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Management and Treatment of Chronic Kidney Disease in Cats - in Practice
Management and Treatment of Chronic Kidney Disease in Cats - in Practice
Management and Treatment of Chronic Kidney Disease in Cats - in Practice
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A rticle
Management and treatment
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Management and treatment of chronic kidney disease PDF
A rticle
in cats FREE
info Sarah Caney
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Making a diagnosis of chronic kidney disease (CKD) in cats marks the start of a new and complex journey to
provide optimal treatment for the patient. A successful outcome depends on attention to detail and a
good working relationship with the carer and patient. If it is possible to institute good treatment measures,
Responses
many patients with CKD survive for several years following diagnosis, with an excellent quality of life.
A rticle
http://dx.doi.org/10.1136/inp.i4901
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AFTER a diagnosis of chronic kidney disease (CKD) attention moves to treating and managing the disease.
Treatment should include addressing any underlying disease which is contributing to ongoing renal
damage, strategies aimed at reducing progression of disease and symptomatic support of complications
of CKD, such as poor appetite and dehydration. CKD is a progressive condition and, ultimately, despite its
chronicity, is likely to be responsible for the patient's death. Phosphate-restriction, ideally through feeding
a specially formulated renal diet, has been shown to be the most effective management option. Cats with
CKD that will eat a renal diet live on average two to three times longer than those fed a standard
commercial cat food, so all efforts should be put into supporting transition to a renal diet. Further
treatments, tailored to the individual's needs, can make a big difference to quality of life.
▪ Where possible, use strategies that are known or thought to slow the progression of renal disease.
In normal cats, excess phosphorus consumed in the diet is excreted by the kidneys and renal excretion of
phosphate is dependent on glomerular filtration. Therefore, cats with CKD are vulnerable to phosphate
retention and hyperphosphataemia. Regulation of phosphate excretion is under the control of parathyroid
hormone (PTH) which has a phosphaturic effect. PTH increases renal reabsorption of filtered calcium while
increasing renal excretion of phosphate. PTH has other effects including mobilisation of calcium (and
phosphate) from bone, and increasing calcitriol production, which facilitates calcium absorption from the
intestine. Hyperphosphataemia and reduced renal production of calcitriol contribute to the development
of renal secondary hyperparathyroidism (R2HPTH); a condition which more recently has been referred to as
feline mineral and bone disorder. In a healthy cat, increased amounts of PTH would help to correct
hyperphosphataemia by increasing renal elimination of this substance. However, this strategy is only
effective when there are sufficient functioning nephrons available to respond. Once the renal mass is
below a critical level, increases in PTH are counter-productive and merely result in mobilisation of calcium
and phosphate from the bone. Calcium and phosphate mobilisation may lead to renal osteodystrophy and
clinical consequences including ‘rubber jaw’. Release of calcium and phosphate also leads to soft tissue
mineralisation. Where present, nephrocalcinosis is especially damaging to renal function.
Unless treated, R2HPTH progressively worsens. High levels of PTH are thought to contribute to the
uraemic state through acting as one of the uraemic toxins. High levels of PTH also contribute to ongoing
renal damage by causing calcium influx into renal tubular cells and precipitation of calcium phosphate in
the lumen of the tubules. R2HPTH is seen in most – if not all - cats with CKD and may precede azotaemia.
Hyperphosphataemia is used as a marker of R2HPTH; if phosphate levels are raised in a cat with CKD they
can be assumed to be suffering from R2HPTH. If phosphate levels are normal unfortunately this does not
rule out R2HPTH. The International Renal Interest Society (www.iris-kidney.com) recommend phosphate
restriction for all cats with azotaemic CKD (IRIS stages 2, 3, 4) irrespective of their blood phosphate levels
and have guidelines regarding ideal (target) blood phosphate levels (Table 1). The aim of phosphate
restriction is to prevent and reverse development of R2HPTH and hence slow progression of renal disease.
Use of a renal diet and/or phosphate binder is effective in achieving phosphate restriction. Acceptance of
a renal diet can take several weeks or months to achieve and success depends on supporting carers
through this period. Cats with CKD can be challenging to transition to a new diet and often require
treatment for complications that have a negative impact on appetite. If feeding a renal diet is not possible
then senior cat food is preferable to standard commercial cat food. If blood phosphate levels remain above
IRIS target levels (Table 1) in spite of phosphate restriction, a combination of renal diet and one or more
phosphate binders may be required.
A number of phosphate binders are available. Used alone with a standard commercial cat food, phosphate
binders may provide sufficient phosphate-restriction for a cat in IRIS stage 2 CKD, but those in more
advanced stages are likely to need a phosphate-restricted diet to maintain normophosphataemia.
‘Veterinary’ formulated options include calcium carbonate (eg, Pronefra, Virbac; Ipakitine, Vétoquinol,
Easypill Cat Kidney Support, Vetinnov); other options include human formulations such as aluminium
hydroxide (eg, Alu-cap, Meda Pharmaceuticals) and lanthanum carbonate (Fosrenol, Shire Pharmaceuticals
Contracts). Phosphate binders should be mixed with food and included with every meal that the cat eats.
They work by binding to phosphate present in the food, retaining this in the bowel and hence limiting the
amount of phosphate that can be absorbed by the body. Calcium-containing binders should be avoided in
hypercalcaemic patients and in those receiving calcitriol.
RAAS suppression
Loss of nephrons leads to activation of the renin angiotensin aldosterone system (RAAS), which results in
hypertrophy of residual nephrons with reduced arteriolar resistance and increased glomerular blood flow.
As renal disease progresses, the afferent arteriolar tone decreases more than the efferent arteriole tone,
resulting in glomerular hypertension and hyperfiltration. Although this increase helps support glomerular
filtration rate and excretory function, ultimately RAAS activation has negative consequences including
proteinuria, renal damage, fibrosis and further progression of renal disease. Angiotensin II is responsible for
many of the damaging effects of RAAS activation.
Two veterinary-licensed options exist for suppression of the RAAS in cats with CKD:
▪ The angiotensin receptor blocker (ARB) telmisartan works by preventing angiotensin II from binding to
one of its receptors, the angiotensin receptor-1 (AT-1). The AT-1 receptor mediates the most harmful
consequences of angiotensin II, whereas the AT-2 receptor is thought to result in some beneficial effects
in cats with CKD.
▪ Angiotensin converting enzyme inhibitors (ACEI) such as benazepril work by blocking the production of
angiotensin II.
IRIS currently recommend that CKD patients are treated with medications that suppress the RAAS if
suffering from a persistent renal proteinuria. Patients are classed as proteinuric if their urine protein to
creatinine ratio (UPC) is over 0.4 and borderline proteinuric if their UPC is between 0.2 and 04. RAAS
suppression using telmisartan or benazepril has been shown to be effective in reducing proteinuria
although as yet a survival benefit has not been shown.
Some clinicians advocate treating borderline proteinuric cats (UPC 0.2 to 0.4) on the basis that survival
times in these cats are reduced compared to non-proteinuric CKD cats (UPC <0.2) and this is considered
logical by the panel responsible for the recently published International Society of Feline Medicine (ISFM)
consensus guidelines on diagnosis and management of CKD (Sparkes and others 2016). ACEI and ARBs should
only be used in clinically stable, normally hydrated cats. There may be some benefits in treating non-
proteinuric CKD patients with an ARB or ACEI since some studies have shown improved quality of life and a
tendency for the renal disease to progress more slowly in these cats.
Telmisartan has a potential advantage over an ACEI by not being susceptible to ‘ACE escape’ – the
phenomenon whereby alternative pathways allow angiotensin II to continue to be produced despite
administration of an ACEI. Telmisartan also offers a more targeted mode of action, sparing the AT-2
receptor which may mediate some beneficial effects. A recent field study of cats with CKD showed that
telmisartan was effective in significantly reducing proteinuria at all assessment points in the 180 day
study, whereas benazepril was not (Sent and others 2015).
Hydration support
Patients with CKD are vulnerable to dehydration. Dehydration worsens renal perfusion and therefore renal
function leading to exacerbation of complications associated with CKD such as metabolic acidosis and
poor appetite. Dehydrated patients should be rehydrated and all patients should be encouraged to
maintain normal hydration through tactics including feeding a moist diet and ensuring that access to
water is easy and plentiful. Detailed guidelines on tactics that can encourage increased water intake are
available in the ‘free downloads’ section of my website (Caney 2011). Subcutaneous fluids (eg, 50 to 100 ml
Hartmann's solution once daily) can be helpful in cats struggling to maintain normal hydration (Fig 1).
Download figure
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Fig 1:
Owners can be taught to administer subcutaneous fluids to their cat at home and this can be helpful in maintaining optimal
hydration in some patients. A typical regime involves giving 50 to 100 ml Hartmann‘s solution once daily, administered via a giving
set and 21 G needle using gravity to aid the flow of the fluid
Prevention/treatment of hyperphosphataemia
Around two-thirds of CKD patients are hyperphosphataemic as a result of their renal disease. This should
be addressed as discussed earlier.
Download figure
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Fig 2:
Placing a feeding tube for nutritional support can be helpful in some cases. A large bore tube is preferable so that liquidised renal
food can be administered
Support of anaemia
Anaemia is a potential complication of CKD, estimated to affect around a third of patients, and may lead to
poor appetite, lethargy and weakness. Anaemia develops due to a lack of production of erythropoietin by
the diseased kidneys, reduced survival of red blood cells and potentially blood loss from gastric ulcers and
excessive blood sampling. Patients may suffer from a relative or absolute iron deficiency, which can
contribute to anaemia development. Iron deficiency should be differentiated from chronic disease by
assessing iron status (iron saturation, total iron binding capacity [TIBC] and iron levels) and looking for
features consistent with iron deficiency, such as microcytic and hypochromic red cells. Low/normal serum
iron and saturation with a low TIBC is generally considered compatible with an anaemia of chronic disease;
in a patient with iron deficiency, iron levels and saturation are low while TIBC is normal. Treatment of
anaemia is generally recommended once the packed-cell volume (PCV) falls to around 20 per cent and
most successful is a combination of an erythrocyte stimulating agent, such as darbepoetin* (induction
dose 1 µg/kg subcutaneously once a week) combined with intramuscular iron dextran (50 mg per cat, can
be repeated monthly if needed). Once the PCV reaches the reference range, the dose and/or frequency of
darbepoetin can be reduced (eg, 1 µg/kg subcutaneously every two to three weeks) to maintain red blood
cell parameters within the reference range. Management of anaemia associated with CKD is reviewed in
detail by Chalhoub and others (2011).
Download figure
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Fig 3:
Clinical evidence of severe muscle weakness, including ventroflexion of the neck, may be seen in cats suffering from severe
hypokalaemia
Renal proteinuria
Proteinuria is an acknowledged complication of feline CKD through activation of the RAAS. Treatment of
proteinuria should be considered as discussed earlier.
Download figure
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Fig 4:
Empty gelatin capsules can be used to combine several medications into one ‘dose’. The photo shows my thumb next to several
size 4 empty gel caps
▪ Do what you can to encourage maintenance of normal hydration: feed a moist diet, encourage drinking
by using water fountains, and so on (Caney 2011).
▪ Do not administer the NSAID if your cat appears unwell (eg, not eating, vomiting).
▪ Mix the NSAID with food: if your cat is unwell and does not eat, it will not receive the medication.
For those cats that cannot tolerate an NSAID, other painkiller options that might be helpful would include
opiates like buprenorphine.
Where anaesthesia is needed in CKD patients, for example for dental treatment, the patients should be
stabilised preoperatively so that their hydration is optimal, electrolytes are normal and they are in as good
a state as possible to cope with anaesthesia. Anaesthetic regimes which may result in hypotension should
be avoided and blood pressure should be monitored and supported, as necessary, throughout the
procedure.
Summary
CKD is often a challenging condition to manage but treatment is extremely successful in most patients
where optimal treatment is possible. Attention to detail and providing an individualised plan leads to the
best treatment outcome.
References
↵ CANEY S. M. A. (2011) Encouraging your cat to drink – a guide for cat owners. www.vetprofessionals.
com/catprofessional/free_downloads.html. Accessed July 27, 2016 Google Scholar
↵ CANEY S. M. A. (2013) An online survey to determine owner experiences and opinions on the
management of their hyperthyroid cats using oral anti-thyroid medications. Journal of Feline Medicine
and Surgery 15, 494–502 Abstract/FREE Full Text Google Scholar
↵ CANEY S. M. A. (2016) An online survey of dietary and phosphate binder practices of owners of cats
with chronic kidney disease. Journal of Feline Medicine and Surgery (In press) Google Scholar
↵ CHALHOUB S., LANGSTON C., EATROFF A. (2011) Anemia of renal disease: what it is, what to do and
what's new. Journal of Feline Medicine and Surgery 13, 629–640 Abstract/FREE Full Text
Google Scholar
↵ SENT U., GÖSSL R., ELLIOTT J., SYME H. M., ZIMMERING T. (2015) Comparison of efficacy of long-term
oral treatment with telmisartan and benazepril in cats with chronic kidney disease. Journal of
Veterinary Internal Medicine 29, 1479–1487 CrossRef PubMed Google Scholar
↵ SPARKES A. H., CANNON M., CHURCH D., FLEEMAN L., HARVEY A., HOENIG M. & OTHERS (2015) ISFM
consensus guidelines on the practical management of diabetes mellitus in cats. Journal of Feline
Medicine and Surgery 17, 235–250 Abstract/FREE Full Text Google Scholar
↵ SPARKES A. H., CANEY S., CHALHOUB S., ELLIOTT J., FINCH N., GAJANAYAKE I. & OTHERS (2016) ISFM
consensus guidelines on the diagnosis and management of feline chronic kidney disease. Journal of
Feline Medicine and Surgery 18, 219–239 Abstract/FREE Full Text Google Scholar
ZIMMERING T. M., HECK E. V., ADAMS J., RAMBAGS B. (2014) Ease of use of Semintra – cat owner
feedback under European field conditions (‘Easy Programme’). Abstract. Journal of Feline Medicine and
Surgery 16, 764–765 FREE Full Text Google Scholar
ZIMMERING T. M. (2015) Ease of use of Semintra® and its effects on quality of life. Abstract. SEVC.
Barcelona,October 15 to 17, 2015 Google Scholar
View Abstract
Footnotes
↵*: Used for products which do not have a veterinary license for use in cats
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