A study published in 2012 found that more than 64 million Americans aged 30 or older had periodontal (gum) disease. Gum disease, also known as periodontitis, is a severe infection of the gums caused by an immune response to imbalanced oral bacteria. Inflammation from periodontal disease can damage gums, destroy the jawbone, and lead to tooth loss. Several studies have shown an association between periodontal disease and other systemic diseases such as heart disease, diabetes, cancer, and dementia. But what about the association between dental health and kidney disease? In this blog, I am going to explore that link.
Periodontal disease and systemic inflammation
The oral microbiome produces metabolic by-products in the mouth. Some of these by-products leak into the blood stream and lead to a low-grade systemic inflammation. Studies have shown that patients with severe periodontitis have elevated levels of pro-inflammatory mediators and increased neutrophil numbers in the blood. In fact, successful treatment of gum disease was associated with improvement in inflammatory markers. Many of these inflammatory markers have been linked to heart disease, diabetes, and other diseases. This may explain the link between periodontal disease and systemic diseases.
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CKD is an inflammatory state
Low-grade inflammation has been shown to be an integral aspect of chronic kidney disease (CKD). Here, too, inflammatory markers were found to be elevated. As kidney function worsens, the levels of these markers increase in the body. They also increase with increasing urine protein (albuminuria), which is common in CKD.
On the other hand, an evaluation of the Chronic Renal Insufficiency Cohort (CRIC) study found that elevated inflammatory markers were associated with rapid progression of kidney disease. So, the relationship between inflammation and kidney disease is bidirectional. CKD can lead to inflammation and inflammation can lead to and worsen CKD.
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Can gum disease cause kidney problems?
Periodontitis can increase the risk of CKD by direct and indirect effects. Directly, periodontitis increases systemic inflammatory burden leading to an increased incidence of CKD. In a recent review of 37 studies, researchers found strong evidence that periodontitis is associated with an increased risk for CKD. This association remained strong after adjusting for other risk factors.
Periodontitis can also increase the risk for CKD indirectly by increasing the risk for insulin resistance and diabetes. In this study, diabetes increased the odds of CKD by twofold, and 6.5% of this effect was mediated by periodontitis.
In addition, some of the increased risk of CKD may have to do with genetics. For example, variants in vitamin D receptor gene were associated with CKD during inflammatory conditions caused by periodontal disease.
There is not a lot of data on how treating gum disease affects CKD. However, in this pilot study, researchers found that treating severe chronic periodontitis for 180 days led to improvement of all periodontal clinical parameters. This was associated with statistically significant improvement in kidney function and markers of inflammation.
CKD and periodontitis: Does kidney disease affect oral health?
On the other hand, CKD can affect oral health by inducing gum overgrowth (known as gingival hyperplasia), dry mouth, calcification of root canals, and delayed eruption of teeth in children. These can lead to increased risk of periodontal disease. In addition, severe periodontal disease was found to be more common in patients with more severe CKD.
Kidney disease, gum disease, and nutrition
There is a triangular interaction between nutrients, CKD, and periodontal disease. Protein wasting that is common in kidney disease, for example, can increase the risk of periodontal disease. Omega-3 fatty acids, on the other hand, were found to be beneficial in the management of chronic periodontitis. Many other nutrients and micronutrients that can be altered in CKD were also associated with periodontal disease.
CKD medications may cause gum and teeth problems
Some of the medications that are used for patients with CKD can also increase the risk for periodontitis. Medications such as calcium channel blockers that are used to treat blood pressure can lead to gum swelling and overgrowth. This was also noted in some transplant medications such as cyclosporine. Other medications can be associated with dry mouth, which can promote gum and teeth problems. These include ACE inhibitors, calcium channel blockers, betablockers, and diuretics.
The bottom line on chronic kidney disease and oral health
Both periodontal disease and CKD are associated with low-level systemic inflammation. The association between the two is bidirectional. Periodontal disease can increase the risk for CKD and the rate of its progression. On the other hand, CKD can also worsen periodontal disease. Paying attention to oral health is essential for the prevention of many chronic diseases. It is also crucial for preventing or slowing down the progression of CKD.
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In a multi-center, nested, case-control study in three Korean hospitals, patients with CKD stage 3 and 4 who are using drugs including colchicine, allopurinol, and febuxostat for high uric acid or chronic gout were studied over a period of 10 years. The progression of CKD was compared between 3085 compared to 11715 control patients.
Colchicine use was associated with a lower risk of adverse kidney outcomes in CKD patients with hyperuricemia, or chronic gout.
Unlike a study published two years ago in NEJM which excluded patients with advanced CKD, this study included patients with kidney function as low as 15 ml/min. Colchicine is known to anti-inflammatory. It also protects against kidney fibrosis.
There are concerns about myopathy and neuropathy with the intake of colchicine. It is, therefore, important to adjust the dose with advanced kidney disease and to be cautious when using it with patients who are on other myopathy-inducing drugs such as statin drugs.
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Long sleep duration is associated with decline in kidney function
This study is retrospective, longitudinal cohort study included 82,001 participants who visited a primary care center in Japan. Patients were categorized into CKD risk groups and sleep duration categories according to their self-reported average nightly sleep duration. The relationship between average nightly sleep duration and the incidence of composite renal outcome was studied.
Researchers found that an average sleep durations ≥8 h/night were associated with an increased risk of kidney function decline over time.
There are many reasons that connect sleep problems with poor kidney function. We summarized these in this blog.
Risk of environmental heavy metal toxicity is higher in CKD
In a study of 5,638 NHANES participants, lead and cadmium levels were higher in patients with CKD than those without it. This was also associated with decreased urinary lead excretion. Each decrease in estimated GFR by 10 ml/min/1.73m2 was associated with 0.05 mcg/dL increase in lead levels and 0.02 mcg/dL of cadmium levels. This association was even stronger among black participants.
The study concluded that CKD increases the susceptibility to heavy metal environmental exposure by reducing its elimination.
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The root cause of IgA nephropathy
IgA nephropathy is a kidney disease that is defined by the pathologic appearance of glomerular deposition of IgA immune complexes. However, this definition does not address the root cause of the disease.
It has been increasingly recognized that IgA immune complex that deposit in the kidneys predominantly contain polymeric IgA1 lacking galactose within its O-glycosylated hinge region.
In this study, researchers found that patients with IgA nephropathy have elevated levels of certain B cells that are enriched for λ light chains. These cells are predestined for homing to upper respiratory and digestive tract mucosal tissues. In the mucosal tissues, these B cells mature and excrete abnormal IgA in the setting of upper respiratory or digestive infection. You can read more IgA nephropathy by reading our blog here.
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Metformin: Some people love it and some people hate it… But it sure is getting a lot of attention lately
This study was done in rats with “non-diabetic kidney disease.” CKD was established in these rats by feeding them high adenine diet. Then they were randomized to receive either metformin or canagliflozin (an SGLT-2 inhibitor).
Metformin, but not canagliflozin, halted the decline in kidney function. Additionally, kidneys of metformin-treated animals showed less interstitial area and inflammation as compared to the vehicle group.
Metformin is increasingly being studied in humans for various kidney diseases. If used judiciously it may be a cheap alternative to preserving kidney function.
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Tremor + gum disease + nephrotic Syndrome = ?
In this study, investigators in Beijing looked into the manifestation of mercury poisoning in 172 patients. 26.74% of these patients had kidney injury (3/4 were women) and most of them had nephrotic syndrome. The most common finding on the biopsy was membranous nephropathy.
Other findings of chronic mercury poisoning were neurotoxicity and gingivitis. Chelation with DMPS alone was as effective as chelation and prednisone in reversing kidney injury.
The most common source of exposure without kidney disease was industrial exposure. Interestingly, the most common source of exposure leading to kidney disease was cosmetics containing ionic mercury (mercury concentration in one of the patients cosmetic was 4600 mg/kg – national standards are < 1 mg/kg).
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Root Causes of Itching in Kidney Disease
Uremic toxin-induced neurologic changes
Several studies showed that patients with CKD have an imbalance of opioid receptors in the central and peripheral nervous system. Interestingly, itching in CKD correlates better with the level of uremic toxins than with glomerular filtration rate (GFR, a measurement of how well the kidneys are working). These toxins play an important role in these neurologic changes that are common in CKD. Most of these toxins are generated by the gut microbiome and are excreted by the renal tubules and not by glomerular filtration (or GFR). Measuring these toxins can be helpful. This can be done by a metabolomic test such as Genova’s Metabolomix+.
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Inflammation
CKD is an inflammatory disorder. Elevated inflammatory markers have been found to be associated with itching in kidney disease. Measuring inflammatory markers such as hsCRP, Th-1 cells, and IL-6 can be helpful in the assessment of the root cause of itching in CKD.
Dehydration
Dehydration can also lead to dry skin and worsens itching in CKD patients. Correcting the dehydration can be important in the management of itching.
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Drug-induced itching
Many medications that are used in CKD have been associated with itching. These include calcium channel blockers, hydrochlorothiazide, and ACE inhibitors. In addition, other medications such as opioids, anticoagulants, and antibiotics can cause itching.
The itch-scratch-itch cycle
One of the major problems with itching is that it leads to scratching, and this can cause skin damage. The latter can cause further itching and the cycle continues.
Natural Treatments for itching in kidney disease
There are many steps you can take to get rid of itching in kidney disease and a kidney disease rash. The first step is to visit a healthcare provider to help you determine the root cause. You can download this two-page handout to guide you in the natural treatment of itching. There is hope that you’ll relieve this frustrating problem and have comfortable skin once again.
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Air pollution is linked to kidney disease
PM 2.5 refers to particulate matters that are up to 2.5 microns in size. Because of their small size, they are considered to be the worst of all air pollutants. They reach the alveoli and enter the blood stream. This study looked at the link between PM 2.5 and chronic kidney disease (CKD) in the Twin-cities area of Minnesota. Researchers found that the risk of CKD increases with higher levels of PM 2.5. This remained true after adjusting to all other variable.
It is, therefore, important to think of air pollution as a mediator of CKD and minimize exposure to it.
Block "fundamentals" not found
A Study reaffirms the role of the gut kidney connection in diabetic kidney disease
You know we discussed the role of the gut-kidney connection in the progression of CKD. You can find many of our blogs discussing this here. Dysbiosis can be a predisposing factor or a mediator when it comes to kidney disease. This study looked at the contribution of impairment in the intestinal barrier (leaky gut) to kidney injury in diabetic kidney disease (DKD). In diabetic mice with impaired intestinal integrity intestine-derived Klebsiella oxytoca and elevated IL-17 were detected in the circulation. This was associated with epithelial renal tubular injury and faster progression to kidney failure as compared to control.
So, always think about the gut when it comes to kidney disease. A personalized comprehensive gut restoration protocol is a must to heal the gut.
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A gut-derived uremic toxin is associated with inflammation
Speaking of the gut, we discussed monocyte to HDL ration (MHR) in a previous email. If you missed it, you can read about it on our Instagram page. This study looked at the connection between Indole-3-acetic acid which is a gut-derived uremic toxin and MHR in patients with kidney disease. The study was conducted on 67 patients with CKD. Researchers found that Indole-3-acetic acid levels are directly related to MHR levels. The latter was associated with higher levels of fibrinogen, arterial hypertension, CRP.
So, as they say, when in doubt think about the gut.
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Cold exposure
Cold exposure, such as cold showers, has many benefits for kidney patients. It increases endorphins and fights off depression. It improves metabolism and circulation. Most importantly, it stimulates the vagus nerve and improves renal circulation. It may also soothe itchy skin which is common in CKD patients. In addition, cold showers help with post-workout muscle soreness.
The benefits of a cold shower begin when the water temperature dips to 60 degrees Fahrenheit. This is 40 degrees lower than the typical steamy shower. To take a cold shower, start with your usual hot shower, then turn the knob to cold at the end of your shower. Lower the temperature gradually at the end of your shower every day. The benefits start with thirty seconds under the cold water. Maximum benefits are reached in three minutes.
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Vagus nerve breathing exercises
Deep and slow breathing can activate the parasympathetic system. In fact, deep breathing is one of the best ways to lower stress in the body. It sends messages to the brain to calm down and relax by activating the vagus nerve which helps lower heart rate and blood pressure. There are various ways to perform deep breathing. Here, I will discuss the 4-7-8 breathing technique.
This technique uses belly breathing. It can be performed sitting or lying down as follows:
- Start by putting one hand on the belly and the other one on the chest.
- Take a deep slow breath from the belly while silently counting to 4. The chest should not move.
- Hold the breath while silently counting to 7.
- Breathe out completely while silently counting to 8.
- The process can be repeated 5 to 10 times until feeling relaxed.
Singing, humming, chanting, and gargling
These activities have also been shown to improve heart rate variability and can also activate the vagus nerve because it is connected to the vocal cords. These benefits can be achieved by 10 minutes of singing, humming, chanting, or gargling every day.
Probiotics
The fact that probiotics have been found to support stimulation of the vagus nerve is another piece of evidence for the importance of the gut-brain axis. Healthy microbiota produce short-chain fatty acids, such as butyric acid, which can activate the vagus nerve and send messages from the gut to the brain. It is highly beneficial to get most probiotics through diet. However, if supplements are used, it is recommended to use good quality broad-spectrum probiotics.
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Meditation
Meditation has been found to increase vagal tone and positive emotions. Meditation for 10-15 minutes is a great way to start the day, manage stress, and stimulate the vagus nerve. There are many ways to meditate and many types of meditations. Mindfulness meditation is the most tested in kidney patients. It has been demonstrated to improve the quality of life, reduce anxiety and depression, reduce sympathetic overactivity,improve sleep, and improve blood pressure.
To practice mindfulness meditation such as Benson’s relaxation technique, follow these steps:
- Sit in a comfortable position or on a meditation cushion.
- Close your eyes.
- Relax your shoulders and muscles.
- Focus on breathing.
- Say a word with every exhalation. A positive word like “gratitude” can be used. As the mind starts racing, which distracts from the breath, the person returns to the word.
Practicing this every day will improve the experience and compound the benefits with consistency.
Omega-3 fatty acids
Among the many benefits of omega-3 fatty acids are increased vagal activity. The best way to reap the benefits of omega-3 fatty acids is by eating fatty fish twice per week, but if that is not an option due to protein restrictions or dietary choices, supplementation is an option. Other food sources include nuts and seeds such as walnuts and flaxseed. It is important that the supplement contains enough eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are the most powerful omega-3 fatty acids. The dose is at least 500-1,000 mg of EPA-DHA three times a day.
Exercise
One of the best vagal tone exercises is exercise itself. Exercise is linked to better mental health and stimulation of the vagus nerve. It may be one of the most underutilized yet effective interventions for the prevention and treatment of kidney disease. It has been shown to reduce the risk of CKD, help with blood pressure and glucose control, and improve health-related quality of life. Exercise also induces a positive influence on mental health, mood, and stress levels by stimulating the vagus nerve.
The best type of exercise is the one that you do. What I mean by that is don’t get discouraged by trying to find the perfect type of exercise and do anything that works best for you. Having said that, studies on exercise in CKD have included resistance training and aerobic activities that use large muscle groups continuously such as walking, cycling, and jogging.
High-intensity interval training (HIIT) offers superior benefits in individuals with metabolic diseases such as diabetic kidney disease. Studies of HIIT in CKD have shown that it is a safe and feasible option for individuals with CKD.
Those who are new to exercising should start slowly and gradually get to 20-30 minutes of strenuous exercises 5-6 days a week. It is best to alternate between aerobic exercises and resistance training. For those who are 50 years of age or older, it is important to check with your provider before engaging in strenuous exercises.
Massage therapy
Massage therapy has also been found to be associated with improved vagal tone. The stimulation of pressure receptors leads to an increased vagal activity which, in turn, seems to mediate the diverse benefits of massage therapy. Functional magnetic resonance imaging data suggested that moderate pressure massage was represented in the part of the brain involved in stress and emotion regulation.
Socializing and laughing
Finally, increased social connection and laughing have been linked to increased positive emotions. Increased
positive emotions, in turn, produced increases in vagal tone, which puts the body in a rest and repair state.
The bottom line
Stimulating the vagus nerve can turn on the parasympathetic nervous system, improve renal blood flow, and modulate inflammation in CKD. Improve kidney health using these natural techniques to turn on the vagus nerve and turn off stress: a cold shower, breathing exercises or meditation, singing or humming, probiotics, omega-3 fatty acids, exercise, massage, and social connection. Check out my 1-hour morning routine for kidney health that incorporates many of these techniques.
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3 years of lifestyle interventions improved exercise capacity and decreased the losses in neuromuscular and cardiorespiratory fitness in CKD patients
In this study, researchers randomized 161 patients with stage 3-4 CKD to either get usual care or usual care plus lifestyle “intervention” for 3 years.
The lifestyle intervention comprised of care from a multidisciplinary team, including a nephrologist, nurse practitioner, exercise physiologist, dietitian, diabetes educator, psychologist, and social worker.
The patients were coached for 8 weeks and then followed for 34 months with a home-based program.
The study did not look at the progression of CKD but it found that a 3-year lifestyle intervention doubled the percentage of CKD patients meeting physical activity guidelines, improved exercise capacity, and decreased the losses in neuromuscular and cardiorespiratory fitness.
It appears that the study mainly focused on exercise. So imagine the benefit of a comprehensive lifestyle modification plan that includes nutrition, exercise, stress management, sleep improvement, and attention to toxin exposure and gut-kidney connection. That’s what we focus on.
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Curcumin powder did not improve markers of vascular dysfunction in PKD
This is essentially a negative study.
It demonstrated that Curcumin powder did not improve markers of vascular dysfunction in children and young adults with PKD. The study was conducted for only one year using a dose of 25 mg/kg per day of curcumin.
This is a classic supplement or nutrient study that is usually underpowered or conducted for short periods of time for a disease that takes years or even decades to evolve. Nevertheless, the study proved that short-term use of curcumin is not beneficial for vascular health for young patients with polycystic kidney disease.
Low serum zinc levels were associated with infections in CKD patients
This did not really need research but it is now studied and it is official: Low zinc levels in patients with CKD lead to infection (..well among other things).
This retrospective study analyzed data from 299 CKD patients who had serum zinc levels checked to evaluate anemia. They used the level of 50 mcg/dl as the cutoff between low or “high” zinc values.
Low serum zinc values remained an independent risk factor for infection-related hospitalization. This was especially true for patients taking proton pump inhibitors (PPIs) medications.
Read about the effect of Zinc on kidney health in this blog.
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Causes of magnesium deficiency
Poor dietary choices
There has been a steady decline in magnesium content in cultivated fruits and vegetables over the past 100 years. This is caused by the depletion of magnesium in soil over time. In addition, utilizing phosphate-based fertilizers leads to the formation of magnesium phosphate salts that are not soluble. This means the soil is deprived of both components: magnesium and phosphorus.
On top of that, the rise of ultra-processed food and drinks have also contributed to the depletion of magnesium in the modern standard American diet. Grain bleaching and vegetable cooking and adding preservatives can lead to a significant loss of magnesium content. Preservatives such as various forms of phosphate and oxalate can bind with magnesium and prevent its absorption. Phosphoric acid in soft drinks has similar effects.
The addition of fluoride to drinking water also prevents magnesium absorption by binding to it and forming insoluble complexes. Finally, drinking caffeine and alcohol can also lead to an increase in the excretion of magnesium by the kidneys, causing magnesium deficiency.
Drug-induced magnesium deficiency
Many medications can interfere with magnesium absorption or increase its excretion, leading to deficiency. Most of the medications leading to magnesium deficiency are summarized in the following table:
| Medication class | Example | Mechanism |
| Anti-diabetic medications | Insulin, insulin mimetics | Interferes with Na/Mg exchange leading to renal loss |
| Antimicrobial | Gentamicin, pentamidine, foscarnet, amphotericin B | Increased renal loss |
| Beta agonists | Salbutamol | Renal loss and cellular shifts |
| Bisphosphonate | Pamidronate | Renal loss |
| Cardiac glycoside | Digoxin | Increased renal loss |
| Chemotherapy agents | Cisplatin | Renal loss |
| Diuretics | Thiazide diuretics | Renal loss |
| Proton-pump inhibitors | Omeprazole | Decreased GI absorption |
Measuring magnesium status
Simply put, there is no ideal test for assessing magnesium status in the body. Mg blood levels are tightly controlled and represent only 0.8% of total body stores (0.5% in red blood cells and 0.3% in the serum). Red blood cell Mg levels have been used as an alternative method, but this too does not represent total body stores and is not well validated. Measuring urine Mg requires measuring a 24-hour urine specimen. This too has been found to be imperfect due to large variations from day to day.
The Mg retention test has been proposed as a more accurate way to assess Mg status. Here, the patient receives an intravenous Mg load (0.25 mmol magnesium/kg body weight at a rate of 2.5 mmol/hour), and a 24-hour urine specimen is collected before and after the load. The percentage of administered magnesium that is retained by the body (not excreted in urine) determines magnesium status. This test is not standardized yet, but retention of 25%-50% may indicate a moderate deficiency, and retention of more than that may indicate severe deficiency.
Ideally, measuring muscle or bone magnesium may be more reflective of accurate magnesium stores but this is obviously not practical. Combining a serum Mg test, a 24-hour urinary Mg, and assessing dietary Mg intake is the most comprehensive and practical evaluation of a patient’s magnesium status.
Combining a serum Mg test, a 24-hour urinary Mg, and assessing dietary Mg intake is the most comprehensive and practical evaluation of a patient’s magnesium status
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Patients at high risk for magnesium deficiency include:
- Diabetics
- Heart disease patients
- Osteoporosis patients
- People who eat a diet high in processed food and soda
- People who suffer from leg cramps
- People with metabolic syndrome
- People who take certain medications
Those patients at risk of magnesium deficiency should be targeted for additional testing and supplementation.
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What type of magnesium should I take?
The type of magnesium supplement used depends on the exact indication. Magnesium supplements are available as oxide, hydroxide, gluconate, chloride, citrate, lactate, malate, taurate, L-threonate, sulfate, glycinate, orotate, and carbonate salts. In addition to magnesium citrate’s direct effects on kidney stones, magnesium benefits the person with kidney disease through its effects on blood pressure, insulin sensitivity, vascular health, and bone. The following indications are listed with the recommended types of magnesium supplements and doses. These doses are for prevention only. Patients who are deficient may need higher doses. Magnesium supplements should be discontinued or decreased in kidney patients if the serum magnesium level is higher than 2.6.
| Indication | Mg type | Dose |
| Prevention of kidney stones | Magnesium citrate | 400 mg daily |
| Bone health | Magnesium citrate or chloride | 400 mg daily |
| Improving blood pressure | Magnesium taurate | 400 mg once or twice daily |
| Improving insulin sensitivity | Magnesium taurate | 400 mg once or twice daily |
| Improving vascular health | Magnesium glycinate or orotate | 200-400 mg daily |
| Phosphate binder | Magnesium carbonate | 250 mg with meals |
We recommend using high-quality supplements. This article can be a useful guide.
The bottom line
Magnesium is essential to many biological functions, as I described in part one, “Magnesium and Kidneys.” It has many health benefits for kidney, bone, and vascular health. Assessing magnesium status is difficult but magnesium deficiency is very common and underrecognized. Supplementing magnesium may be important for patients with kidney disease. The type of supplement used depends on the indication. As always, it is recommended that you check with a Functional or Integrative Medicine provider and nephrologist before taking any new supplement.
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Altered vitamin K biodistribution may decrease the benefit of vitamin K2 supplementation in advance CKD
In this study, investigators sought to determine if there are other causes for vitamin K deficiency in advanced CKD beyond decreased dietary intake. They compared vitamin K uptake and distribution into circulating lipoproteins after a single administration of vitamin K1 plus K2 (MK-4 and MK-7) between patients on dialysis and healthy individuals.
They found that patients with uremia and advanced kidney disease don’t incorporate MK-7 well into HDL and LDL particles compared to healthy individuals. In addition, the combination of a statin and PPI was associated with signs of functional vitamin K2 deficiency in these patients.
In essence, patients with advanced kidney disease may not benefit as well from vitamin K2 supplementation. This highlights the importance of optimizing vitamin K2 status at earlier stages in CKD.
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Higher levels of deoxycholic acid were associated with a higher risk of progression in CKD
Deoxycholic acid is one of the secondary bile acids, which are metabolic byproducts of intestinal bacteria. Intestinal bacteria metabolize the primary bile acid, cholic acid, into deoxycholic acid (DCA).
Researchers studied 3,147 CRIC study participants who had fasting DCA levels. DCA levels above the median were independently associated with higher risks of ESKD and all-cause mortality.
This study highlights the importance of the microbiome and dysbiosis in the progression of kidney disease as we discussed in our blog.
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The higher number of medications a kidney patient takes the faster her kidney disease progresses
In a study performed in Japan of 1117 CKD patients under nephrological care, the use of a higher number of medications was associated with an increased risk of kidney failure, cardiovascular events, and all-cause mortality in patients with CKD. This is one of the major reasons we advocate for lifestyle modifications and coaching as the first and major step in the management of kidney disease.
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Low magnesium levels have been associated with a number of adverse events, such as high risk for heart disease. However, little is understood about magnesium and kidney health. Here, we will discuss the potential benefits of magnesium on the kidneys. This is one of two articles on magnesium and kidneys. For more on how to test and treat kidney patients with magnesium deficiency, see part two, “Magnesium Deficiency: Assessment and Management for Better Kidney Health.”
Dietary sources of magnesium
A daily intake of 3.6 mg/kg is necessary to maintain magnesium balance in humans under normal conditions. This is estimated to be between 320 to 420 mg/day (13–17 mmol/day) for adults. Sadly, there has been a steady decline in magnesium content in cultivated fruits and vegetables over the past 100 years. This is due to depletion of magnesium in soil over time. This, along with the rise of ultra-processed food, sodas, and taking medications such as proton pump inhibitors and diuretics that deplete magnesium levels (polypharmacy), has led to rising prevalence of magnesium deficiency.
Traditionally, the highest food sources of magnesium are:
- Leafy greens (78 mg/serving on average)
- Nuts (80 mg/serving on average)
- Pumpkin seeds have the highest level of magnesium per serving (156 mg).
- Whole grains (46 mg/serving on average)
A complete list of foods high in magnesium can be found here.
Can Magnesium Help Kidney Function?
There are many potential benefits of magnesium for kidney health including improving blood pressure control, insulin sensitivity, bone health, vascular health, and preventing kidney stones. Let’s explore the data.
Magnesium and blood pressure control
Magnesium supplementation may help reduce blood pressure (BP) by increasing the production of nitric oxide. Nitric oxide acts as a signaling molecule that helps relax blood vessels, which lowers BP. In fact, a review of 34 studies showed that supplementing magnesium with an average dose of 368 mg per day for 3 months can decrease systolic BP by 2.00 mmHg and diastolic BP by 1.78 mmHg. This supplementation was accompanied by 0.05 mmol/L increase in serum magnesium levels.
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Magnesium and insulin sensitivity
Diabetes is one of the major risk factors for kidney disease worldwide. Higher dietary intake of magnesium has been correlated with lower diabetes incidence. A review of 18 studies in people with diabetes showed that magnesium supplements reduced fasting plasma glucose levels. In people who are at high risk for diabetes, magnesium supplementation significantly improved plasma glucose levels after a 2-hour oral glucose tolerance test. These effects are thought to be due to the effects of magnesium on insulin receptors and signaling that allows for improvement in glucose transport and utilization.
Magnesium and vascular health
Magnesium levels have been associated with a lower incidence of cardiovascular disease. In fact, supplementing with magnesium was associated with improvement in vascular flow and endothelial function. Endothelial function refers to the lining of the blood vessels, which is involved in regulating blood vessel health and blood clotting.
Studies in patients receiving dialysis have shown that having a lower serum magnesium level is a significant risk for cardiovascular mortality. Laboratory data show that magnesium inhibits high phosphate-induced calcification of vascular smooth muscle cells. Calcification of arteries is a strong predictor of heart disease and heart-disease-related death.
Magnesium and vitamin D
Magnesium is essential to vitamin D metabolism. Vitamin D that we eat or make in our skin from sun exposure circulates in the blood and is bound to vitamin D binding protein (VDBP). VDBP binding activity depends on adequate magnesium levels. In addition, magnesium is an essential cofactor for the enzymes that activate vitamin D. Studies have demonstrated that magnesium deficiency is associated with impaired vitamin D metabolism.
On the other hand, taking large doses of vitamin D can induce severe depletion of magnesium. This is thought to be due to the overutilization of magnesium. Therefore, adequate magnesium supplementation should be an important part of vitamin D therapy.
Adequate magnesium supplementation should be an important part of vitamin D therapy.
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Magnesium and bone health
Besides magnesium’s effects on vitamin D metabolism, it is an essential component of hydroxyapatite, an essential component of bone and teeth. In fact, 60% of total Mg is stored in the bone. Low magnesium intake was found to be associated with lower bone mineral density in postmenopausal women. Magnesium deficiency contributes to osteoporosis directly by acting on crystal formation and on bone cells and indirectly by impacting the secretion and the activity of parathyroid hormone (PTH) and by promoting oxidative stress and inflammation.
In addition, a review of 8 studies looked at magnesium and chronic kidney disease (CKD). The study investigated magnesium supplementation on parameters of CKD-related mineral bone disease (CKD-MBD). Mg supplementation improved PTH levels and carotid intima-media thickness (CIMT). Low serum Mg levels were also found to impact PTH and worsen osteoporosis in CKD patients, particularly with diabetes.
Magnesium and kidney stones
Mg acts as an inhibitor of calcium oxalate crystallization and stone formation in the urine. It also decreases the absorption of dietary oxalate in the gut. Mg supplementation in patients with kidney stones was found to decrease the incidence of stone formation even in patients without signs of Mg deficiency.
Magnesium as a phosphate binder
Hyperphosphatemia (high phosphate level) is common in advanced kidney disease. Many kidney patients with stage 4 and above use binders that bind phosphate (or “phosphorus,” as it is commonly known) in the food and prevent it from getting absorbed. High phosphate levels have been associated with poor bone and vascular health in kidney patients. In fact, higher dietary phosphate load can be seen in earlier stages of CKD, and it can do harm even before it is detected.
Magnesium carbonate has been successfully used as a phosphate binder. Magnesium based phosphate binders were also found to reduce vascular calcifications in rats with kidney disease. Iron-magnesium hydroxycarbonate was also studied and found to be well tolerated and can effectively lower phosphate levels in dialysis patients. It is essential to know that most of the magnesium used as a phosphorus binder will not be absorbed.
The bottom line on magnesium and kidneys
Magnesium is essential to many biological functions. It has many health benefits for kidney, bone, and vascular health. Optimizing magnesium status is, therefore, an important step in the integrative approach to kidney health. In part two of this blog, “Magnesium Deficiency: Assessment and Management for Better Kidney Health,” we will discuss practical steps for figuring out a person’s actual magnesium status, the best form of magnesium to take, and the dose I recommend for each condition.
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