About 700,000 individuals are affected by chronic kidney disease (CKD) throughout the world. In fact, according to the CDC, 1 in every 7 people in the US have CKD. The majority of risk factors for CKD are related to lifestyle factors or conditions related to lifestyle disease. These lifestyle factors include impaired fasting glucose, elevated blood pressure, high body mass index, a high sodium diet and exposure to lead. In this blog, we will focus on the link between lead exposure and kidney health.

Although there has been a considerable reduction in lead exposure over the last few decades, low level exposure is still common, globally. Concerns about chronic low-level lead toxicity are associated with gradual accumulation of the heavy metal in the body. 


Sources of lead exposure

Lead contamination can be due to exposure to various household products, water, soil, and air. Most significant sources of lead include:

  • Homes built before 1978 (when lead-based paints were banned) probably contain lead-based paint. 
  • Water pipes may contain lead (recently we learned about the impact on which can lead to contamination of community water crisis as it has happened in Flint, MI).
  • Some toys
  • Jewelry
  • Cosmetics 
  • People involved in jobs and hobbies working with stain glass, ceramic glazing, welding and batteries
  • Aviation fuel (living near airports may increase risk of exposure in air and soil)

It is estimated that a large population of adults and children in the United States have blood lead levels that are higher than what is considered safe. 



How does the body handle lead?

When it enters the GI tract, lead utilizes the iron gates (Divalent metal transporter (DMT1)) in the gut to enter systemic circulation. In the case of mineral deficiency, especially iron deficiency, lead can more easily compete for absorption via DMT1. This is significant, considering the low mineral status of the Standard American Diet (SAD). Furthermore, lead can compete with iron for incorporation into heme by inhibition of an enzyme called 6-aminolevulinic acid dehydratase (ALAD), increasing risk of iron-deficiency anemia. 

Lead cannot be converted by the body, and is either stored in tissue (primarily in bone, replacing calcium) or eliminated (primarily through the kidneys and gut). It can accumulate and remain stored in the bones for decades, and is released into the blood under certain circumstances such as pregnancy, breast-feeding, menopause, weight loss and advancing age.

How the kidneys handle lead

Lead competes with  iron and calcium due to similarities in atomic size. After lead is filtered by the glomeruli, it enters the proximal tubular cells via calcium channels. In fact, lead is 10 times more efficient at utilizing calcium channels than calcium itself. Some of it returns to recirculate in the blood while some is transported back to the tubular lumen through other transporters. This constant exposure causes damage to the tubules and increases oxidative stress by using up glutathione, an antioxidant. 


The effect of lead on the kidneys

The kidneys are the major site of elimination for lead and appear to be one of the primary sites of accumulation. Even exposure to small levels of lead early in life can lead to glomerular hypertrophy and may disrupt glomerular development leading to renal insufficiency later in life. 

However, the majority of lead toxicity in the kidneys is due to its effects on the tubules. Chronic exposure has been shown to lead to progressive tubulointerstitial nephritis including inflammation, fibrosis, and atrophy. The mechanism involves oxidative stress, mitochondrial injury, and acting as a functional substitute to calcium and increasing unchecked activity of protein kinase C. Lead can also replace calcium in the cellular tight junctions compromising its integrity. Finally, lead decreases the ability of the tubules to eliminate uric acid.

Collectively, these lead to the classic triad of lead exposure, which includes progressive kidney disease, elevated blood pressure, and gout.


Nutrients and lead exposure

It makes sense now to understand that a deficiency in iron and calcium can lead to an increase in lead toxicity. It has been documented that the absorption of lead in the gut is actually inversely proportional to dietary levels of calcium. Studies in children demonstrated a relationship between dietary calcium and blood levels of lead by linking a low dietary intake of calcium to higher lead levels. Indeed, increasing dietary calcium intake has been shown to decrease blood levels of lead.


Genetics and lead exposure

Genetic mutations in iron and calcium metabolism can greatly impact lead toxicity. In fact, genetic mutations in the gene coding for ALAD have been shown to affect blood and bone lead levels. In addition, polymorphisms in the gene for vitamin D receptor (VDR) were found to influence the accumulation of lead in bone. VDR is involved in calcium absorption from the gut and its placement in bone.

Finally, variations in the hemochromatosis gene that codes for the HFE protein associated with iron absorption can also increase the risk of lead absorption. These genetic variations can increase an individual’s susceptibility to lead toxicity even from relatively low-level exposure. In other words, what may be a “safe” exposure level to one person may be a toxic level to another depending on genetic variables, especially when combined with other lifestyle or occupational factors.

The microbiome and lead exposure

Metabolomics is the study of the substrates and byproducts of metabolism of various microbes found in the body and their impact on the system. Studies in this emerging field have demonstrated that exposure to lead causes alterations in gut microbiome diversity and metabolic functions. These changes are responsible for the development of obesity when exposure to lead occurs in early childhood. Some of these changes are mediated through epigenetics

On the other hand, there is some evidence that preexisting depletions in the diversity and quantity of the gut microbiome increases the risk for lead toxicity. This may be independent or further complicated by the impact of dysbiosis on digestion, especially on calcium and iron absorption.

Neutralizing lead exposure

There are medications that are used to chelate lead including calcium disodium edetate (EDTA) which can be used for assessing body stores of lead and for treatment. Interestingly, calcium channel blockers such as verapamil have been found to protect the kidneys against the effects of lead toxicity.

Curcumin has been found to protect kidney cells from the oxidative stress of lead toxicity.
In addition, baicalin, a traditional Chinese herb, has been found to protect the kidneys in a similar manner.
Therapeutic treatment of iron or calcium deficiency can also be effective in reducing lead absorption. Therefore, monitoring mineral levels and supplementation might be a useful approach in management of these cases. 

Protecting the body from lead 

There are ways to protect the body from the negative effects of heavy metals, including lead. Incorporating therapeutic foods on a regular basis such as cilantro, blueberries, garlic, ginger, onion, green tea, and tomato supplies the body with vitamins, minerals, and nutrients that decrease the risk of lead toxicity. Certain essential metals and vitamins (zinc, calcium, iron, selenium, magnesium, vitamin C, B1, and B6) may be supplemented to provide protection and boost antioxidant levels. Other practices that help the body with detox are exercise, sweating, dry brushing, drinking enough water, and lymphatic massage. Correcting nutrient deficiencies through food and supplements, as well as incorporating routine detox practices, is key to prevent lead absorption and safely remove it from the body, especially in those at high-risk of exposure.

The Bottom Line

Lead exposure remains a global public health issue. Even low levels of lead exposure have been associated with decreased kidney function. In addition to addressing possible sources of exposure, an integrative medicine approach to lead toxicity should use appropriate nutritional evaluations and interventions, as well as biotransformation and antioxidant support to help decrease the impact of toxicity and the risk of chronic kidney disease.