In the early 1950’s, researchers declared that age-related kidney decline reduced function at a rate of about 8% every 10 years after the age of 40. More recently, it was noted that the decline may begin as early as 20 years old. In this blog, we will discuss age-related kidney decline.

Each of us are born with a specific number of nephrons, the functional kidney units which does the job of filtering toxins out of our system. Depending on factors like diet, lifestyle factors, and genetics/epigenetics (to name a few), the rate of decline varies and results in different outcomes to each patient. So, is there anything we can do to reduce our risk of age-related kidney function decline to avoid dialysis?

What causes the Age-related kidney decline?

1. Blood flow

Recent studies demonstrate that the blood flow to the kidneys decreases by approximately 10% every 10 years after age 40, affecting each nephron. In addition, the arteries of each nephron become less responsive to changes in blood pressure, increased pressure leads to damage and accelerated loss of kidney mass.

2. Inflammation

Furthermore, as the lining of the filters inside the nephron become more permeable protein begin to seep through, contributing to increased inflammation. As time passes, inflammation leads to scarring of the filtration units. In fact, on average by the time an individual reaches the end of their 80’s, 30% of the nephrons are too damaged to be functional.
[bctt tweet=”Inflammation leads to scarring of the filtration units. In fact, on average by the time an individual reaches the end of their 80’s, 30% of the nephrons are too damaged to be functional” username=”inkidney”]

3. Renin-Angiotensin System (RAS)

Factors that affects the blood flow to each nephron includes a system called the Renin-Angiotensin System (RAS). So that if the blood flow to the nephron declines, the nephron produces a chemical called Renin which promotes the production of another chemical called Angiotensin (Angiotensin I then Angiotensin II).
Angiotensin II increase the pressure inside the nephron and maintain adequate function by promoting “clamping” of some of the vessels in the nephron. With aging, production of Renin decreases. This results in a subsequent decline in the kidney’s ability to maintain good flow in response to changing blood pressure.

4. Nitric Oxide production

Blood vessels are also controlled by Nitric oxide (NO₂), another system that functions by expanding the blood vessels inside the nephron to help maintain good blood flow. This system also serves to protect the kidney from the formation of scar tissue.
Many factors help improving the production of NO₂ while others lead to its breakdown. One example, are factors like genetics or availability of precursors that can influence the action of the enzyme responsible for making NO₂, Nitric Oxide Synthetase (i.e. eNOS, iNOS, and nNOS). Another factor affecting the breakdown of Nitric Oxide are sex hormones. Estrogen, the dominant sex hormone in females, prevents the breakdown of NO₂keeping its level high. Meanwhile, testosterone, the male dominant sex hormone, has the opposite effect of increasing its breakdown. This may in part explain why hypertension and kidney function decline is more pronounced in men than in women.
With aging, NO₂ production declines and leads to the closing of the arteries in the kidney, sodium retention, and scar tissue formation. These factors make the aging kidneys more vulnerable to even minor changes in blood pressure, changes in hydration, and medication – in turn, making them more susceptible to acute kidney injury.
[bctt tweet=”With aging, NO2 production declines and leads to the closing of the arteries in the kidney, sodium retention, and scar tissue formation” username=”inkidney”]

What can be done to slow the rate of age-related kidney decline?

Conventional medicine focuses on using medications that block the RAS system such as Angiotensin Converting Enzyme (ACE) Inhibitors (i.e. enalapril, lisinopril) or Angiotensin II Receptor Blockers (ARBs) (i.e. losartan, irbesartan). There are a multitude of studies demonstrating their effectiveness in delaying the progression of various forms of kidney disease, including diabetic kidney disease, age-related kidney decline and others.
However, despite the delayed progression, patients continue to lose kidney function and end up requiring dialysis. Additionally, like all drugs, these medications come with side effects and risks*. Adverse effects include increased potassium retention, zinc depletion, and swelling of the throat, among other side effects. In fact, these medications have an established increased risk of acute kidney injury, particularly in elderly with kidney disease.
Arginine (or L-Arginine, we’ll use the terms interchangeably) is an amino acid that is essential for the body to produce NO₂. It’s labeled as a conditionally essential amino acid because although the body can make it, production is dependent on factors including health and nutrition status. Levels tend to decline with age, therefore ensuring adequate intake through food sources or supplementation is important.

Arginine-rich foods include animal proteins, eggs fish, nuts (including walnuts, hazelnuts, pecans, peanuts, almonds, cashews, and Brazil nuts), seeds (especially pumpkin, also sesame and sunflower), oats, buckwheat, and cacao. Note, some of these foods are also high in phosphate which should be restricted in kidney patients even at early stages. (link-blog to write). With age and reduced gut function, absorption of nutrients from food may be diminished, so supplementation may be in order to prevent/slow age-related kidney decline. For kidney patients over 50-years-old, the recommendation* is to supplement 2 grams of L-Arginine three times a day to maintain good kidney circulation, stabilize function and prevent age-related kidney decline.
*Reminder: Always consult with your kidney doctor or primary care physician before taking any supplement, and never change or discontinue your medication without the instruction of your doctor.

References:

1. Davies Df, Shock NW, Age Changes in glomerular filtration rate, effective plasma flow, and tubular excretory capacity in adult males. J Clin Ivest 1950; 29:496-507
2. Llorens S, Fernandez AP, Nava E. Cardiovascular and renal alterations on the nitric oxide pathway in spontaneous hypertension and aging. Clin Hemorheol Microcirc 2007; 37:149-156
3. Delp MD, Behnke BJ, Spier SA, Wu G, Muller-Delp JM. Aging diminishes endothelium-dependent vasodilation and tetrahydrobiopterin content in rat skeletal muscles arterioles. J Physiol 2008; 586:1161-1168
4. Auelo JG. Normotensive ischemic acute renal failure. N Engl J Med 2007; 357:797-805
5. Ahmed SB, Fisher ND, Hollenberg NK. Gender and the renal nitric oxide synthase system in healthy humans. Clin J Am Soc Nephron 2007;2:926-931