This is where things get interesting. Even if healthy kidneys have no problem with a high dietary protein intake, once someoneâs 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 weâre 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?
Iâm 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.
âNot only are there zero case reports of kidney injury from high protein dietsâthe medical dogma of restricting protein in chronic kidney disease is almost purely mythical.â (Theodore Naiman, MD.)
Protein restriction being warranted in those with advanced kidney disease is less convincing than youâd 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. Itâs 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 âtoo high,â so far, is very vague.)
Even in studies where protein reduction is shown to be beneficial in those with kidney disease, the results typically arenât all that spectacular. At best, restriction merely slows the decline in function, rather than halting or reversing it. This isnât reason to dismiss protein reduction as a therapeutic strategy (because why wouldnât you want to slow the decline?), but patients should be made aware of the cost/benefit ratio. Iâd 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 Iâve heard âanecdotalâ 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 canât 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 Alzheimerâs disease, I would speculate that, if impaired kidney function were identified early enough, and a ketogenic diet implemented immediately, thereâd be a stronger potential for restoration of healthy function. The problem with chronic kidney disease, just like with Alzheimerâs, 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 âdiminished renal reserve,â and this is the state someoneâs 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 happenâârenal insufficiency.â 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 bloodworkâitâs an indicator of kidney function.) But by this point, youâre 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 âunexplained proteinuriaâ compared to the standard control diet. Oddly enough, this standard control diet was called a âprotein restrictedâ 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 thatâs the maximum they should be consuming. Oh, manâŠthe 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.