eat a prescription diet (and also have stable renal function for the first few months following their diagnosis). Some may live upwards of 2 years. While a renal diet is a known protective factor, other factors may shorten a canine’s survival, including having an initial systolic blood pressure reading of >160 mmHg and having a urine protein : creatinine (UPC) ratio of ≥ 1.

Cats tend to fare a bit better with CRF than do dogs. However, a prescription renal diet certainly helps extend these cats’ lives as well. Cats not consuming a renal diet live only 7-9 months of average versus 18-29 months while eating a renal diet. With loads of TLC, some kitties with CKD may live several years with a decent quality of life. Though feeding a prescription renal diet is known to improve these cats’ lifespan, proteinuria with a UPC ratio >0.2 decreases survival.

Since idiopathic CKD tends to have a later onset, occurring in older dogs and cats, the likelihood that your pet has a concurrent health condition is high. The presence of another disease process in addition to CKD may complicate the management of both diseases. A good example of this catch-22 is is a patient that has both CKD as well as congestive heart failure (CHF). With kidney disease, we want to preserve renal function by keeping the dog or cat well hydrated with fluid therapy. However, with cardiac disease, a damaged heart cannot pump blood as effectively as it should, resulting in fluid to backup in and/or around the lungs, causing respiratory distress and possible death. The goal of certain cardiac medications (such as furosemide) is to slightly dehydrate the body in order to improve function of the heart and to protect the lungs. The goals of each of these diseases oppose one another, and can therefore make managing both disorders difficult. A balance must be met to try to keep both the heart and the kidneys as healthy as possible while their therapies conflict with one another. Another example of “frenemy” illnesses is CKD and feline hyperthyroidism: medications which treat excessive thyroid hormone production in hyperthyroid cats can worsen pre-existing kidney disease. A balance between managing these two disorders must also be met.

 

What Can I Do At Home to Help My Pet with CKD?

• Provide access to plenty of fresh water at all times (including inside your pet’s crate if he or she sleeps in one overnight)
• At-home fluid administration: It may seem daunting at first, but many owners of pets with CKD quickly learn how to deliver subcutaneous (sub-Q) fluids to their pets at home. This is especially helpful for those cats (or dogs) who dislike vet visits. From the comfort of their own environment, these pets can receive their weekly, bi-weekly, or even daily fluid therapy (whatever frequency is recommended by your veterinarian). Supplies you need include sterile 18-gauge needles (they seem large, but they allow fluid to flow quickly for easier administration), an IV bag (usually LRS) and IV line from your vet (although, yes the fluids are given subcutaneously, not IV), and a high place to hang the bag (on an IV pole or somewhere else up high as gravity will help facilitate the quick flow of fluids). Do not squeeze the bag to push fluids out more quickly; this can cause discomfort to your pet. Always use a new needle with each fluid administration; we want them to be sterile to prevent introducing bacteria under the skin, and we don’t want them to dull (ouch!). Your veterinary team can show you how to administer the sub-Q fluids under your dog or cat’s skin and allow you to practice until you get comfortable. Opt for a different site each time you give fluids to decrease your pet’s chances of becoming overly sore at that area and to minimize scar tissue formation (which can happen over time). Only administer the type of fluids your vet prescribes: they must be sterile and specially balanced (never use plain water!). Furthermore, only give your pet the exact amount of fluids that your vet recommends: if you don’t deliver enough, your pet may remain dehydrated; if you deliver too much, your pet (especially cats) can experience fluid overload, in which the body cannot effectively handle so much water content, which can leak into or around the lungs and impair breathing. If you’re still not comfortable performing at-home fluid therapy, no problem. Either continue with your regular veterinary appointments or enlist a visit by a mobile veterinary service who can administer the fluids at home for you.
• Strictly adhere to your pet’s prescription diet and medication regimen: Remember, a prescription renal diet is the sole identified way of increasing your pet’s lifespan!
• Keep your pet away from hot outdoor temperatures to prevent dehydration.
• Protect your pet’s health in other ways: Other illnesses, such as GI upset with vomiting and diarrhea, can cause your pet’s CKD to decompensate due to dehydration. Therefore, ask your vet how best to keep your dog or cat healthy in all other areas to prevent other diseases.
• Monitor that your pet is urinating: Usually, CKD patients are polyuric (meaning they produce a large volume of urine frequently, as we’ve discussed). However, if they become severely dehydrated or experience end-stage renal failure, they may stop producing any urine (anuria). This condition is an emergency requiring veterinary attention ASAP!
• Heed your vet’s recommended re-check schedule
• Recognize when your pet is suffering: Keep track of how your dog or cat is doing with a quality of life chart to help you understand if your pet is improving with his or her prescribed renal therapies or is suffering. This will guide you in determining when the time is right to grant your brave warrior permission to end his or her fight with chronic kidney disease and cross the “rainbow bridge” with the selfless and kind gift of euthanasia. Hopefully, you will have many months (or even years) of a good quality life with your dog or cat before the time comes to make this decision.

– Maranda Elswick, DVM

 

The Meowing Vet urges you to consult with your personal veterinarian at the earliest indication that your dog or cat may have kidney disease. Follow your vet’s advice regarding medical therapy and religiously adhere to the recommended re-check schedule to give your pet the best chance of having a longer, happier life with CKD.

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Special thanks to David C. Grant, DVM, MS, DACVIM (Internal Medicine) for excellent clinical teaching.