Cats: Causes of Chronic Renal Failure

What causes chronic renal failure(CRF) or chronic kidney disease(CKD)?  That is one of the most important questions that remains unanswered in veterinary medicine.  The problem, as I see it, is the cause in one cat may be different from the cause in another cat, which may explain the different progressions of the disease.

A small percentage of cats with CRF have this disease clearly because of genetic problems.  In Persians and related cats, the PKD (polycystic kidney disease) gene goes produce kidney failure due to the growth of multiple cysts in the kidneys which eventually are destroyed by the cysts.  Similarly, amyloidosis is a genetic disease in Abyssinians, Oriental shorthairs, and Devon rexes.

With the exception of genetic problems, the causes of CRF are not clearly known, but there is a list of potential causes.

1.  The after effect of acute renal failure.  Often any type of acute renal failure will scar the kidneys enough that full function is never restored.  With prompt treatment, some of these cats can reach a status where the damage does not lead to more kidney problems.  With others, the damage is too much and the scarring seems to hasten the development of CRF.  This latter group experiences a feedback cycle of lowering kidney function which leads to more stress on the kidneys which leads to lowering the function more.

2.  Immune problem which attack the kidneys.  The main two agents in this category are FeLV and mycoplasma polyarthritis (haemobartonella – feline infectious anaemia).

3.  Infections in the kidneys.  These range from chronic bacterial, to viral (FIP, FIV), to fungal.  Untreated, these infections interfere and then destroy the kidneys’ ability to function.

4.  Cancer.

5. Mechanical problems, such as large kidney stones, granulomas, or even the occasional cyst.

6. Idiopathic – no known cause.  This is, unfortunately, for most cats the ‘cause’ of CRF.   As late as 2 years ago, researchers still had no clear clue as to the causes (and there are probably multiple causes) for the development of most cases of CRF/CKD.  See http://www.ncbi.nlm.nih.gov/pubmed/21262581 

What is interestingly missing from this list is food.  As I will explain in a future post, the moment a cat is diagnosed as having CKD, many veterinarians ask clients to switch the cat to a low protein food.  A few vets and some pet owners have taken this a step further and argued that the protein level in a cat's food should be restricted to prevent CKD from developing.  While researchers have looked into this, there is no scientific support for limiting protein levels to prevent CKD and there are a number of reasons why this could lead to other health problems.

Cats: Demographics of Chronic Kidney Disease (CKD)

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.

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.

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.

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.

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.

Bertie's $500 Paper Ball

The last two weeks have been interesting for Bertie, one of my DLH cats.  He's always drank a lot and pee-ed a lot since I got him, but recently I noticed he had lost some weight and was hesitant to eat.  So, since I had to take Wendy to my vet, I took Bertie along to be checked out and have bloodwork done.  My vet examined him thoroughly and felt a large, strange mass in his intestines.  I figured it was paper, since he likes to eat (not nibble) paper.  I know he got into some a few days before the visit -- he ate most of a 9x12 inch envelop.  We both figured it was paper, but like other times, it would pass.

His bloodwork came back fine except that his BUN was 57 and the creatinine was 2.6 (2.4 is the upper end of normal).  He's only 6 years old, so CRF (chronic renal failure) seems very early.  But he's got either Persian or British short hair in his background and both can carry PKD (poly-cystic kidney disease).  So, I'm guessing it is PKD, but he's doing okay and thanks to other cats, I hope I can keep him healthy for a long time.

He came home, ate for a few days, and then threw up.  Then refused to eat.  I figured it was the paper ball, especially since he got into some credit card offers which my husband left by the shredder -- Bertie shredded them instead.  I tried laxatone.  Nothing.  I then tried lactulose.  Again nothing.  I even tried an enema.  Still nothing.

So, I called my vet -- she was on vacation.  I called my back-up vet -- he was on vacation.  Finally I took him to the VCA Hospital.

X-rays showed a large blockage in his lower intestines, about 6-7 inches long.  They wanted to try some meds and fluids on Thursday, and if it didn't work, do surgery on Friday.  So, he stayed over night.  While he didn't poop for them, more x-rays showed it was moving, which then moved any surgery to Monday.  On Friday night, he pooped!  And only cat lovers can understand -- I was doing a happy poop dance!!!  They wanted to keep him until they were sure it was all out.  More poop on Saturday night and he started to eat.  Still more poop on Monday morning, right before I picked him up.  Monday's x-rays showed a clean intestinal tract.

The x-rays also showed his hips are degenerating, which explains why he walks funny.  I need to work on that.

But, I'm so glad that he didn't need surgery and that he's now home, eating and pooping.  And 'his' room is paper free!!!  All this for only $500.  LOL!

Clancy Keeps Going

I just thought I should update how Clancy is doing.

Fine.

Yes, the cat who had a creatnine level of ~8.2 over  two years ago is fine.
Yes, the cat I treated for thyroid problems even though his bloodwork said it was okay is fine.
Yes, the cat who was drooling and not eating 4 months ago is fine.
And yes, the cat who couldn't walk for 2 hours a couple of weeks ago is fine.

Clancy, the Conundrum, continues on....

Seriously, the only noticeable 'problem' he has right now is that his fur is oily and matted near his tail and had to be shaved off.  I would have bathed him, but I worry about over stressing him.

I know we are on borrowed time and he has cashed in several lives.  He has, however, become more affectionate and snuggly, so I do wonder if he understands that his time is limited.

I'm also very thankful for him.  More than ever before.  He has taught me a lot about CRF, trusting my instincts, and diet.

I wish there was more I could do for him and truly heal him.  But I know that physically that won't happen.  I am beginning to believe that his shattered little personality is beginning to heal.  He is so enjoying the petting and snuggling now -- until a couple of years ago.

Poor Bertie...

Not a happy day here.

I discovered that Bertie had huge hard mats on his haunches and some on his tummy, so I am giving him a lioncut, one area at a time.  He hates sitting still in the best of times -- he's feline ADHD -- and with clippers going, he especially doesn't want to sit still.  Apparently, I had only been combing above the mats...

But that's not the worst of it.

For some time, I've noticed he drinks a lot and pees a lot.  His coat is oily.  And today, while he was complaining about being shaved, I noticed he had a small mouth ulcer.  I've wondered and the ulcer basically confirms it -- I'm fairly sure he has PKD.  PKD is polycystic kidney disease.  Cysts grow in the kidneys and eventually damage the kidneys so much that they stop functioning and the cat dies of kidney failure.  Basically it is the same as chronic kidney failure (CRF), but mechanical in nature and not old age.  It's associated with Persians, but not always.  Bertie probably has some British shorthair in him and that breed has Persian stock in it, so PKD isn't a surprise.

The bad part is Bertie isn't old.  He's only about 4 or 5 years old.  For him to show symptoms at this age probably means the cysts are already good sized.  And there's nothing I can do to stop them growing.

Poor baby....  He's a beautiful cat, although a bit strange.  He's like I said, feline ADHD and is always on the move.  He wants to be petted twice and then walks off.  He squeaks instead of meows.  He loves to eat paper.  And he has a mildly deformed backbone so he has a hump.

Unfortunately, he doesn't get along with James so we have to keep them separated most of the time.  And that's why I feel especially bad about this turn of events.  I've been working on getting him more integrated with the others so he can be loved on more...

Just not something I wanted to deal with....