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Review Article: Is there any point in referring cases of chronic renal failure?

The traditional view of chronic renal disease is that, with the exception of instigating a proprietary ‘kidney diet’, there is very little that can be done to help. In fact there are a number of therapeutic options that have the potential to improve quality of life and to slow disease progression. As with most diseases, a prerequisite to good management of chronic renal disease is to obtain as much information as possible regarding specific diagnosis, staging and underlying cause. In particular, there are four important questions to be answered:


1. Is this definitely renal disease?

Azotaemia can be a consequence of pre-renal, renal or post-renal pathology and it is extremely important that this distinction is ascertained:

Pre-renal azotaemia is often characterised by a disproportionate increase in urea compared with creatinine. Kidney function, and thus urine concentrating ability, is not affected and urine specific gravity should therefore be high (dogs >1.020, cats >1.030). Causes include dehydration, congestive heart failure and shock, which can usually be distinguished clinically.

Intrinsic renal failure results in a lack of urine concentrating ability and can only be diagnosed when this is demonstrated. If azotaemia is present, the body’s response should be to conserve water and urine should be maximally concentrated. Azotaemia in combination with a low urine specific gravity (<1.20 in dogs, <1.30 in cats) is inappropriate and suggests impaired renal function. In the majority of cases this is due to intrinsic renal failure but there are exceptions. Some conditions resulting in electrolyte imbalance and diuresis (eg. hypoadrencorticism, frusemide administration, hypercalcaemia) can impair concentrating ability resulting in low urine specific gravity, even in the face of pre-renal azotaemia. These patients are identified based on a thorough clinical history, physical examination and laboratory results.

Post-renal azotaemia is usually easily identified clinically, being characterized by acute onset illness accompanied by a distended bladder and lack of urine production as a result of urethral obstruction. If untreated, this will quickly progress to secondary renal failure. Since nephrolithiasis and ureteral obstruction invariably result in unilateral obstruction, renal failure is not generally a feature unless there is pre-existing kidney disease. 


2. Is this acute or chronic disease?

Patients with chronic renal disease initially develop polydipsia and polyuria (PUPD) and, if detected early, a lack of concentrating ability may be identified without associated azotaemia. However, unless an owner is very observant, these early stages of disease are often missed, particularly in outdoor cats. Most patients are diagnosed later once the disease has progressed and azotaemia has developed. A significant number of patients are not presented until they have advanced disease with secondary complications such as weight loss and vomiting. The phenomenon of ‘acute on chronic’ disease may therefore confuse the clinical picture and a detailed history is a useful tool with respect to this. The distinction is clinically important because, unlike chronic renal failure, acute renal failure is potentially reversible and thus may carry a very different long-term prognosis.


3. Is there an identifiable underlying cause?

The majority of patients with chronic renal disease are elderly with what is generally believed to be idiopathic or age-related kidney degeneration. However, it is worth ruling out other more specific causes (figure 1) for which alternative treatment options may be available. This is particularly important in younger patients.


4. Are there secondary complications?

Once a diagnosis of chronic renal disease has been established, treatment should be tailored to the individual patient based on disease staging and assessment of complicating factors.

Chronic renal disease is classified as stage 1 (non-azotaemic, creat <120), stage 2 (mild azotaemia, creat 125-180), stage 3 (moderate azotaemia, creat 180-440) or stage 4 (severe azotaemia, creat >440). It is only stage 4 disease that is associated with uraemia and chronic renal failure. Care must be taken because creatinine is not 100% specific for glomerular filtration rate and reduced muscle mass, common in chronic renal disease, can give a false impression of creatinine reduction. In addition, intrinsic renal failure and pre-renal failure often co-exist, thus complicating the picture. For each stage, proteinuria and hypertension are defined separately. Both these complications are known to accelerate the progression of renal disease and patients should therefore be regularly monitored with specific treatment being initiated as soon as they are identified.

As well as proteinuria and hypertension there are many other potential complications of chronic renal disease that should be identified and addressed (table 1). These complications are not uncommon and a minimum database for an animal with renal failure should therefore include the following:

(1)     full history and physical examination (including ophthalmoscopy and systolic blood pressure measurement)

(2)     serum biochemistry and electrolytes (including calcium and phosphate)

(3)     complete blood count and leucocyte differential

(4)     full urinalysis (dipstick evaluation, specific gravity, sediment analysis, urine protein:creatinine ratio, culture and sensitivity)

Only when this information is known can a comprehensive treatment strategy be formulated.

In summary, while chronic renal disease is incurable and progressive, there is often much that can be done to improve or maintain quality of life and to extend life expectancy. As is common practice, a prescription ‘renal diet’ is invariably indicated. This provides a palatable source of reduced high quality protein with high calorific value, reduced phosphorus and sodium, increased vitamin B and increased omega-3:omega-6 ratio, thus helping to address some of the common problems associated with chronic renal disease.  However, each patient also presents a unique combination of secondary complications and, by identifying and specifically addressing each of these issues, a more holistic and effective therapeutic plan can be formulated.   


Figure 1:

List differential diagnoses for chronic renal disease

Familial or congenital disease


  • Amyloidosis (Shar pei and Beagle)
  • Cysadenocarcimona (German Shepherd Dog)
  • Renal dysplasia (Shi Tzu, Lhasa Apso, Golden Retriever, Chow)
  • Glomerulopathy (English Cocker Spaniel, Doberman, Bull Terrier)
  • Fancomi syndrome (Basenji)
  • Polycystic disease (Cairn Terrier)


  • Amyloidosis (Abyssinians and Orientals)
  • Polycystic Kidney Disease (Persians and Himalayans)


Acquired disease

  • Infectious (bacterial, mycotic, leptospirosis, leishmania, FIP)
  • Immune complex glomerulopathy
  • Reactive amyloidosis
  • Neoplasia (lymphoma, renal carcinoma, nephroblastoma)
  • Sequelae of acute renal failure
  • Bilateral hydronephrosis (spay granuloma, transitional cell carcinoma, nephrolithiasis)
  • Polycystic disease
  • Hypercalcaemic nephropathy (malignancy, hyperparathyroidism)
  • Idiopathic


Table 1:

Treatment considerations for chronic renal disease

Complication Cause Treatment options
Dehydration Polyuria Maximise fluid intake (water fountains, flavoured water), subcutaneous fluids (consider indwelling catheter), IVFT
Proteinuria Glomerular damage ACE inhibitor
Hypertension Response to increased fluid loss ACE inhibitor, amlodipine
Anaemia Erythropoeitin deficiencyGastrointestinal bleeding

Chronic disease

Recombinant erythropoietinGastroprotectants

Iron supplementation

Weakness/myopathy Hypokalamia Potassium supplementation (po, iv)
Renal secondary hyperparathyroidism ↑ PO4, ↓ ionised Ca2+, low calcitriol, PTH resistance Low phosphate diet, oral phosphate binders, calcitriol therapy? (efficacy still under review)
Gastrointestinal signs (vomiting, gastric ulceration, stomatitis) Uraemic toxins irritate mucosa Anti-emetics, gastroprotectants
Malnutrition AnorexiaProtein loss


Appetite stimulants, tube feedingACE inhibitors

Palatable, high calorie diet (vitamin B2, B6, B12, folate, niacin) +/- anabolic steroids*

Urinary tract infection Impaired innate immunity Antibiotics
Haemorrhage Uraemic platelet dysfunction DDAVP may improve clotting times
Metabolic acidosis Impaired renal excretion of H+, impaired re-absorption of bicarbonate IVFT (+ bicarbonate therapy in severe cases)
Encephalopathy Uraemic toxins Supportive therapy +/- anti-seizure medications
Nephrotic syndrome Hypoalbuminemia Oncotic support


* Note that use of anabolic steroids reduces serum creatinine levels as a result of reduced muscle catabolism and creatinine reduction observed with this therapy does not imply improvement in renal function.