One of the leading causes of death among cats over 10 years old is chronic kidney disease (CKD), which is when the kidneys slowly lose functionality. A note about the name of the problem: A decade ago, this was called chronic renal failure (CRF) because it involved the kidneys failing over a long period, as opposed to acute kidney failure. In recent times, the preferred description is chronic kidney disease (CKD) because this name emphasizes the idea that many cats can live with diminished kidney function for years. I became a 'cat person' when CRF was the term to use and often use that in preference to CKD, but I will try to follow the veterinary trend and use CKD.
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| Emily -- died of complications due to CKD |
In terms of who is getting CKD, the ratio of females to males is 1.06:1, with a
population ratio of 1.15:1.0, so females are a tiny bit less likely to get it
than would be expected.
Some of the purebreds, eg. Birmans, British shorthairs, and Angoras, seem to be over-represented. For example, DSH was 11.7%, Angora was 36.4%, Persians 9.9%. This could be either due to the owners of these cats being more able to do repeated early testing, or some yet-to-be discovered genetic factor, or small sample sizes on the rarer breeds.
In researching this topic, I ran across an interesting and horrifying statistic on the incidence of CKD. In 1990, the estimated rate of CKD was 16 cases for every 1000 cats examined. Looking at just the older cats, the rate was 77 per 1000 for cats over 10 yrs and 153 per 1000 for cats over 15 years. The same type of study was conducted in 2000. For cats of all ages, the rate increased to 112 per 1000, for 10 yrs or older 269 per 1000, and for 15 yrs or older it was 491 per 1000.
Some of the purebreds, eg. Birmans, British shorthairs, and Angoras, seem to be over-represented. For example, DSH was 11.7%, Angora was 36.4%, Persians 9.9%. This could be either due to the owners of these cats being more able to do repeated early testing, or some yet-to-be discovered genetic factor, or small sample sizes on the rarer breeds.
In researching this topic, I ran across an interesting and horrifying statistic on the incidence of CKD. In 1990, the estimated rate of CKD was 16 cases for every 1000 cats examined. Looking at just the older cats, the rate was 77 per 1000 for cats over 10 yrs and 153 per 1000 for cats over 15 years. The same type of study was conducted in 2000. For cats of all ages, the rate increased to 112 per 1000, for 10 yrs or older 269 per 1000, and for 15 yrs or older it was 491 per 1000.
While some of this is due to the increased awareness of CKD and the importance of early detection, it is my opinion and the opinion of my
vet that there has been an actual increase in the rate. My vet started practicing in the mid
1980s. She says she saw CKD in cats 12
yrs or older, but not at a high rate.
This summer we got discussing this and now she is seeing cats as early
as 8 yrs old having the same symptoms and bloodwork as the 12 yrs cats in the
1980s. She also commented that she now
expects any cat over 15 to have CRF and is surprised when they don’t. (She’s in awe of Dante at ~22 with no CKD!)
So, the question becomes what has changed in the last 20
years. While one might want to blame
inbreeding among some purebreds as a cause, this would not explain the increase
among randomly bred cats, namely DSH and DLH.
My vet and I agree that there have been 2 significant changes which MAY
explain part of the increase.
1. Vaccines. In the 1970s, most cats were not vaccinated. In the 1980s, there were pushes to vaccinate cats for a variety of things. By the 1990s, cats began to be vaccinated for 5-8 different diseases each year. Some of the vaccines are grown on kidney tissue, which has lead to the speculation that the residue proteins from the kidney tissue in the vaccines may actually be causing inflammation of the kidneys which then leads to CRF over time.
This actually has been researched (2005) and the conclusion reached was “Parenteral administration of vaccines containing viruses likely grown in CRFK cells induced antibodies against CRFK [Crandell-Rees feline kidney] cell and FRC[feline renal cell] lysates in cats. Hypersensitization with CRFK cell proteins did not result in renal disease in cats during the 56-week study.” (http://www.ncbi.nlm.nih.gov/pubmed/15822597) Now, on the surface, this seems to rule out that vaccines are related to CKD. Looking at the methodology, I do begin to wonder. First, only 14 kittens were used. Not only was the numbers low (14), but these began as 8-week old kittens which means the kidneys and other organs were still growing. Second, they received 4 FVRCP vaccines at 0, 3, 6, and 50 weeks. Basically one year of vaccines. Third, the study concluded at 56-weeks, which is only 6 weeks after the last vaccine. No one is saying that a vaccine causes immediate detectable damage, so 6 weeks seems far too short.
1. Vaccines. In the 1970s, most cats were not vaccinated. In the 1980s, there were pushes to vaccinate cats for a variety of things. By the 1990s, cats began to be vaccinated for 5-8 different diseases each year. Some of the vaccines are grown on kidney tissue, which has lead to the speculation that the residue proteins from the kidney tissue in the vaccines may actually be causing inflammation of the kidneys which then leads to CRF over time.
This actually has been researched (2005) and the conclusion reached was “Parenteral administration of vaccines containing viruses likely grown in CRFK cells induced antibodies against CRFK [Crandell-Rees feline kidney] cell and FRC[feline renal cell] lysates in cats. Hypersensitization with CRFK cell proteins did not result in renal disease in cats during the 56-week study.” (http://www.ncbi.nlm.nih.gov/pubmed/15822597) Now, on the surface, this seems to rule out that vaccines are related to CKD. Looking at the methodology, I do begin to wonder. First, only 14 kittens were used. Not only was the numbers low (14), but these began as 8-week old kittens which means the kidneys and other organs were still growing. Second, they received 4 FVRCP vaccines at 0, 3, 6, and 50 weeks. Basically one year of vaccines. Third, the study concluded at 56-weeks, which is only 6 weeks after the last vaccine. No one is saying that a vaccine causes immediate detectable damage, so 6 weeks seems far too short.
A different study (2006) did produce interesting results. Researchers sensitized cats to CRFK lysates (remains of cells) and several cats did develop lymphocytic-plasmacytic interstitial nephritits after 2 years. (http://www.ncbi.nlm.nih.gov/pubmed/16713319 ) A study from 2010 confirmed that vaccination with FVRCP vaccine grown on CRFK (kidney tissue) does produce antibodies after 2 years which have been associated with nephritis in humans. (http://www.ncbi.nlm.nih.gov/pubmed/20136712 )
So, bottomline… There is no clear evidence that vaccines cause (and I mean this is a statistical sense) CKD. There seems to be evidence that vaccines grown on kidney tissue do cause antibodies against that tissue which (speculation here) may lead to antibodies against all feline kidney tissue which leads to CKD. What I don’t know (because I don’t follow vaccine stuff) is how common it is for FVRCP to be grown on kidney tissue or if there are other options.
2. Food. (And note:
this is MY pet theory which my vet agrees with now.) When meat is processed into cat food, the
proteins undergo a structural change when cooked. They are denatured – like the clear egg white
cooked becomes white opaque solid. The
cooking process also can create partially denatured proteins. My personal opinion is that these denatured
proteins and especially the partially denatured ones are not easily nor
thoroughly digested but are absorbed anyway into the blood stream. There, the kidneys then must filter out these
forms of proteins which they were not designed to handle. (Think of putting diesel fuel in a car
instead of gas.) These ‘foreign’
proteins then begin to clog the tiny tubules in the kidneys which then lead to
more problems and eventually full scale CKD.
My evidence for this is twofold. First, 40 years ago, the rate of CKD seems to be exceedingly low and many cats were let outside to catch mice, etc. As the commercial pet food industry grew, so has the rate of CKD. Yes, this is guilt by association and not causation.
Second, I have observed in my CKD cats virtually none of the secondary problems associated with CRF even in cats that are in stage IV. My CKD cats in stage IV live an average of 4 years. I have taken cats in stage IV, put them on raw, given no fluids, and have had the creatinine level drop so that the cat was as low as stage II. The only explanation I can give is the raw food has a purer protein which spares the kidneys further damage.
My evidence for this is twofold. First, 40 years ago, the rate of CKD seems to be exceedingly low and many cats were let outside to catch mice, etc. As the commercial pet food industry grew, so has the rate of CKD. Yes, this is guilt by association and not causation.
Second, I have observed in my CKD cats virtually none of the secondary problems associated with CRF even in cats that are in stage IV. My CKD cats in stage IV live an average of 4 years. I have taken cats in stage IV, put them on raw, given no fluids, and have had the creatinine level drop so that the cat was as low as stage II. The only explanation I can give is the raw food has a purer protein which spares the kidneys further damage.
Are there other things that may cause problems? Sure.
Some drugs are excreted via the kidneys and when given in large enough
doses can cause kidney failure. The
question remains for some of these drugs what are the long-term low dose
effects on the kidneys. I’m one of
‘those’ people that given any drug, if it can possible affect the kidneys, I
immediately ask for an alternative. Other
things, such as water impurities, do affect kidneys both directly and via stone
formation. Scented oils seem to be more
of a liver function problem.
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