The Mythology of Protein Restriction in Dogs with Reduced Kidney Function

By 24 December 2021 BLOG / NEWS, Diet

SYNOPSIS

For more than four decades, limiting protein in the dog’s diet has become widely accepted as a method of nutritional management – support in animals with impaired renal function. Although no substantiated scientific evidence has been presented, this view has been widely applied.

Claims that dogs with urinary tract problems could benefit from restricting protein in their diets have been the subject of much speculation by many industrialized pet food companies for diets for kidney, adult or elderly animals.

However, modern research and studies have shown that the reduction of proteins in the diet of kidney patients leads to a reduction in glomerular filtration, ie the reduction of the volume and the rate of filtration of blood in the kidneys, which is not desirable. When we have a reduction in the functioning of the renal units, we are interested in the remaining ones working at a faster pace in order to be able to filter the same volume of blood. If we do not achieve this rate then instead of having a reduction of the relevant indicators e.g. urea, BUN, creatinine we will have an increase in them and the corresponding symptoms caused mainly by urea (nausea etc). On the other hand, the reduction of proteins below predetermined levels leads to the reduction of muscle mass with other serious consequences.

In fact, given that the possibility of dialysis in dogs practically does not exist the golden rule based on the above is NOT the reduction of protein in the diet of kidney disease dogs but the administration of a food with proteins of HIGH BIOLOGICAL VALUE.

For over four decades, dietary protein restriction has been widely accepted as a method of nutritional management for animals with impaired renal function. Although no scientific evidence has been presented, this method is especially used in dogs. Advertising claims that dogs with multiple urinary problems could benefit from protein restriction including those with renal insufficiency, progressive renal insufficiency, acute renal failure, normal aging, polydipsia / polyuria, glomerulus, prostatitis, urticaria. The most widely accepted of all of the above is the notion that dogs with impaired renal function or advanced age will benefit from reduced protein intake.

In recent years, 10 experimental studies have been published using dogs, which shed light on the controversy over protein restriction. A multicenter research conducted in human medicine is still worth mentioning.

Numerous misconceptions have been made about the need to reduce protein intake for kidney disease that have been perpetuated in the literature for many years, including:

  • Elevated urea levels lead to an increased “workload” for the kidneys.
  • High dietary protein intake damages the kidneys.
  • High dietary protein intake causes hyperkalemia
  • High consumption of dietary protein causes acidosis.
  • Reduced protein intake delays the progression of kidney disease.

Recent research in dogs has challenged the validity of the above hypotheses and raises questions about the factors that lead to the progression of renal failure. Beliefs about protein restriction will be discussed as a medical myth. It is being investigated why the exercise of reduced protein intake persists, despite the lack of scientific evidence.

The History of Protein Restriction

The results of 10 experimental studies have failed to provide evidence for the benefit of reduced dietary protein in influencing the course of renal failure.

Two general reasons are commonly given to support the reduction of dietary protein in animals with renal insufficiency. First, reduced protein can lead to reduced azotemia, which reduces the nausea of ​​kidney failure and allows animals to continue eating. While this condition / proposition is widely accepted, its clinical significance has not been taken into account. Second, reduced protein can affect the course of kidney failure.
The first evidence in the literature on the deterioration of the clinical condition of people with renal insufficiency from protein intake dates back to 1920. Ambard stated that uremic patients were weakening and their condition was declining when they ate meat.1 This clinical description led to efforts mitigation of so-called “uremic toxins” by reducing dietary protein. Newburgh and Curtis in 1928 reported the development of kidney damage in rats fed a variety of protein amounts and suggested that rats fed large amounts of protein containing 75% dehydrated liver developed more rapidly than those with or with casein diets.2 Rodents have been widely used to study possible contributors to the progression of renal failure.

Some species of rats have a high incidence of autoimmune renal glomerular and renal tubular injuries associated with aging alone.3-8 Progression and severity can be improved by increased dietary protein, 2,9,10 sodium and phosphorus.11 Surgery Detachment of renal mass accelerates renal glomerular injury as diabetes does in these rats.12-14 Although these observations are limited to specific species of rats, many researchers have suggested that the risk of kidney disease in other rats .

The first published data linking dietary protein to renal function in dogs appeared in the 1930s. could increase significantly with high protein intake. 15-17 Subsequent studies by Pitts showed that intravenous infusion of amino acids dramatically increased renal hemodynamics. 18
It should be remembered that in the 1930s and 1940s the basic parameters of renal function were studied for the first time. For example, at that time they first mentioned the use of blood urea concentration as an accurate method of measuring renal function and the idea of ​​extrarenal azotemia. protein was beneficial to human patients as Addis claimed.20 This notion lost its favor in human medicine when they realized that renal function was closely linked to the reabsorption of active sodium and that urea was handled passively. Special dietary restrictions were not considered necessary in humans with chronic renal failure as there was a lack of evidence that normal protein intake had a damaging effect on the kidneys. Addis reported that urea production, urea secretion, and Urea Nitrogen in the Blood (BUN) increased to normal levels when dietary protein was increased. The uselessness of urea emptying and creatinine limitations were not assessed at that time.

In 1941, Allison et al. delivered a report on 10 dogs with renal disease as a result of measuring increased BUN and decreased urine specific gravity, which were believed to be consistent and were of great clinical importance in the determination of renal damage. They were unaware of the extrarenal and renal factors that differentiate the renal coil filtration rate and possibly affect BUN, and stated that serum creatinine concentration was not a reliable indicator of renal damage.22 Morris later developed reduced protein, KD, for dogs with renal insufficiency. He and others were influenced by the wrong exercise of urea secretion promoted by Addis.20 While no experimental or clinical data were provided to support the value of this diet or other diets, the idea was widely accepted without question by the veterinary literature. .23 Diets were promoted as a means of reducing BUN and the amount of urine.

The notion that feeding high-protein dogs can be harmful was also adopted by the National Research Council of the National Academy of Sciences in 1972. 24 It was argued that high-protein foods in some commercial diets increased the “workload”. of the liver and kidneys and how they contribute to kidney disease in dogs. There is no evidence to support this view, and the recommendation has been overturned. In contrast, there is evidence that high-protein diets enhance renal function in normal dogs. This has led to confusion among veterinarians who have learned for decades that low-protein diets can be beneficial for kidney function so high-protein diets can have a detrimental effect on normal dogs.

While Addis’s hypothesis of the practice of hypertrophy for the secretion of urea is incorrect, a more modern conception of renal coil hyperfiltration was made in the 1980s by Brenner.25 This hypothesis states that after any Significant loss of renal function is followed by the survival of the renal kidney undergoing functional and structural changes including increases in the filtration rate of the renal coil in the single kidney and an increase in the pressure in the vessels of the renal coil. These changes are called renal coil hyperfiltration and renal coil hypertension. Micro-puncture studies in rats have shown that the result of these adaptations is a progressive “decline” in kidney function. In addition, renal coil enlargement, hypertrophy, and deposition in the medial petal of the vascular renal glomerulus lead to gradual hardening of the renal coil and eventual renal loss. The surviving kidney undergoes further increases in vascular pressure, filtration rate, and size, thus following a vicious cycle of pathogenic renal injury. Reduction in dietary protein and / or calories has been shown to limit this process in certain species of rats. 26 If this mechanism were functional in the dog as well, it would make sense to limit the dietary protein.

Experimental Research in Dogs

Due to the confusion between the veterinary literature and the lack of supporting data for the exercise of low-protein diets, numerous experimental studies have been conducted in recent years. These studies have followed the standard experimental model of reduced renal function and have addressed many questions as the dogs were fed a variety of proteins in different forms and amounts at different levels of renal function. These studies represent a tremendous amount of work that required the sacrifice of hundreds of dogs in the overall effort to elucidate the potential role of dietary protein in the onset, maintenance, and progression of renal impairment.

Measuring the progression of renal insufficiency requires specific clarity. In these studies, the use of clinical symbols, decreased urinary concentration, increased BUN, and elevated serum creatinine have limited the ability to detect the effectiveness of protein restriction. Similarly, the presence of hyperphosphoraemia, acidosis and proteinuria can be misleading as depending on the experimental model and diet may not represent an accurate measure of progress. The only most reliable method is to measure the filtration rate of the renal coil using inulin. This is considered the gold standard for the progression of the disease, and all other measurements are considered secondary.
The deterioration of the condition can still be calculated on the basis of morphological measurements. The agreement of morphological and functional measurements is extremely complex and seems to differ depending on the form of kidney disease and the experimental model. A synthesis or comparison of functional and morphological measurements may be useful in some cases. However, the results may or may not agree. Although histological or electron microscopic differences are indications of pathophysiology, their relationship to worsening of the condition can be difficult to describe. It is generally difficult to quantify histological lesions as they are not evenly distributed, there may be confusion due to hypertrophy and hyperplasia and in some forms of extrarenal disease it may obscure the histological architecture.

The results of 10 experimental studies have failed to provide evidence for the benefit of reduced dietary protein in influencing the course of renal failure. 27 -36 These results of this research should allow veterinarians to reposition themselves and get rid of the six protein consumption issues starting at the beginning of this article. It is clear that the perception of increased “workload”, the cause of kidney damage from protein consumption, and the delay in the course of kidney disease by reducing protein consumption are wrong. The other three hypotheses concerning hyperkalemia, acidosis and urinary toxins require comment. In the above studies, hyperkalemia was not found to be associated with increased dietary protein. The ability to excrete potassium and maintain a normal serum potassium concentration until the final stages of chronic renal failure has been studied in detail in dogs. 37.38 The secretory mechanism in the peripheral tubules represents the critical area for increased potassium excretion in renal failure. Potassium balance is maintained in chronic uremic state in dogs even with the appearance of changing rates of potassium excretion of sodium, phosphorus and ammonia. Acidification is also uncommon due to altered tubes of the mechanisms in dogs with reduced renal function.39-41 The dog is unique in that the fractional carbon reabsorption increases after reduced renal function. This enhanced carbon dioxide resorption capacity prevents acidification and is present despite the adjustment of piping to regulate other electrolytes such as sodium, potassium and phosphorus. Finally, the notion that dietary protein is responsible for the so-called “uremic toxin” has not been proven in any species despite extensive research.

Nutritional Protein and Progress in Kidney Failure in Humans.

The controversy over the restriction of dietary protein in humans has been perpetuated by “anecdotal” reports and uncontrolled clinical trials since the early 1960s. patients with chronic renal failure. Patients were fed a standard protein diet and a low-protein diet for 18 to 45 months. Renal coil filtration rate measurements and standard chemistry measurements were used. The mean decrease in renal coil filtration rate at 3 years did not differ significantly between the two groups.

Among patients with more severe renal impairment, a diet very low in protein compared to one that was simply low in protein did not significantly delay the progression of renal failure.

Advantages and Disadvantages of Restricting Dietary Protein in Dogs

Based on previous data, the only benefits that seem to exist are the reduction of BUN and the possibility of reducing nausea. The value of these effects in dogs has not been reported. In contrast to the disadvantages that occur due to reduced protein consumption. These include decreased renal function according to measurements of renal coil filtration rate and renal serum flow, possibility of negative nitrogen balance and promotion of catabolic status in the presence of proteinuria. In practice, the use of vague dietary guidelines seems to lead to reassurance about the long-term monitoring of the animal or the need for individualized treatment. Because some kind of management seems available, research for a more specific etiological diagnosis is usually not organized. Finally, the use of arbitrary diets leads to the illusion of treatment and increases the cost to the owners.

Why Is Dietary Change Still Used Since There Is No Proven Benefit?

The continued use of protein restriction in the absence of scientific evidence is worth considering. I would suggest that dogma and mythology for a possible benefit are ingrained in the thinking process of veterinarians and owners who can not easily “detach” despite scientific evidence. I would refer to this as the myth of dietary protein and characterize it as a negative myth.
What is a myth? Myths are a way of understanding a difficult and “incomprehensible” world. Myths give society a degree of relief from neurotic guilt and excessive anxiety. Philosophers, psychiatrists and theologians tell us that people have always needed myths. Myths are an interpretation of ourselves and our inner self in relation to a larger world. All societies and people are built on a series of myths that are not automatically obvious. If society does not give us myths, we invent them so that we can understand our personal experiences. 44 There are both positive and negative myths. Positive myths support and affirm the value of ourselves. They provide guidance and support. These positive myths are used as an important model in human consciousness, allowing us to cope with a difficult world, as the psychiatrist Rollo May, 44 Carl Jung, 45 and the philosophers Mortimer Adler 46 and Joseph Campbell remind us.47 There are many in Our modern popular culture, however, is clearly wrong, taking myths for granted. I believe that a really negative myth is one that misleads or has destructive effects. These could be defined as pseudo-myths or exaggerations and seem to be almost magical. These are associated with beliefs without benefit or responsibility.

There are many types of myths: personal, social, and professional. We use personal myths to develop our identity, our image, and our moral values. We use myths to identify within society. Social myths include the New World, the Western frontier, the lone cowboy, national heroes, and the so-called “American Dream.” Professional veterinary myths include images related to the stories of James Herriott, the kind doctor as projected by our industry, and the healing power of modern science.

Are there conflicts between science and myth? As it turns out, many of our scientific theories are a kind of mythology. Many scientific discoveries start as myths or have questions about myths. In many ways, science is the critique of myths (W.B Yeats) .44

Why Do We Associate Protein Restriction with Myth?
I think we have used the myth of dietary protein restriction because it is psychologically reassuring when dealing with a deadly disease. Chronic renal failure presents with many difficult problems in the absence of adequate medical treatment despite all efforts to date. In the absence of dialysis, which is impractical for the vast majority of animals, and kidney transplantation, which is not successful in the dog due to immune barriers, medical treatment has little to offer.

Most cases occur slowly in the natural course, are usually irreversible, and are usually followed by a uniform pattern of failure and eventual death over the months. Because of these factors, a sense of resentment, shame and even guilt prevails in the vet and the owner. Veterinarians are desperately looking for something they can offer to maintain their professional position, prestige, and power in this dilemma with respect to the owner. Restricting dietary protein is simple, relatively inexpensive, usually harmless, and has the ring of validity. We can offer vague but firm assurance of its value, as it has been in the spotlight for such a long time. The owners feel this dilemma and appreciate our efforts. These are the ideal conditions to trap one, along with the customer, in a false myth.

Why Have We Chosen to Keep the Reduced Protein Myth?
The myth has persisted even in the last decade despite the negative scientific evidence because the doctrine has insisted on its value for the last 40 years. If we, as professionals, are unsure about the facts of a controversy, we should probably put ourselves in the hands of someone else who seems to have power. The commercial power of these special products with deceptive messages has the power to invoke this power. Marketing dynamically targets veterinarians and homeowners. There is a profit motive for veterinarians selling these diets. The public has a nutritional mania and deals with nutrition in our society. Dietary change has assumed the validity of medical treatment using terms such as surgery, maintenance and correction. The profession and the public do not realize that advertising claims are made without proof in the case of referees. Owners can easily join such a diet because they feel involved in something constructive. Professional responsibility has been lost in this case. The case may remind us that we are part of an industry that lacks prudent judgment with little inspection or few standards. When scientific evidence fails to justify an exercise, a false myth may be perpetuated.
In conclusion, perpetuating this false myth about dietary protein is a disturbing reminder of the lack of evolution, critical thinking, and reliance on oversimplified and attractive doctrines that persist in our profession. This is just one example of the many myths, misinformation, and half-truths that are repeated from decade to decade. Until a more critical approach emerges with standards and oversight are brought to bear in our profession, we will probably continue to be trapped in false myths despite the presence of fundamental science.

Kenneth C. Bovee, DVM, MMedSe

Department of Clinical Studies, School of Veterinary Medicine
Pennsylavania University, Philadelphia, Pennsylvania