A study just published in the Annals of Internal Medicine concluded that reducing the amount of protein in the diet "significantly reduced the risk for renal failure or death" by slowing progression of the underlying kidney disease. To reach this conclusion, the authors closely analyzed randomized, controlled studies in diabetic and other types of renal disease done from 1966 through 1994. They also concluded that the beneficial effect of a low-protein diet was independent of its possible beneficial effects on blood pressure.

The massive Modification of Diet in Renal Disease study, the results of which were published two years ago, reported that patients on a low-protein diet initially showed a faster decline in their glomerular filtration rate (GFR) during the first four months, but then the rate of decline became much slower than that of patients on a normal diet. As the present authors point out, a "low-protein diet initially reduces the single-nephron glomerular filtration rate but subsequently slows the progression of renal disease." In addition to slowing progression, low-protein diets also ameliorate uremic symptoms in patients suffering from chronic renal failure, a prelude to loss of the kidneys.

Two cautionary notes, however: patients with proteinuria that exceeds 10 g/day are at greater risk for malnutrition, which is the major potential adverse effect of a low-protein diet, and the study did not deal specifically with IgAN, although its results are no doubt applicable to IgAN patients. The studies analyzed used a prescribed protein intake of 0.6 g/kg of body weight per day (or about 40 grams for a 150-lb. individual), a very low amount usually suggested only for patients with chronic renal failure. Apparently, quite a few patients exceeded these protein levels, meaning that the diet's true beneficial effects may have been understanted.

Many of the IgAN patients we hear from have drastically reduced their consumption of meat; some have even adopted wholly vegetarian diets. A vegetarian diet, as the Network's literature points out, saves the kidneys a lot of hard work in clearing the body of the byproducts of protein metabolism. By reducing strain on the kidneys, we hope to preserve function longer.

That's the simple explanation. A more technical one was given years ago by Drs. Barry Brenner, Timothy Meyer, and Thomas Hostetter, who were concerned that not enough attention was being paid to the influence of diet upon the progression of renal disease.

There are significant changes in renal blood flow and glomerular filtration rate (GFR) in animals fed intermittently: during intervals between meals, the glomeruli close to the surface of the kidneys show very low GFR, as if at rest; but after a meal, filtration rates increase more markedly in these superficial glomeruli than in the deeper ones. In other words, the superficial glomeruli are like reserve troops, only called upon as needed.

As Brenner and his co-authors note, this reflects the kidney's evolutionary adaptation to the needs of meat-eaters whose protein intake is not constant. Our hunter-gatherer forebears lived through feast-or-famine situations. When there was a kill, their kidneys had enough excess capacity to handle the huge influx of protein metabolites produced by gorging on mastodon.

Our kidneys still have that excess capacity for dealing with the occasional feast, but our eating habits have changed. Now the feast is continual. We eat smaller meals more often, taking in substantially higher amounts of food overall and protein specifically. There is, the authors conclude, "a fundamental mismatch between the evolutionary design characteristics of the human kidney and the functional burden imposed" by modern eating habits.

When animals are fed at will, their overall protein intake increases and all their glomeruli are continually called into action. There's no rest for the superficial glomeruli that used to be called upon only occasionally. This leads to higher pressures within the kidneys, which in turn contribute to the glomerulosclerosis (scarring of the glomeruli) found normally in older people and animals.

Even in healthy humans, renal blood flow and GFR decline progressively after age 30. By the time we've reached 70, these values have declined to two-thirds or half of what they were when we were young adults, and 10-30% of our glomeruli are showing signs of scarring -- even if we don't have a disorder like IgAN. This wear-and-tear on the kidneys poses no threat to healthy people, but it does pose one to people whose kidneys are further damaged by renal disease. Hyperfunctioning [excessively active] glomeruli are like hyperactive kids, only in the case of the former excessive pressures within the kidney lead to eventual deterioration of the glomeruli.

There is no way to predict how long it will take the glomeruli (and eventually the nephrons) of a given patient to shut down. Brenner and his colleagues note that nephron function declines at rates that are peculiar to each patient rather than characteristic of the underlying disease. Progression to renal failure can even go on even when the underlying disease is controlled medically, or when the original cause has been removed (as in patients who develop renal failure after post-streptococcal glomerulonephritis). They conclude that once the initial injury or disease has attacked and destroyed a certain number of nephrons, increased pressure on the remaining glomeruli destroy more, eventually causing renal failure. They do not, however, know how many nephrons must be lost to begin this process of progressive renal disease in the absence of ongoing injury.

Fatty acids are mediators of inflammation becuase of their ability to form compounds known as prostaglandins. There are good and bad prostaglandins; the good kind have anti-inflammatory effects, the bad kind fuel the fires.

A "bad" fatty acid is arachidonic acid, which is derived almost entirely from meat and dairy products. Animal foods also tend to be high in saturated fats, which can also increase the inflammatory response. One of the products of arachidonic acid metabolism is thromboxane, which plays a role in glomerulosclerosis, or the scarring of the glomeruli.

A "good" fatty acid is eicosapentaenoic acid (EPA), the active ingredient in the fish oil that is widely being used now to treat IgAN and which helps form anti-inflammatory prostaglandins. A recent study of fifteen IgAN patients found they were deficient in certain beneficial fatty acids. Supplementing the diet with fish oil increased plasma levels of certain beneficial fatty acids, such as EPA, and suppressed harmful ones.

Dr. Michael T. Murray observes that a vegetarian diet can also be beneficial in treating inflammatory conditions (of which IgAN is one), for it decreases the availability of arachidonic acid for converstion to inflamatory prostaglandins and leukotrienes. It also supplies such "good" fatty acids as linoleic and linolenic acids. Good sources for these fatty acids are also flaxseed oil, canola oil, and evening primrose oil.

In sum, a vegetarian diet may a doubly protective effect in IgAN, first, by reducing the strain on the kidneys of metabolizing animal proteins, and second, by reducing the inflammatory response that damages the kidneys.