Last fall when I first posted on this topic (Rimadyl Toxicity – I wish I weren’t an expert), I had just brought Billy home from an 8-day hospitalization for a mega-toxic overdose of Rimadyl. We were sure we were going to lose him and went to hell and back during those 8 days. Somehow he survived, but the discharge instructions were very discouraging and included the following quotes from the doctor (my comments and thoughts in italics):
- “The overdose has injured his liver and kidneys. He will need to be managed as a chronic renal failure patient for the rest of his life. His level of kidney disease is currently Stage 2 (out of 4).” This was accompanied by a verbal warning that he had to have sustained damage to at least 70% of his kidneys to show these findings.
- “Resume normal activity.” Really? He’s not just a pet, he’s a 4-year-old Border Collie that just started his competitive agility career. Not sure we have the same interpretation of “normal”…
- “Part of managing Billy’s chronic kidney disease will be feeding a low protein diet … [examples] … Hill’s k/d or Royal Canin LP… ” For this dog, low protein = not compatible with “normal” activity. And furthermore, both of those foods are grain-based (especially corn), which I concluded years ago was not the healthiest option for my dogs.
As I absorbed these paragraphs of doom and gloom, I was confronted with a happy hungry energetic young Border Collie who was thrilled to be home and more than willing to work (i.e. weave) for his breakfast. And who, after sleeping through the night zipped in a crate, showed no desperation to drink or pee when released. In other words, this dog didn’t display any classic “kidney dog” symptoms (lethargy, anorexia, polyuria, polydypsia).
Where was the disconnect between the diagnosis and the dog? Whereas some might blindly follow the discharge instructions and ignore the dog, and others might look only at the dog and ignore the history and evidence, anybody who knows ME knows what happened next – an intense flurry of activity involving hours and hours of web crawling, review of anecdotal evidence, personal conclusions and changes, and follow-up labs and appointments with specialists. I believe that I chose the informed and responsible route, and what follows is what I learned during the weeks and months following his crisis.
If you have a dog with kidney issues, whether acute or chronic, let me save you a lot of trouble. Here’s where you need to go:
DogAware.com. Read it all, click on all the links. In fact, I printed out most of the pages and have them organized in a binder.
K9KidneyDiet Yahoo group. Join it, follow the instructions to post your introduction, review the files and links, then decide what you want to get out of it.
RainGoddess. Phosphorus content of prescription and commercial dog foods. It’s a little dated, but it’s a starting point.
NutritionData. Nutritional content (including phosphorus) of human food. The FDA does not require phosphorus to be reported on labeling. This site overcomes that, though it’s a little tedious because you have to look up each individual item and make a note of what you find.
I’m fortunate to be very connected with the dog agility community, which includes many regular folks who have faced extreme acute kidney crises, as well as veterinarians who have experience that they’re willing to share. Here is some of what I learned through that network:
Case study #1: 10-wk old Border Collie puppy with suspected mushroom ingestion in 2001. Extreme liver and kidney toxicity, not expected to live. 10 days in ICU. Discharged with ALT level of 414, creatinine 2.74, dietary restrictions TBD. 4 days later, ALT 134, creatinine 1.57, no dietary restrictions. Dog went on to have an extremely successful agility career culminating with an 8th place finish at Nationals in 2007. Retired from competition at the age of 10 due to unrelated neurological issues and is happy and healthy today at age 11-1/2.
Case study #2: Young adult PyrShep with a similarly extreme Rimadyl ingestion. Parallel treatment, equally grim findings and prognosis. Dog was treated with only moderate dietary restrictions, kidney values improved over a period of months, and the dog continued to compete until retired due to unrelated neurological issues.
Phosphorus/Protein: Everything I read suggests that the issue for kidneys isn’t protein as much as it is Phosphorus (the elemental symbol is “P” – in the interest of space, that’s how I’ll refer to it). As one vet friend put it, “The P is the Key”. Since protein is a primary source of P, that explains the automatic “low-protein k/d diet” recommendation. But as it turns out, the equation is far more complex than that. Proteins vary widely in two important measures: Biological Value (BV), which is amount of absorbed protein that is actually used by the body (loosely, “efficiency”), and P content. Here is a summary of what I have gleaned so far:
- Animal protein has a higher BV than plant protein. And eggs and milk are even higher. But that’s not the whole story because of the role that P plays.
- Within a food category, medium-to-high fat versions have a lower P level than low-fat foods. This seems to be true for both meat and dairy.
- The exception to #2 is oily fishes (mackerel, sardines), which are relatively high in P. But the Omega-3 oils in salmon offset this to some extent because they are supportive to the kidneys.
- Whole eggs have one of the highest BV values. The yolks are much higher in P than the whites, but the balance is still pretty good for low-level kidney dogs.
- Green Tripe is one of the lowest P proteins, as long as it doesn’t have additives.
- Bones have off-the-charts high P levels. So bone meal is an ingredient I’ll be avoiding when I look at dog foods in the future.
- Processed white grains are lower in P than whole grains.
Water quality: I have lived in the country for 10 years and have never thought twice about giving my dogs untested well water out of the tap (which I won’t even drink). No more. My dogs now get purified water from the Glacier vending machines or the water store – it may not be perfect, but it has to be a hell of a lot better than what’s coming up from my well.
Before: Innova Adult (239 mgP/kcal)
Now: Innova Senior (186mgP/kcal).
Update 10/28/13: My trust in Innova began to wane when they were bought by P&G, and following the recent salmonella scares and resultant recalls, I decided to switch. I repeated my Phosphorus research and landed on Wellness Super5 Chicken – 197mgP/kcal.
Update 2/11/15: Wellness went through a rebranding about a year ago. I have confirmed with the company that the changes are in name and packaging only, the formulas didn’t change. The new name for Super5 Chicken is Complete Health Chicken and Oatmeal.
Before: Turkey hearts, green tripe K9 Delight (which has additives), string cheese
Now: green tripe K9 Krackle (no additives), Bravo Turkey Bites (all thigh meat), Natural Balance Duck & Potato Treat Roll, and limited string cheese for variety
Labs – What Do The Numbers Mean and Which Ones Matter?
Disclaimer: I am not an expert. This section is intended as a lay introduction to understanding lab values in acute liver and kidney toxicity. Reference values (aka Normal Limits or NL) vary by lab/machine and are here only for illustration.
Urine Specific Gravity (USG): represents the degree to which the kidneys are able to concentrate urine. The USG has high variability even in healthy animals because it is influenced throughout the day by exercise and hydration. To ensure the most meaningful results, you need to always test consistently, which we were advised is first catch in the morning. NL=1.015 – 1.045.
Creatinine (CRE): creatinine phosphate is a natural breakdown product of protein which is normally filtered out of the blood by the kidneys. If the filtering capacity of the kidney is compromised, creatinine levels in the blood rise. NL = 0.4 – 1.8.
Blood Urea Nitrogen (BUN): Urea is a by-product from metabolism of proteins by the liver and is removed from the blood by the kidneys. The BUN test is a measure of the amount of nitrogen in the blood in the form of urea, and is thus a measurement of renal function. NL = 7 – 27.
Alanine Transaminase (ALT ): Elevated ALT levels often suggest liver health problems, but this value is highly variable and cannot be used alone – other values need to be considered to narrow down the significance. NL = 5 – 107.
Total Bilirubin (TBIL): Bilirubin is a breakdown product from red blood cells which is normally excreted by the liver (bile) and kidneys (urine). Elevated bilirubin levels indicate liver cell damage, which causes the bilirubin to “spill” into the blood. NL = 0.0 – 0.4
What about Billy?
We have done regular follow-up lab work since Billy’s hospitalization. The initial results were encouraging, but the results at 3 months post-insult were nothing short of miraculous: ALL of his numbers have recovered to WNL (Within Normal Limits), suggesting that his liver has recovered and his kidneys are compensating.
Advice from the Specialist
Six weeks after discharge and the questionable “resume normal activity” recommendation, we consulted with a Board-Certified Internist who is also an avid agility competitor. We knew that she would understand our concept of normal activity and offer a much clearer perspective on what that meant in terms of Billy’s prognosis and dietary recommendations.
After reviewing the numbers and examining Billy, she was much more encouraging. She had no concerns about competing him as long as we watched out for his hydration and conditioned him to get his fitness level back. She went on to say that she thought he could even return to a regular adult diet at some point. She reminded me that even if he does have 50% kidney damage (which is likely), mammals do quite well at that level, as evidenced by the humans who donate one of their kidneys for transplant. Kidney function is aggregated, so it doesn’t matter if the 50% comes from a well-functioning single kidney or from the remaining nephrons in two damaged kidneys.
I have always accepted the common wisdom that kidneys don’t repair themselves (in contrast to the liver), so I asked about the discrepancy between the recovering lab values and the likely extent of damage. She explained that acute kidney injury is different from chronic kidney disease, and when the former happens in young healthy animals, they can often compensate. The toxicity causes nephrons to die and slough off, leaving gaps. There is evidence that the neighboring healthy nephrons grow and expand into the gaps and become super-nephrons. There is even some evidence suggesting that stem cells may come into play and develop new nephrons.
We walked away from that consult with renewed optimism, a prescription for several months of medication for kidney support (Ursodiol and Vitamin E) and liver support (Denamarin), and no unusual dietary restrictions.
Where are we now?
I’ve written up the one year status report in a separate post: Life Is Good – Rimadyl Toxicity Part 3
I want to reiterate that my discovery and decisions are specific to my dog, with his history and clinical findings. I don’t want anyone to walk away from this article thinking that what I did for Billy translates to another dog, especially a dog who truly does have chronic kidney disease. That said, the web resources are outstanding for those dogs, and I plan to follow up with a reference post on some of the data I gathered on Phosporus guidelines.