Does Protein Harm the Kidneys?

Hey kids! My previous blog post laid waste to the myth that a high protein intake is harmful for bone health. This time, it’s my great pleasure to decimate another “high protein is bad for you” thing. Today, it’s kidney function. Many of you have been eagerly awaiting this post. Here’s hoping I don’t disappoint.

Even if you’ve accepted that everything we thought we knew about saturated fat and cholesterol in our diets was almost completely wrong, and you’ve been following a low-carb or ketogenic diet confidently for fat loss, migraines, GERD/acid reflux,  reversing type 2 diabetes, reducing insulin needs and evening out blood sugar for type 1 diabetes, or for some other health issue, maybe there’s still some lingering fear in the back of your mind that the protein you’re eating—especially animal protein—is bad for your kidneys.

We’ve heard this over and over from just about everyone with an agenda to discredit the efficacy of low carb diets. Now, mind you, low carb diets are not, by definition, high in protein, but in walking away from sugars, grains, beans, and starchy vegetables, many of us find that, compared to our former high-carb life, our protein consumption does increase, whether in absolute grams, as a percentage of total calories, or both. Not to mention the growing carnivore movement, where people are eating only animal foods. For these folks, protein consumption almost certainly increases compared to a standard Western diet, and likely even compared to if/when they were following a ketogenic diet.

So with all this in mind, it’s important that we set the record straight about the influence of dietary protein on kidney function.

Isn’t all that protein bad for the kidneys?

No.

So where did the idea come from that it is?

Well, protein is the source of nitrogen in our diets, and the kidneys (and liver) are taxed with getting rid of nitrogenous wastes. (Physiology textbooks use this phrase, but please understand that these “wastes” are products of normal metabolic processes and are impossible to avoid producing unless you’re dead.) This is why they measure creatinine, urea, and BUN (blood urea nitrogen) in your blood or urine—they’re nitrogen-containing compounds, and are indicators of kidney function.

It’s assumed that consuming more protein “strains” the kidneys, because they have to deal with more nitrogen. But there’s no reason to suspect that changes that occur with increased protein intake (e.g., increased urea in the urine) indicate that harm is being done to the kidneys. This would be like suggesting that gluconeogenesis is a “strain” on the liver, rather than a very normal, totally expected physiological adaptation to fasting or to a very low carbohydrate intake. Just because something changes doesn’t mean it’s automatically bad:

“…evidence suggests that protein-induced changes in renal function are likely a normal adaptative mechanism well within the functional limits of a healthy kidney.” (Source)

The second reason people assume higher protein is bad for the kidneys is that low protein diets are the primary go-to intervention for kidney disease. Diseased, damaged kidneys seem to not handle protein as well as healthy kidneys. However, this doesn’t mean that it was protein that caused the damage or disease.

Think of it this way: just because damaged and poorly functioning kidneys may not be able to handle a “normal” protein load doesn’t mean it was protein that caused the damage. If someone breaks a leg in a skiing accident and they can’t walk for a few weeks, they can’t walk, but it wasn’t walking that caused the break. The leg was damaged by something else that then affected the ability to walk. Such is the story with protein and the kidneys:

“Although excessive protein intake remains a health concern in individuals with pre-existing renal disease, the literature lacks significant research demonstrating a link between protein intake and the initiation or progression of renal disease in healthy individuals.” (Source)

According to Stuart Phillips, PhD, one of my most trusted protein researchers:

“Increased dietary protein is thought to have impact on renal function. What needs to be recognized is that the thesis that dietary protein is causative for renal disease is not supported by evidence.” (Source)

Dr. Phillips pulled no punches when he wrote that the idea that protein is harmful for the kidneys is “usually derived from circular logic of people’s experiences in renal wards where there’s little doubt that lower protein diets can help extend a person’s health and life due to the lower urea and therefore less ‘work’ filtering such substances by the kidney. The incorrect circular logic that is then applied is that ‘therefore’ [sic] high protein diets cause renal disease. That’s poor logic, flawed reasoning, and just plain wrong.” (Source; emphasis mine)

We’ve got a lot to cover, but we’ll come back later to the concept of protein restricted diets for people with compromised kidney function, because even there, results from low protein diets aren’t exactly worth celebrating.

What do kidneys do, anyway?

Beyond low protein diets being recommended for people with already compromised kidney function, I think another reason for fearmongering with regard to protein intake and kidney health is that the kidneys play a big role in maintaining blood pH (acidity). Along with those that occur in the lungs, biochemical reactions and ion exchanges in the kidneys help ensure that your blood stays within a very narrow pH, neither too acidic nor too alkaline. And everyone seems to think that if you eat a lot of protein, your kidneys (and presumably lungs) have to work a lot harder to buffer the resulting acid. (I explained the protein/acid load thing in the post about protein & bones.) The kidneys aid in maintaining blood pH by getting rid of hydrogen ions (H+), and synthesizing and reabsorbing bicarbonate ions (HCO3-).    

Aside from helping to regulate blood pH, the other main function of the kidneys is to filter the blood—to get rid of toxins and normal metabolic waste products (e.g., creatinine, urea), and retain or reabsorb things the body needs, like sodium, potassium, chloride, uric acid, and other fun stuff. This is pretty important when you think about it. I mean, unless you’re completely neurotic, you really have no way of ensuring your daily intake of sodium, potassium, chloride, and other electrolytes will exactly meet your needs, so it’s a good thing your kidneys look out for you and can hang on to what you need, when you need it, and get rid of any excess.

And it’s not just a matter of having the right mix of these things in the blood or delivered to the cells that need them. The reason these matter is because these minerals may be required cofactors in a host of enzymatic reactions that quite literally keep you alive and functioning properly. They also influence fluid balance—that is, keeping the right amount of water and other fluids in the right bodily compartments. When this is a bit off, you might have edema (abnormal fluid retention) in different parts of your body, depending on where the problem is. It’s also why diuretic medications, which are prescribed for hypertension, often result in edema, hyper- or hypokalemia (high or low blood potassium, respectively), and other gnarly and downright dangerous side effects. Diuretics work by changing the way the kidneys hold on to or don’t hold on to various electrolytes, with the goal of inducing them to get rid of more water, which, in theory, lowers blood pressure.    

Your kidneys are small, but man, they are hardworking little buggers! They typically constitute less than 0.5% of total body mass, but they receive 20-25% of resting cardiac output (blood flow). In adults, renal blood flow—the blood flow through both kidneys—is about 1200 mL per minute. (Translated into other units to make sure we all understand just how much this is, every 60 seconds, your kidneys receive about 40.5 ounces of blood or about 5 cups.) Assuming a healthy filtration rate, the kidneys filter 180 liters of water per day. (Source)    

Together with your colon, your lungs, and your skin, your kidneys constitute your body’s sanitation crew—the parts of you that collect and get rid of waste. So you really don’t want to mess with them. When your kidneys have become damaged to the point that they can no longer perform this critical function, you get put on dialysis, where a machine performs this filtering action for you several times per week. This is not a fate anyone ever hopes to arrive at. So what tends to make it happen, then?

What causes chronic kidney disease?

It’s probably easier to say what doesn’t cause it: a high protein intake.

In a paper that covered over 13 risk factors and influences on development of chronic kidney disease, there was ZERO MENTION of a high protein intake. They mentioned proteinuria—the presence of protein in the urine—but that goes back to what I said earlier about the broken leg: the presence of protein in the urine that results from kidneys that are damaged to the point they are unable to properly filter the blood doesn’t mean that eating protein caused the kidneys to become damaged. Don’t confuse these two things—dietary protein and protein in the urine—because they are entirely different.

Even the Mayo Clinic, the National Kidney Foundation, and the US National Institutes of Health—as conventional as you can possibly get—make ZERO MENTION of high dietary protein intake as a risk factor for kidney disease. Seriously, these institutions are as mainstream as mainstream gets. Considering how committed the powers that be in governmental and medical health and nutrition authoritative organizations are to demonizing animal protein consumption as fervently as they can, you can bet your bum that if there were any connection—even the slightest hint of a connection—between a high animal protein intake and kidney disease, these folks would be shouting it from the rooftops. You’d never hear the end of it. That they say nothing about it speaks volumes.      

So if a high protein intake doesn’t cause kidney disease, what does?

Diabetes (especially type 2) is the leading cause of chronic kidney disease and end-stage renal disease (ESRD) in the world, and hypertension is a close second. According to the US Centers for Disease Control and Prevention (CDC) and the American Kidney Fund, diabetes accounts for 44% of kidney failure, and hypertension accounts for about 28%. And if you’ve read my blog for any amount of time—especially my insulin series—then you know that T2D and hypertension are both hyperinsulinemic conditions, so we could say that, considered collectively, chronically high insulin and/or blood glucose is the number one cause, by far, of chronic kidney disease, responsible for 72% of it. The chronic kidney disease fact sheet from the CDC says, “Keep your kidneys healthy by controlling your blood sugar and blood pressure.” Notice there’s nothing—nothing—about limiting protein. Again, if there was even a whiff of a possibility that a high protein intake caused kidney disease, the CDC would be banging that drum loudly.

I reread the urinary system chapter from my trusty ol’ anatomy & physiology textbook to get a refresher on the kidneys. Let me tell you, dear readers, the kidneys are complex. They are quite an engineering marvel! There are several reasons why chronically high blood glucose and insulin are so damaging to them, but one of them is because the glomerulus—the structure inside the nephron (main kidney cell) responsible for much of the filtration—is a capillary. It’s a teeny, tiny, microscopic blood vessel whose walls are one cell thick. This is not a big, strong, muscular vessel like your aorta or an artery. The glomerulus is very tiny and very fragile.

As I explained way back in part 2 of the insulin series, highly glycated blood is sticky, thick, sludgy blood. And glycated blood vessels under the influence of insulin are hard, stiff, and unaccommodating. In this scenario, instead of water flowing easily through a rubbery, pliant, flexible, and accommodating garden hose, we have something more like thick, sticky molasses trying to force itself through a narrow glass tube. Higher pressure, more breakage. It’s just a bad situation all around. Protein does not damage the microscopic blood vessels in the kidneys. Constant, unrelenting exposure to high levels of glucose and insulin does. (Same goes for the microscopic blood vessels in the eyes. Diabetic nephropathy, retinopathy…different tissues, same disease, same cause.)     

To revisit the protein and kidney function “thing” again:

A paper from the American Journal of Clinical Nutrition—another uber-conventional publication—stated: “Diets higher in plant and animal protein, independent of other dietary factors, are associated with cardiometabolic benefits, particularly improved central adiposity, with no apparent impairment of kidney function.”

This little tidbit was based on food recall questionnaires, so we can’t rest our case there, but it’s still interesting to note. Association doesn’t prove causation, but lack of association certainly suggests lack of causation. Meaning, if there were an association between higher protein intakes and compromised kidney function, we wouldn’t be able to conclude that it was the protein, by itself, that was responsible for the kidney damage. But since there wasn’t an association at all, we can safely assume that protein isn’t harmful for kidneys.  

And while those researchers were digging around looking to see if higher protein diets had an adverse impact on kidney function, they happened to notice that higher protein diets (whether from animals or plants) were associated with “cardiometabolic benefits,” such as decreased central adiposity (being smaller around the middle) and higher HDL. Oh, and by the way, BMI and waist circumference were inversely associated with protein intake: higher protein intake, lower BMI and waist circumference. Maybe not causal, but just sayin’.  (It’s almost like some of the low carb MDs who encourage higher protein rather than super high fat are on to something…)

What about people who already have kidney disease?

This is where things get interesting. Even if healthy kidneys have no problem with a high dietary protein intake, once someone’s kidney function is already compromised, there does seem to be some merit in reducing protein consumption. However, even here, the evidence is less impressive than we’re usually led to believe. I mean, this is sort of the third rail of low carb diets, right? Sure, healthy kidneys can handle however much protein you cram down your piehole (Steakhole? Do we need a new slang term for this?), but people who are already dealing with kidney disease need to go low protein. Need to. Right? Right?  

I’m not ready to say that protein restriction is unnecessary in cases of impaired kidney function, but like I said, with all the buzz about this, you would think the clinical evidence would be more compelling.

“Not only are there zero case reports of kidney injury from high protein diets—the medical dogma of restricting protein in chronic kidney disease is almost purely mythical.” (Theodore Naiman, MD.)

Protein restriction being warranted in those with advanced kidney disease is less convincing than you’d expect. In a study of patients with chronic renal failure, a low protein diet (0.4 to 0.6 g/kg/d) delayed the progression rate of renal failure only in patients with primary glomerular disease, and only in males. Female patients did not benefit at all. Considering primary glomerular disease accounts for only about 7% of all kidney disease (with 44% attributed to diabetes and 28% to hypertension, which, as I mentioned, are basically the same disease, so really, 72%), this is an intervention that would benefit very few people. Protein restriction should not be dismissed for the few individuals whom it would help, but it should not be recommended across the board for all kidney patients, and certainly not for healthy people with no valid reason to limit protein intake.

A different study of patients with chronic renal failure showed that a diet of 0.6g/kg/d led to no significant difference in rate of fall of creatinine clearance compared to a diet that met the RDA of 0.8g/kg/d. It’s possible that an even greater reduction in protein intake might have resulted in a more favorable outcome, but 0.5g/kg/d or lower would likely not be sustainable and could conceivably lead to problems from protein malnutrition. (Yes, there most definitely is such a think as a diet too low in protein, but “too high,” so far, is very vague.)

Even in studies where protein reduction is shown to be beneficial in those with kidney disease, the results typically aren’t all that spectacular. At best, restriction merely slows the decline in function, rather than halting or reversing it. This isn’t reason to dismiss protein reduction as a therapeutic strategy (because why wouldn’t you want to slow the decline?), but patients should be made aware of the cost/benefit ratio. I’d like to see studies on carbohydrate restriction in kidney disease. It is very, very difficult to reverse kidney damage and restore healthy function. Maybe the most people can hope for is to slow the decline or maybe stop it from getting worse. But I’ve heard “anecdotal” reports that kidney function improves, if only slightly, after a while on a ketogenic diet.

Considering the role of diabetes and hypertension in causing kidney disease, I can’t imagine carbohydrate restriction would be any worse than protein restriction, and I can imagine multiple ways that it would be better. As I have argued with regard to Alzheimer’s disease, I would speculate that, if impaired kidney function were identified early enough, and a ketogenic diet implemented immediately, there’d be a stronger potential for restoration of healthy function. The problem with chronic kidney disease, just like with Alzheimer’s, is that by the time you start showing signs & symptoms, the disease is already quite advanced: the first stage of chronic renal failure is called “diminished renal reserve,” and this is the state someone’s in until 75% of functioning nephrons are lost. During this stage, the remaining nephrons enlarge and compensate for the loss of the others, so the person has no signs or symptoms. Only when things get even worse than this does stage 2 happen—“renal insufficiency.” This is when the glomerular filtration rate decreases (the kidneys are much slower at filtering blood) and abnormalities are measurable in the blood and urine. (This is why you see GFR measured on routine bloodwork—it’s an indicator of kidney function.)  But by this point, you’re already down to less than 25% of healthy kidney function!

One of the low carb MDs I know sent me a link to this paper, in which a low(er) carb diet that was also low in bioavailable iron and high in polyphenols delayed progression of kidney disease and reduced mortality (at least during the follow up period of 3.9 ± 1.8 years) in type 2 diabetics with kidney disease or “unexplained proteinuria” compared to the standard control diet. Oddly enough, this standard control diet was called a “protein restricted” diet, yet it called for 0.8g/kg. Funny how these kidney researchers even considered 0.8g/kg to be a restricted protein intake, huh? (And so many keto newbies think that’s the maximum they should be consuming. Oh, man…the LOLZ.) (The control diet was 65% carb, 25% fat, 10% protein; the low carb diet called for 35% carbs, 30% fat, 25-30% protein, 5-10% alcohol [for the red wine polyphenols or some such]. So the low carb diet was nowhere near ketogenic, but compared to 65% carbs, 35% is a substantial reduction.) To be clear, most of the subjects on the lower carb diet still declined; they just declined more slowly, and there were fewer deaths during the follow-up period. How much better might the results have been if this was actually a truly low carb diet? This is quite promising, though, because it shows that even when the diet is still 35% carbs, a low-ish carb diet has a more favorable impact on kidney disease progression than a low protein diet.

What do physicians and researchers say?

I know I’m like a broken record with quoting Ted Naiman, but sometimes what he says is just too darn good not to. The following comes from an episode of the Human Performance Outliers podcast:

“The kidney thing is 100% mythical. There’s absolutely no data anywhere that says that a high-protein diet harms your kidneys. We have zero case studies in the bodybuilding community, which means it’s absolutely impossible for high protein to damage your kidneys. There are all kinds of studies and meta-analyses that completely refute the thought that high protein is bad for your kidneys. Even in kidney failure, protein restriction being beneficial is almost completely mythical. The vast majority of chronic kidney disease is diabetes and high blood pressure, and in none of these people has protein restriction ever been found to be beneficial.”

“There’s a tiny subset of primary glomerular disease, which is less than 7% of all chronic kidney disease, and in women, protein restriction was not beneficial at all. In men, there was possibly a low single digits improvement with protein restriction, so like maybe 7% of all chronic kidney disease, there’s maybe a few percent of just men who might benefit from protein restriction, but there were other studies that were equivocal and said that they basically didn’t see a difference there.”

“Honestly, protein restriction in chronic kidney disease is nearly mythical, and protein causing kidney damage is just a giant load of crap.”

How could I not quote that?

If you wish I would branch out and give you some juicy bits from other sources, your wish is my command:

A systematic review of renal health in healthy subjects consuming protein at levels above the US RDA determined that “increased protein intake had little or no effect on blood markers of kidney function,” and that, “at least in the short term, higher protein intake within the range of recommended intakes for protein is consistent with normal kidney function in healthy individuals.” Within the range of recommended intakes for protein means up to 35% of calories, since the Food and Nutrition Board of the Institute of Medicine of the U.S. National Academies of Sciences determined that the acceptable range of protein intake as a percentage of total calories for adults is 10-35%. I dislike using percentages with regard to macronutrients, but the point here is, depending on someone’s total energy intake, 35% of calories from protein could be a lot more than 0.8g/kg.

According to a report by the World Health Organization, Protein and Amino Acid Requirements in Human Nutrition: “the suggestion that the decline of glomerular filtration rate that occurs with advancing age in healthy subjects can be attenuated by reducing the protein in the diet appears to have no foundation.”

English translation: the WHO—yet another super-conventional body—says that there’s no evidence to support that eating a lower protein diet improves kidney function in older people. GFR tends to decrease with age, but that’s not necessarily because the kidneys are damaged, but more likely because older people typically eat less protein!

What is a “high” protein intake?

I’ve been using the phrase “high protein” throughout this post. Because I think it’s safe to say that even vegans understand the human body does require some protein, even if they think we can get all we need solely from plant sources. So even people who think a “high” protein intake might be bad for the kidneys would have to acknowledge that protein, per se, isn’t a one-way ticket to kidney disease. After all, the long-lived, healthy populations in their precious “blue zones” weren’t eating protein-free diets.

So what, exactly, is a “high” protein intake?

As I discussed in the post on protein and bones, the 0.8g/kg is more of a bare minimum of protein to aim for, not a goal or a target. So if 0.8g/kg is on the low end, then the high end is up for debate. 

“Current evidence indicates intakes in the range of at least 1.2 to 1.6 g/(kg·day) of high-quality protein is a more ideal target for achieving optimal health outcomes in adults.” (Source)

“Anyone who thinks the RDA for protein should be 0.8 g/kg/d has apparently missed the last 3 decades of scientific progress in nutrition.” (Source)

That shiny gem comes from Jose Antonio, PhD, a researcher and associate professor of exercise and sport science. Dr. Antonio has done extensive research into protein and the athletic community, with relatively long-term studies employing higher protein intakes (2.0g/kg/d and higher). If higher protein intakes were harmful for the kidneys, it’s likely the bodybuilding community, chugging whey and casein shakes, would be rife with kidney problems, and high-protein eating bodybuilders would be a dialysis clinic’s best customers. To the contrary, you don’t see lean, strong, well-muscled people lining up at these centers.

Even in people at “higher risk” for kidney disease, higher protein diets are not contraindicated:

“Although the efficacy of high protein diets for weight loss has been evaluated, there have been no reports of protein-induced diminutions in renal function despite subject populations that are generally at risk for kidney disease (e.g., dyslipidemia, obesity, hypertension).” (Source)

The same was seen in a study of type 2 diabetics on a low carb, higher protein diet (28% protein, 58% fat, 14% carbs) – “consumption of an LC high protein diet does not adversely affect clinical markers of renal function in obese adults with T2DM and no preexisting kidney disease.” (Source)

In obese, non-diabetic subjects, a low carb, high protein diet (actually named straight-up as the Atkins diet!), “over 2 years was not associated with noticeably harmful effects on GFR, albuminuria, or fluid and electrolyte balance compared with a low-fat diet.” (Source)

Basically, you just don’t see kidney problems in people eating higher protein diets when carbs are low. Even if subjects have type 2 diabetes.

Donald Layman, PhD, is tied with Dr. Phillips for nabbing the number one spot as my favorite protein researcher. (Dr. Phillips might have a slight edge, as he seems more friendly to low carb diets than Dr. Layman, but Dr. Layman is still wonderful, IMHO.) Watch this video from Dr. Layman when you get a chance. Even if, for some reason, you’re still worried about this kidney thing and you’re worried that you might be eating “too much” protein, rest assured, none of us is approaching anything near a “high” protein intake. (Just ignore what he says about low fat toward the end. The rest is golden.)

A Final Note

I don’t want to give the impression that chronic hyperglycemia and hyperinsulinemia are the only things that damage the kidneys. Many other things can impair kidney function, including congenital defects, viruses, chronic urinary tract infections (UTIs), kidney stones, various cancers, and problems of unknown origin specific to nephrons or the glomerulus. There’s also polycystic kidney disease, but that makes me wonder…if polycystic ovarian syndrome is driven by hyperinsulinemia, is there a role for that in polycystic kidney disease? Insulin is great at promoting aberrant growth of random tissues.

My point is, I don’t want to “blame the victim” here. Not every case of kidney disease originates from diet and lifestyle. As much as we like to believe we can control every single aspect of our health and longevity via a low carb, ketogenic, or carnivorous diet, sometimes stuff just happens. But that being said, let’s prevent what we can prevent, like kidney damage from a ceaseless onslaught of glucose and insulin.   

Disclaimer: Amy Berger, MS, CNS, NTP, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician. Links in this post and all others may direct you to amazon.com, where I will receive a small amount of the purchase price of any items you buy through my affiliate links.