By Dr. Francesco Casillo
It is now a notion "known and established" by the multitude (including certain experts) - and it does not matter how unfounded it is, as will be explained below - that protein inputs exceeding the RDA are first a metabolic and then an important nutritional stimulus stress on the kidney, thus causing a negative impact on him that would have inevitable negative consequences for his health.
Premise
A "high -protein diet" means a pro-die protein intake equal to or greater than 1.5g per kg of body weight (13). Chronic kidney disease is characterized by renal damage (documented by laboratory, pathological and instrumental findings) or a decline in renal function as a result of a decrease in glomerular filtration rate for at least 3 months (14). Thus, hyperfiltration and increased glomerular pressure as a consequence of excessive protein intake and as responsible for renal damage.
The most cited and accredited reference to possible kidney damage caused by protein excesses is the Brenner hypothesis.
Brenner 's hypothesis states that conditions associated with increased filtration and pressure would cause kidney damage, compromising the function itself. Although the effects of hyperfiltration - induced by the hyperproteic nutritional structure - on renal function in patients with pre-existing renal diseases is documented (21), it is also true that the scientific evidence cited by the authors on the harmful effects of hyperprotein approaches with respect to kidney health, derives from studies on animal models and from patients with pre-existing renal diseases.
Therefore, any speculation concerning the extension and application of these conditions detected in certain and precise contextualities, even to healthy subjects and / or with normal kidney functions, is somewhat out of place and inappropriate . In fact, the changes in renal function that are observed in healthy subjects and healthy kidneys are the reflection of a natural, physiological adaptation to the nitrogen load and to the incremental need for renal clearance . Evidence of this is the occurrence of alterations in renal function - hyperfiltration and increase in glomerular pressure - in subjects with normal renal function in which, in fact, no sign of an increased risk of renal disease has been recorded.
This is what happens to pregnant women (15). In healthy pregnant women there is an increase in glomerular filtration rate of 65% (16); and despite this change in renal function, pregnancy is not a risk factor for chronic kidney disease (17).
Again, renal hypertrophy and improvements in the renal function of the contralateral kidney following unilateral nephrectomy (renal removal) suggest that these processes are adaptive and possibly beneficial for kidney health (18).
Other evidence in the scientific literature shows that, despite the presence of prolonged hyperfiltration processes, the functionality of the residual kidney in nephrectomized patients has remained normal without deteriorating in the long term - over twenty years (19, 20) . And yet no adverse effects on renal function and / or renal damage were recorded in response to a hyperprotein regime on 1135 women with renal normal function (22).
Proteins and Renal Stress
Protein consumption is positively related to urea production (23) and its excretion is controlled by the kidney. These physiological processes would be considered renal stress induced by protein consumption (24).
In a press release it was asserted (as it will be shown below: speculated ) how dangerous the high-protein contributions on renal function are especially in athletes and body-builders ; more precisely, the high protein intake determines an increase in nitrogen levels in the blood, nitrogen reaches the kidneys in the form of urea to be eradicated with urine. The resulting and incremental urination process "could" cause dehydration, thereby increasing renal stress . And, therefore, body builders may be at risk of chronic kidney disease since hyperfiltration "could" produce renal lesions, thereby reducing renal function itself (25).
Scientific research, in this context, is often widely misrepresented. Indeed, laboratory research does not support such claims (26). Indeed, it has been found that high-protein diets have had minimal influences on the individual's state of hydration (26).
Why, then, is dehydration cited as a physiological consequence - in turn a factor of renal stress - to the incremental protein-nutritional intake? This speculation could derive from an extrapolation of a 1954 review on the literature of the nitrogen balance, which was then extended without foundation to contextual-applicative contexts different from the one of origin (27). This review took into consideration the survival rations of soldiers on missions in the desert and in concomitance with limited water and energy supplies!
Since the excretion of one gram of urea nitrogen requires 40-60ml of extra water intake, the increased protein intake forming part of the study resulted in an increased water requirement for urea nitrogen excretion: for example, 250ml d water for every 6 grams of nitrogen in a dietary framework of 500kcal. Therefore, it is clear that the increased water requirement is " context-specific " and is not necessarily applicable to contexts of adequate caloric and water intake.
Despite what is reported in the statement: "the protein intake could induce dehydration and stress the kidneys ...", there are no studies conducted on healthy subjects with normal kidney function that objectively attest to the relationship "hyperproteic intake and dehydration = renal stress ”. Therefore any assertion that denounces the protein intake as a promoter of dehydration and / or renal stress remains at a purely and purely speculative level. The evidence that emerges from the studies in the literature is exactly the opposite: that is, there are no cases of decrease in renal function in response to high protein intake even in those (obese, hypertensive, dyslipidemic) who are more at risk due to the onset of kidney problems (28, 29, 30, 31, 32).
In a study conducted on 65 healthy and overweight individuals, the subjects underwent a hyper or hypoproteic regimen for 6 months. In the group with high protein intake there was an increase in kidney size and an increase in glomerular filtration rate compared to the baseline values prior to the study. No change in albumin excretion was found in either group; despite acute changes in renal function and size, hyperprotein intake did not cause any effect to the detriment of renal function in healthy subjects (33).
Finally, in another study 10 individuals respected the diet to which they were accustomed for 7 days, followed by a high-protein diet for 14 days. There were no significant changes in serum and urinary creatinine levels, much less in reference to urinary albumin excretion; all facts that reinforce the belief that hyperproteinics do not create kidney damage on healthy subjects (34).
And let's get to the athletes! Athletes of disciplines of strength and power are known to consume high amounts of dietary protein and also introduce amino acid and protein supplements that significantly increase nitrogen levels. Despite this, there is no evidence that this type of individuals is at high risk of renal damage or loss of renal function (35).
Furthermore, it was found that a protein intake fluctuating between 1.4g and 1.9g per kg of body weight per day or its introduction according to values fluctuating between 170 and 243% of the RDA did not result in alterations of renal function in a group of 37 athletes (36).
Proteins and kidney stones
High protein intake increases the excretion of potentially lithogenic compounds (tending to form sediments - Ed), including calcium and uric acids (37, 38). In an accredited study Reddy et al. they showed how a high -protein approach led to increased aciduria and calcium in the urine, claiming that these factors represented an incremental risk for the formation of kidney stones in the 10 individuals who had taken part in the study. But none of the 10 subjects reported kidney stones (39)!
The drastic glucidic restriction adopted in the study in question could have favored an increase in keto-acid production, thus contributing to acid formation; given that food categories such as fruit and vegetables represent an important and sensitive source of basic-alkaline load, their restriction - foreseen by the protocol adopted in the study - may have certainly influenced the resulting final net acid load.
Diet alone does not result in the formation of kidney stones. This is testified by a study in which, under the same nutritional and hydration conditions, healthy subjects eliminated single crystals of calcium oxalate with a diameter of 3-4 microns where subjects prone to the formation of kidney stones produced crystals of 10-12 microns in diameter, which most often they were joined in polycrystalline aggregates with a diameter of 20-300 microns (40).
Instead, the real causes of kidney stones lie behind important metabolic alterations (41). In fact, this is also witnessed in another study, with which Nguyen et al. found that high protein intake negatively affects markers of kidney stone formation (such as, for example, increased oxalate excretion) in subjects with metabolic problems underlying the formation of kidney stones (ICSFs, or "Idiophatic Calcium Stone Formers" ) but not on healthy subjects (42).
Causes of Chronic Kidney Disease
The factors that affect the risk of contracting chronic kidney disease are: obesity, hypercholesterolemia, insulin resistance, hyperuricemia, hypertension (43). As can be deepened by the bibliographical note (44) to the reference study, subjects with blood pressure values greater than or equal to 160/96 mmHg have a more marked decline in the glomerular filtration rate on an annual basis and a risk of early decline in renal function 5.21 times higher than those with blood pressure values below 140/90 mmHg.
The counter-evidence of the importance of arterial pressure on renal function is found in various studies showing how anti-hypertensive therapy decreases the progression of chronic kidney disease in patients suffering from it (45, 46).
What instead surprises and goes against the common "pseudo-knowledge" and the myth of the dangerousness of the high-protein order is the literature that highlights the inverse relationship between protein intake and systemic blood pressure (47, 48). The evidence proves the confirmation of how much the protein intake, together with that of the fibers, has additional benefits in inducing the lowering of the 24-hour systolic pressure in a group of 36 hypertensives (49).
