Cobalt-Induced Chronic Kidney Disease

Cobalt (Co) is mostly known from cobalt-based blue pigments and these have been used since antiquity for jewelry and paints, and to impart a distinctive blue tint to glass. Its name was derived from kobold ore (German for 'goblin' ore) because they were poor in known metals and gave off poisonous arsenic-containing fumes when smelted. These days, Cobalt is primarily used in lithium-ion batteries.

[Roman Cobalt Blue Glass Unguentarium]

The blue pigment, cobalt blue, is toxic when ingested or inhaled. Its use requires appropriate precautions to avoid internal contamination and to prevent cobalt poisoning, otherwise known as cobaltism.

Still, Cobalt is an essential element for health in animals, including humans, in minute amounts as a component of vitamin B12, the deficiency of which can be fatal, as in the disease pernicious anemia.

Recent research shows that 'Higher levels of .. Co are significantly associated with increased advanced CKM risk among US adults'[1]. CKM means Cardiovascular-Kidney-Metabolic syndrome, which is defined as a health disorder attributable to connections among obesity, diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD), including heart failure, atrial fibrillation, coronary heart disease, stroke, and peripheral artery disease. CKM syndrome includes those at risk for CVD and those with existing CVD.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Cobalt-Induced Chronic Kidney Disease.

[1] Yan et al: Urinary metal exposure, systemic inflammation, and advanced cardiovascular-kidney-metabolic syndrome risk in US adults in Biometals - 2026

Arsenic-Induced Chronic Kidney Disease

From reading Agatha Christie's mysteries you will probably know that arsenic poisoning occurs over a brief period, symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhoea that contains blood[1]. Chronic exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhoea, heart disease, numbness, and cancer.

Ah, you might think, arsenic poisoning is a thing of the past, when (mostly) female murderers were using rat poison to get rid of the philandering husbands. Not so.

Inorganic arsenic (as opposed to the less poisonous organic arsenic) is naturally present at high levels in the groundwater of a number of countries, including Argentina, Bangladesh, Cambodia, Chile, China, India, Mexico, Pakistan, the USA, and Vietnam. Drinking water, crops irrigated with contaminated water, and food prepared with contaminated water are sources of exposure. Thus, arsenic poisoning is still a global health problem affecting many millions of people [Source: Fact sheet WHO].

Additionally, you can get poisoned from mining and other industrial processes where arsenic is inadvertently inhaled or ingested.

People who smoke tobacco can also be exposed to the natural inorganic arsenic content of tobacco because tobacco plants can take up arsenic that is naturally present in the soil.

Arsenic is also present as a contaminant in many traditional remedies.

Arsenic exerts its toxicity by inactivating up to 200 enzymes, especially those involved in cellular energy pathways and DNA synthesis and repair.

There are no evidence based treatment regimens to treat chronic arsenic poisoning.

A systematic review of the recent literature suggests evidence that exposure to arsenic may be associated with Chronic Kidney Disease[2]. Studies of arsenic exposure were mixed, but the highest quality studies reported negative impacts of arsenic on kidney function and Chronic Kidney Disease incidence.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Arsenic-Induced Chronic Kidney Disease.

[1] Ratnaike: Acute and chronic arsenic toxicity in Postgraduate Medical Journal – 2003. See here.
[2] Moody et al: Toxic metals and chronic kidney disease: A systematic review of recent literature in Current Environmental Health Reports – 2019. See here.

Chronic Kidney Disease and Mees' Lines

Mees' Lines are also known as Aldrich–Mees lines and leukonychia striata. They are white lines of discoloration across the with of the nails of the fingers and toes (leukonychia). As the nail grows they move towards the end, and finally disappear when trimmed.

Mees' lines appear after an episode of poisoning with arsenic, thallium or other heavy metals*, such as lead and chromium, or selenium, opioid MT-45, fluorine, and can also appear if the subject is already suffering from kidney failure. They have also been observed in chemotherapy patients. Other possible causes include altitude sickness, cancer, carbon monoxide poisoning, heart failure, tuberculosis, leprosy, and malaria.

Although the phenomenon is named after Dutch physician Rudolf Adriaan Mees, who described the abnormality in 1919, earlier descriptions of the same abnormality were made by Englishman Ernest S. Reynolds in 1901, and by American Charles John Aldrich in 1904.

Mees described three patients with ‘polyneuritis arsenicosa’ (polyneuropathy due to acute arsenic intoxication) as a result of ingesting a large single dose of arsenic salts[1]. He discussed two cases of attempted suicide and one of attempted murder.

Mees lines can be linked to Chronic Kidney Disease as a sign of systemic stress or toxin buildup. While Chronic Kidney Disease patients often get distinctive 'Lindsay's nails' (half white/half brown), Mees' lines indicate a serious underlying issue affecting nail matrix development, needing medical investigation for the root cause.

To conclude: Mees' lines can occur [1] if you already have Chronic Kidney Disease, because your kidneys cannot process the toxins anymore, or [11] if the toxins themselves have damaged the kidneys so much that Chronic Kidney Disease is the resulting effect.

* The most widely used toxicology textbook, Casarett & Doull’s Toxicology: The Basic Science of Poisons, 9th edition (2018) uses term 'toxic metal', not 'heavy metal', which is more illuminating.

[1] Mees: Een Verschijnsel bij Polyneuritis Arsenicosa in Nederlands Tijdschrift voor Geneeskunde 1919. See here.

Sickle Cell Disease-Induced Chronic Kidney Disease

Sickle Cell Disease (SCD), also simply called sickle cell, is a group of inherited haemoglobin-related blood disorders. The most common type is known as sickle cell anaemia. This results in an abnormality in the oxygen-carrying protein haemoglobin found in red blood cells. This leads in turn to the red blood cells adopting an abnormal sickle-like shape under certain circumstances. With this shape, they are unable to deform as they pass through capillaries, causing blockages, which really hurts.

People with this mutation are (relatively) protected against the danger of dying of malaria[1].

Sickle Cell Disease causes several negative kidney manifestations. These include defects in urine concentration, impaired handling of potassium and hydrogen ion, albuminuria, acute kidney injury, and Chronic Kidney Disease just to name a few[2].

Glomerular hyperfiltration, tubular hyperfunctioning, endothelial damage from repeated sickling and vaso-occlusive episodes, and iron-induced proinflammatory changes in the glomerular mesangium and tubulointerstitium are some of the mechanisms of kidney damage.

Albuminuria is one of the most and common clinical features of kidney disease and progresses with age. Kidney disease in patients with sickle cell is also associated with increased mortality.

Adequate hydration, angiotensin-converting enzyme inhibitors, and adequate control of sickle cell are the main stay of treatment for albuminuria. The haemoglobin goal for patients with sickle cell nephropathy is lesser (10 g/dL) than that for patients with Chronic Kidney Disease due to other causes, given that a higher haemoglobin level increases viscosity and the risk of precipitating vaso-occlusive episodes.

Also, recurrent episodes of vaso-occlusion and inflammation will result in progressive damage to most organs, including the brain, kidneys, lungs, bones, and cardiovascular system, which becomes apparent with increasing age[3].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Sickle Cell Disease-Induced Chronic Kidney Disease.

[1] Luzzatto: Sickle Cell Anaemia and Malaria in Mediterranean Journal of Hematology and Infectious Diseases - 2012
[2] Amarapurkar et al: Sickle Cell Disease and Kidney in Advances in Chronic Kidney Disease – 2022
[3] Rees: Sickle-cell disease in The Lancet - 2010

Hemochromatosis-Induced Chronic Kidney Disease

Hemochromatosis is a (mostly) genetic disorder characterized by an abnormal increase in iron absorption from the diet, leading to iron overload in various organs including the liver, heart, pancreas, and kidneys[1].

Kidney damage and dysfunction results from excessive iron accumulation. In hemochromatosis, excess iron is deposited in the kidney glomeruli and distal tubules, resulting in progressive damage and kidney dysfunction[2].

Several mechanisms contribute to kidney injury, including inflammation, oxidative stress, and fibrosis[3]. The accumulation of iron in the kidney tubules can also impair their function, resulting in inadequate reabsorption and secretion processes, leading to electrolyte imbalances such as hypokalemia, hypomagnesemia, and hyperphosphatemia. It may also cause impaired acid-base balance, which leads to metabolic acidosis.

Excessive iron deposition in the renal parenchyma may cause nephrocalcinosis. Consequently, kidney function may be impaired, resulting in kidney stones. Chronic iron overload in the kidneys triggers fibrotic changes, leading to progressive kidney damage and eventually end-stage renal disease. Hemochromatosis renal manifestations can vary from mild abnormalities in kidney function to more severe conditions such as end-stage renal disease.

Hemochromatosis can therefore lead to Chronic Kidney Disease (CKD) due to excess iron accumulation in the kidneys, causing progressive damage through inflammation, oxidative stress, and fibrosis.

What could be the first symptom you might find if you're afflicted with Hemochromatosis? Possibly melanoderma (darkening or 'bronzing' of the skin), especially of your hands. Which also explaines the name of this disease: From hemo- ('blood') + chromat- ('colour') + -osis ('abnormal condition'). It describes the changing colour of blood affected by the disorder.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Hemochromatosis-Induced Chronic Kidney Disease.

[1] Piperno et al: Inherited iron overload disorders in Translational Gastroenterology and Hepatology - 2020
[2] Ozkurt et al: Renal hemosiderosis and rapidly progressive glomerulonephritis associated with primary hemochromatosis in Renal Failure - 2014
[3] Lv et al: Oxidative Stress and Renal Fibrosis: Recent Insights for the Development of Novel Therapeutic Strategies in Frontiers in Frontiers in Physiology - 2018

Chronic Kidney Disease and Vitamin D Deficiency

Vitamin D
Vitamin D, also known as calciferol, is a fat-soluble vitamin. It is an essential nutrient that supports strong bones by helping the body absorb calcium and phosphorus. It also plays a vital role in the functioning of the immune system, muscles, and nerves. The body produces vitamin D when exposed to sunlight, but it can also be found in certain foods such as fatty fish, eggs, and fortified milk.

In foods and dietary supplements, vitamin D has two main forms, D₂ (ergocalciferol) and D₃ (cholecalciferol), that differ chemically only in their side-chain structures. Both forms are well absorbed in the small intestine. The concurrent presence of fat in the gut enhances vitamin D absorption, but some vitamin D is absorbed even without dietary fat. Neither aging nor obesity alters vitamin D absorption from the gut.

Vitamin D Deficiency
Vitamin D deficiency is more common among people who are lactose intolerant, have a milk allergy, or follow an ovo-vegetarian or vegan diet. Deficiency may also occur in people who have limited exposure to sunlight, those whose kidneys cannot convert 25(OH)D (or 25-hydroxyvitamin D) to its active form, 1,25-dihydroxyvitamin D (calcitriol), or those who cannot absorb vitamin D efficiently in the digestive tract. Vitamin D deficiency can manifest as rickets in children and as osteomalacia in adolescents and adults.

Growing evidence has indicated that vitamin D deficiency may contribute to deteriorating kidney function, as well as increased morbidity and mortality in patients with Chronic Kidney Disease[1].

Vitamin D Deficiency and Chronic Kidney Disease
Vitamin D deficiency does not directly cause Chronic Kidney Disease, but it is strongly associated with its progression and complications[2].

Vitamin D deficiency is common in patients with Chronic Kidney Disease, because the kidneys play a key role in converting 25-hydroxyvitamin D to its active form. As kidney function declines, this conversion is impaired, leading to low vitamin D levels.

These low vitamin D levels can exacerbate Chronic Kidney Disease-related issues, such as secondary hyperparathyroidism, bone disease (renal osteodystrophy), and cardiovascular complications, by disrupting calcium and phosphorus metabolism.

Supplements
Recent studies have suggested that treatment with active vitamin D or its analogues can ameliorate kidney injury by reducing fibrosis, apoptosis, and inflammation (in animal models). This treatment also decreases proteinuria and mortality in patients with Chronic Kidney Disease[3].

[1] Andreas: Vitamin D in chronic kidney disease: a systemic role for selective vitamin D receptor activation in Kidney International - 2006
[2] Dusso, Tokumoto: Defective renal maintenance of the vitamin D endocrine system impairs vitamin D renoprotection: a downward spiral in kidney disease in Kidney International - 2011
[3] Alvarez et al: Effects of high-dose cholecalciferol on serum markers of inflammation and immunity in patients with early chronic kidney disease in Europese Journal of Clinical Nutrition - 2013

Baclofen-Induced Chronic Kidney Disease

Baclofen is a medication often used to treat muscle spasticity, such as from a spinal cord injury or multiple sclerosis. It may also be used for intractable hiccups and muscle spasms near the end of life, and off-label to treat alcohol abuse or opioid withdrawal symptoms. Baclofen is also used in the treatment of sleep-related painful erections.

Chemically, baclofen is a derivative of the neurotransmitter GABA (γ-aminobutyric acid). It is believed to work by activating (or agonizing) GABA receptors, specifically the GABAB receptors.

It can be administered orally or (in severe cases) by intrathecal pump (delivered directly into the spinal canal via an implantable pump device). It is sometimes used transdermally (applied topically to the skin).

Adverse effects of baclofen include drowsiness, dizziness, weakness, fatigue, headache, trouble sleeping, nausea and vomiting, poor concentration and recall (resembling dementia), urinary retention, or constipation.

Around 70 to 85 percent of baclofen gets excreted unchanged in the urine. Which means that the duration of its action gets prolonged in patients with kidney problems. Reports have suggested that patients with Chronic Kidney Disease may be especially at risk for the adverse effects[1]. Older patients appear to be even more sensitive to baclofen's adverse effects[2].

As baclofen does not readily cross the blood-brain barrier, patients may require a high dose to treat their spasticity effectively. As a result of this, most of the patients also develop neurotoxicity with encephalopathy (a change in how your brain functions)[3].

It will not come as a great surprise, but in the US baclofen has been increasingly used as a recreational drug by adolescents. Also, from 2014 to 2017 baclofen misuse, toxicity and use in suicide attempts among adults in the US have significantly increased[4].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Baclofen-Induced Chronic Kidney Disease.

[1] Wolf et al: Baclofen Toxicity in Kidney Disease in American Journal of Kidney Diseases – 2018
[2] Chauvin et al: Baclofen has a risk of encephalopathy in older adults receiving dialysis in Kidney International - 2002
[3] Muanda et al: Association of Baclofen With Encephalopathy in Patients With Chronic Kidney Disease in JAMA – 2019
[4] Reynolds et al: Trends in gabapentin and baclofen exposures reported to U.S. poison centers in Clinical Toxicology - 2020

Diabetes-Induced Chronic Kidney Disease

Diabetes type-2 is a major health concern, and one of its most serious complications is Chronic Kidney Disease (CKD). Chronic Kidney Disease is a common comorbidity in patients with type-2 diabetes mellitus and both conditions are increasing in prevalence[1].

Over time, high blood sugar damages kidney blood vessels, leading to diabetic nephropathy, which can progress to Chronic Kidney Disease. Up to one-third of people with diabetes may develop Chronic Kidney Disease, making awareness and early action vital.

Chronic Kidney Disease often develops ever so slowly and with just a few symptoms. As it worsens, you may notice swelling, fatigue, frequent urination, or high blood pressure.

Many people don't even realize they have Chronic Kidney Disease until it's well advanced (read: too late). At that point, you need dialysis (a treatment that filters the blood) or a kidney transplant to survive.

Therefore, if you have diabetes, get your kidneys checked regularly. This is done by your doctor with simple blood and urine tests. Regular testing is your best chance for identifying Chronic Kidney Disease early if you do develop it. Early treatment is most effective and can help prevent additional health problems.

Key risk factors include uncontrolled diabetes, hypertension, obesity, and smoking. Regular screening with blood and urine tests is crucial for early detection.

Some medications can somewhat slow the progression of Chronic Kidney Disease. Stay proactive to keep your kidneys healthy.

But the problems do not stop here, because heart failure is often linked to diabetes and Chronic Kidney Disease[2]. These are commonly occurring and interlinked conditions. Approximately 25% to 40% of patients with heart failure have diabetes, and approximately 40% to 50% of patients with heart failure have Chronic Kidney Disease. Thus both diabetes and Chronic Kidney Disease are associated with increased risk of heart failure.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Diabetes-Induced Chronic Kidney Disease. progression.

[1] Thomas et al: Changing epidemiology of type 2 diabetes mellitus and associated chronic kidney disease in Nature Reviews. Nephrology - 2016
[2] Vijay et al: Heart Failure in Patients with Diabetes and Chronic Kidney Disease: Challenges and Opportunities in Cardiorenal Medicine – 2022

Borax-Induced Chronic Kidney Disease

Exposure to boron and related compounds, such as borax, have been recently implicated as a potential cause of Chronic Kidney Disease in Southeast Asia[1].

For readers that do not have a clue about chemistry: boron (B) isn't the same as borax (Na₂H₂₀B₄O₁₇) as some websites erroneously claim.

Borax (or sodium borate) is not safe for human consumption. It is a naturally occurring mineral used in cleaning products, laundry detergents, pesticides, and industrial applications. Ingesting borax can cause serious health issues, including nausea, vomiting, diarrhoea, abdominal pain, and, in severe cases, organ damage or death.

Some online sources, particularly in 'alternative health communities', have promoted borax for supposed health benefits, like treating arthritis or balancing hormones. These claims lack any scientific evidence and are potentially dangerous. Studies indicate borax can cause toxicity at doses as low as 2-3 grams in children and 10-20 grams in adults. There is no established safe level of borax for human consumption. The FDA has not approved borax as a food additive, and it is considered toxic when consumed, even in small amounts.

A recent TikTok trend involves ingesting borax mixed with water, with some claims suggesting it can reduce joint pain, inflammation, body weight, body toxins, and more. But in the real world, where science reigns supreme, there are no proven health benefits associated with drinking borax, and it has not been approved for any health-related use.

Drinking toxic borax is extremely dangerous — even when diluted in water – and can lead to serious health problems, such as neurological problems, gastrointestinal issues, headaches, mood changes, hormone disruption, and chronic kidney damage. Toxicity of borax may lead to cellular toxicity and even genetic defects in humans[2].

Unfortunately, false claims spread on social media, may influence worrisome behaviours, particularly among children and mentally challenged adults.

Scientific research suggests that acute borax toxicity can lead to acute kidney insufficiency in humans[1].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Borax-Induced Chronic Kidney Disease.

[1] Pahl et al: Boron and the kidney in Journal of Renal Nutrition - 2005
[2] Pongsavee: Effect of borax on immune cell proliferation and sister chromatid exchange in human chromosomes in Journal of Occupational Medicine and Toxicology - 2009

Chronic Kidney Disease in Cats

Chronic Kidney Disease in cats is one of the most prevalent diseases in older cats, affecting up to 40% of cats over the age of 10 and 80% of cats over the age of 15.

Like in humans, healthy kidneys perform many functions in cats, including filtering the blood, making urine, and helping to regulate blood pressure.

Chronic Kidney Disease in cats refers to the persistent loss of kidney function over time and can have many health consequences.

The only known risk factor for the development of CKD in cats is age, so it is very important for all senior cats to be regularly monitored for this disease.

In the early stages of Chronic Kidney Disease in cats, it is very common for cats to show no obvious clinical signs, as their body is able to compensate for the decrease in kidney function. As the kidneys lose their ability to concentrate urine effectively, cats may begin to urinate greater volumes and drink more water to compensate. The loss of important proteins and vitamins in their urine may contribute to abnormal metabolism and loss of appetite. Eventually, cats with Chronic Kidney Disease may experience a buildup of the waste products and other compounds in the bloodstream that are normally removed or regulated by the kidneys. This accumulation may make them feel ill and appear lethargic, unkempt, and lose weight.

Dietary modification is an important and proven aspect of treatment for Chronic Kidney Disease in cats. Therapeutic diets that are restricted in protein, phosphorus and sodium content and high in water-soluble vitamins, fiber, and antioxidant concentrations may prolong life and improve quality of life in cats with Chronic Kidney Disease.

Paracetamol-Induced Chronic Kidney Disease

New research, led by scientists at the University of Nottingham, has found that repeated doses of paracetamol in people aged 65 and over, can lead to an increased risk of gastrointestinal, cardiovascular and renal complications[1].

The new study shows that care must be taken when repeated doses are required for chronic painful conditions such as osteoarthritis in older people.

“Due to its perceived safety, paracetamol has long been recommended as the first line drug treatment for osteoarthritis by many treatment guidelines, especially in older people who are at higher risk of drug-related complications,” Professor Weiya Zhang explained.

The study analysed data from the Clinical Practice Research Datalink-Gold. Participants were aged 65 and over with an average age of 75, and had been registered with a UK GP practice for at least a year between 1998 and 2018.

Researchers looked at the health records of 180,483 people who had been prescribed paracetamol repeatedly (≥2 prescriptions within six months) during the study. Their health outcomes were then compared to 402,478 people of the same age who had never been prescribed paracetamol repeatedly.

The findings showed that prolonged paracetamol use was associated with an increased risk of peptic ulcers, heart failure, hypertension and chronic kidney disease.

Professor Zhang adds: “Whilst further research is now needed to confirm our findings, given its minimal pain-relief effect, the use of paracetamol as a first line pain killer for long-term conditions such as osteoarthritis in older people needs to be carefully considered.”

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Paracetamol-Induced Chronic Kidney Disease.

[1] Kaur et al: Incidence of Side Effects Associated With Acetaminophen in People Aged 65 Years or More: A Prospective Cohort Study Using Data From the Clinical Practice Research Datalink in Arthritis Care and Research - 2024. See here.

High Protein Diet-Induced Chronic Kidney Disease

Some of us are forever trying to lose weight. Theoretically, you should consume fewer calories than you spend. But that easier said than done and people often try to lose weight by dieting. All sorts of diets exist, but most of them will not work in the long term.

In the last few years, people often decide to adopt a high-protein diet. Eating protein helps a person feel full, which can lead to them eating fewer calories overall. High-protein diets typically include large quantities of protein and only a small amount of carbohydrate. High-protein diets are thus the same as low-carbohydrate diets (or Lo-Carb Diets).

Most people can follow a high-protein diet by eating mostly meat, fish, and dairy products. This diet will help you to reduce your weight in the short term, but a life without carbohydrates (bread, pasta, potatoes, etc) isn't the most healthy option.

In fact, a high protein diet is a bit of a double-edged sword. Yes, you can lose weight with it, but it can also have some detrimental effects on your kidneys.

Scientific evidence suggests that kidneys might be damaged in individuals with—and perhaps without—impaired kidney function. High dietary protein intake can cause intraglomerular hypertension, which may result in kidney hyperfiltration, glomerular injury, and proteinuria. It is possible that long-term high protein intake may lead to de novo Chronic Kidney Disease[1].

It is prudent, so concludes another study, to avoid recommending high-protein intake for weight loss in obese or diabetic patients or those with prior cardiovascular events or a solitary kidney if kidney health cannot be adequately protected[2].

Red and processed meat are being adversely associated with the risk of Chronic Kidney Disease risk, while nuts, low-fat dairy products, and legumes being protective against the development of Chronic Kidney Disease[3]. That means that following the so-called Mediterranean Diet is possibly the only healthy option if you want to lose weight, while at the same time protecting your kidneys.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): High Protein Diet-Induced Chronic Kidney Disease.

[1] Ko et al: The Effects of High-Protein Diets on Kidney Health and Longevity in Journal of the American Society of Nephrology – 2020. See here.
[2] Kalantar-Zadeh: High-protein diet is bad for kidney health: unleashing the taboo in Nephrology, Dialysis, and Transplantation – 2020. See here.
[3] Haring et al: Dietary Protein Sources and Risk for Incident Chronic Kidney Disease: Results From the Atherosclerosis Risk in Communities (ARIC) Study in Journal of Renal Nutrition – 2017. See here.

Smoking-Induced Chronic Kidney Disease

Everybody knows (of should know) that smoking is a habit that isn't particularly healthy. Cigarette smoke contains several poisonous chemicals of which nicotine is the best known.

Cigarette smoke contains 4,000 or more chemicals, such as nicotine, tar, phenol, acetic acid, CO, CO₂, NO, and NO₂. Nicotine is an alkaloid that has a significant effect on your blood vessels. It is a vasoconstrictor. When you smoke, nicotine causes your blood vessels to constrict, which reduces the amount of blood that can flow through them. Blood transports vital oxygen to your organs.

Plus, over time, the continual vascular constriction from smoking makes your blood vessels more narrow and stiff. The organs, body tissues, and cells throughout your entire body receive much less oxygen and nutrients than they would if you didn’t smoke. Constricted blood vessels also make your heart beat faster and your blood pressure go up.

If you smoke long enough, the people around you will start to notice that the skin on your face has become greyish and pale. The tiny veins in your outer skin (epithelium) are chronically devoid oxygenated blood and are starting to die.

But that effect not only causes your skin to slowly deteriorate. The nicotine will have the same effect inside your body. In your lungs, the smallest arteries, called arterioles, will also chronically constrict and eventually cause shortness of breath and chronic obstructive pulmonary disease (COPD).

Other organs, like your kidneys, are under threat too.

In a study, scientists found that current and former smokers had significantly increased odds of Chronic Kidney Disease compared with never smokers[1]. If you stop smoking, the risk of suffering from a Chronic Kidney Disease will decrease with 18%. Another study showed that smoking was associated with a higher risk of incident Chronic Kidney Disease among healthy middle-aged adults[2]. Furthermore, the risk of adverse kidney outcome was incrementally higher as smoking pack-years were higher[3].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Smoking-Induced Chronic Kidney Disease.

[1] Kelly et al: Modifiable Lifestyle Factors for Primary Prevention of CKD: A Systematic Review and Meta-Analysis in Journal of the American Society of Nepnhrology – 2021. See here.
[2] Jo et al: Association of smoking with incident CKD risk in the general population: A community-based cohort study in PloS One 2020. See here.
[3] Lee et al: Smoking, Smoking Cessation, and Progression of Chronic Kidney Disease: Results From KNOW-CKD Study in Nicotine and Tobacco Research – 2021. See here.

Chromium-Induced Chronic Kidney Disease

Chromium is steely-grey, hard, and brittle metal. As chromium metal has a high corrosion resistance and hardness, it is added to iron to form an alloy called stainless steel (or rather rustless steel). The name of the element is derived from the Ancient Greek word chrōma (χρῶμα), which means 'colour'.

As a trace element, chromium is naturally present in many foods, including meats, grain products, fruits, vegetables, nuts, spices, brewer’s yeast, beer, and wine. However, chromium amounts in these foods vary widely depending on local soil and water conditions, as well as the agricultural and manufacturing processes used to produce them.

In the United States, trivalent chromium (Cr(III)) ion is considered an essential nutrient in humans, supposedly necessary for the metabolism of insulin, sugar, and lipids. However, in 2014, the EFSA (European Food Safety Authority) concluded that there was insufficient evidence for chromium to be recognized as essential.

While chromium metal and Cr(III) ions are considered non-toxic or even beneficial, hexavalent chromium, Cr(VI), is toxic and carcinogenic. Chromium trioxide that is used in industrial electroplating processes is a substance of very high concern.

Kidney disease is often cited as one of the adverse effects of chromium. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by some reports in chromium workers[1]. It raises the possibility that low-level, long-term exposure may produce persistent kidney damage, researchers wrote in 1991.

However, in 2023 the situation has dramatically changed. Now even beauticians are at risk for chronic kidney diseases. Some cosmetic products, such as eye shadows, may contain worrying levels of chromium, and if you are in daily contact with these products your kidneys may be in danger of irreversible damage[2][3].

Scientists also found that the older you get, the more kidney damage you may have[4].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Chromium-Induced Chronic Kidney Disease.

[1] Wedeen, Qian: Chromium-induced kidney disease in Environmental Health Perspectives – 1991
[2] Mahmoodi et al: Urinary levels of potentially toxic elements (PTEs) in female beauticians and their association with urinary biomarkers of oxidative stress/inflammation and kidney injury in The Science of the total Environment - 2023. See here.
[3] Kang et al: Determination of hexavalent chromium in cosmetic products by ion chromatography and postcolumn derivatization in Contact Dermatitis - 2006
[4] Wu et al: Threshold effect of urinary chromium on kidney function biomarkers: Evidence from a repeated-measures study in Ecotoxicology and Environmental Safety - 2023

Chronic Kidney Disease and Cannabis

The Cannabis plant is a known bioaccumulator of non-essential harmful heavy metals such as arsenic (As), lead (Pb), chromium (Cr), mercury (Hg) and cadmium (Cd). It scavenges these heavy metals from the soil and these are distributed up through the stalk and into the leaves and flowers of the plant[1].

Arsenic, lead, chromium, mercury, and cadmium are toxic metals that have long-lasting detrimental effects on your body. All are causes for serious and potentially fatal Chronic Kidney Diseases.

Because smokers of cannabis inhale, researchers speculated that these users would have statistically higher levels of lead and cadmium in their blood than people who do not use weed[2].

They collected data from a group of more than 7,200 adults, of which 358 reported using marijuana within the past 30 days.

The marijuana users had 22% higher cadmium levels in their blood than non-users, and they had 27% higher blood lead levels than those who said they didn’t use either marijuana or tobacco.

“Both cadmium and lead stay in your body for quite a long time,” explained Tiffany Sanchez, an author of the study and an assistant professor of environmental health sciences at Columbia's Mailman School of Public Health. “Cadmium is absorbed in the renal system and is filtered out through the kidney. So, when you’re looking at urinary cadmium, that’s a reflection of total body burden, how much you have taken in over a long period of chronic exposure.”

Cadmium has been linked to kidney disease and lung cancer in people and fetal abnormalities in animals, according to the EPA, which has set specific limits for cadmium in air, water and food.

There is no safe amount of lead exposure, since even low levels can slow children’s brain development and result in learning and behavioral problems. In adults, chronic exposure to lead increases the risk of high blood pressure, heart problems and kidney damage.

Cadmium, meanwhile, is considered a human carcinogen by the World Health Organization. Exposure to low levels, such as through tobacco smoke, may lead to kidney disease and fragile bones.

[1] Bengyell et al: Global impact of trace non-essential heavy metal contaminants in industrial cannabis bioeconomy in Toxin Reviews - 2021
[2] McGraw et al: Blood and Urinary Metal Levels among Exclusive Marijuana Users in NHANES (2005-2018) in Environmental Health Perspectives - 2023

Lead-Induced Chronic Kidney Disease

Heavy metals are chemical elements that have a relatively high density and is toxic or poisonous at low concentrations. Examples of heavy metals include mercury (Hg), cadmium (Cd), arsenic (As), chromium (Cr), thallium (Tl), and lead (Pb).

Heavy metals are dangerous because they tend to bioaccumulate in your body. Compounds accumulate in living things any time they are taken up and stored faster than they are broken down (metabolized) or excreted.

Your kidneys are specifically designed by Mother Nature to rid your body of toxins.

Lead and its related components remain widely distributed in the environment and in some workplaces. Think of paint, old water mains and even food, cosmetics, and some folk medicine. For many years adverse human health effects have been recognized after heavy lead exposure. Only recently more subtle human effects have been suggested invoking nervous system, reproductive and kidney function. Chronic low level environmental lead exposure may subtly effect kidney function[1].

Scientists always want proof of cause and effect and therefore adult rats were subjected to exposure to lead to assess the effects of that lead administration on the kidney and testicular structure. They were killed 48 hours following lead administration. Yes, that's sad, but it was done in the name of science. Scientists found a negative effect of lead on the structure and function of kidney and testes[2].

Smoking seems to be one of the key factors responsible for high concentrations of lead in the kidneys. Furthermore, blood lead levels were 14% and 24% higher in children who lived with one or with two or more smokers, respectively, than they were in children living with no smokers[3].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Lead-Induced Chronic Kidney Disease.

[1] Bernard, Becker: Environmental lead exposure and the kidney in Journal of toxicology. Clinical toxicology – 1988
[2] Massanyi et al: Lead-induced alterations in rat kidneys and testes in vivo in Journal of Environmental Science and Health - 2007
[3] Apostolou et al: Secondhand Tobacco Smoke: A Source of Lead Exposure in US Children and Adolescents in American Journal of Public Health - 2012

Ethylene Glycol-Induced Chronic Kidney Disease

Ethylene glycol and diethylene glycol are odorless, colorless, flammable, viscous liquids. Both have a sweet taste, but they are lethally toxic in higher concentrations.

The major use of ethylene glycol and diethylene glycol is as an antifreeze agent in the coolant in for example, automobiles and air-conditioning systems. In the plastic industry, ethylene glycol is an important precursor to polyester fibers and resins.

Upon ingestion, ethylene glycol and diethylene glycol are oxidized into glycolic acid, which is, in turn, oxidized to oxalic acid, which is toxic. It and its toxic byproducts first affect the central nervous system, then the heart, and finally the kidneys. Ingestion of sufficient amounts is fatal if left untreated.

So, why would you ingest this highly toxic fluid? Why would you drink your car's antifreeze? You can ingest it because of criminal neglect.

The were a number of incidents in which glycerine (glycerol), one of the regular ingredients in cough syrup, has been replaced with ethylene glycol and/or diethylene glycol leading to some mass poisonings. Ethylene glycol and diethylene glycol simply are less-expensive alternatives to glycerine for industrial applications, however, both nephrotoxic and can result in Multiple Organ Dysfunction Syndrome (MODS), especially in children.

Toxic effects can include abdominal pain, vomiting, diarrhoea, inability to pass urine, headache, altered mental state, and acute kidney injury which may lead to death.

The latest cases of toxic cough syprup occured in The Gambia and Indonesia. In October 2022, the WHO announced a link between four brands of paediatric cough syrups from one Indian pharmaceutical company and the deaths of (to date) 66 children in The Gambia from kidney failure[1]. The products (Promethazine Oral Solution, Kofexmalin Baby Cough Syrup, Makoff Baby Cough Syrup, and Magrip N Cold Syrup) are believed to be contaminated with diethylene glycol and/or ethylene glycol. The products involved were manufactured by the Indian producer Maiden Pharmaceuticals. The syrups have been imported via Atlantic Pharmaceuticals Company Ltd, an somewhat shady US-based pharmaceutical company.

On October 20, 2022, Indonesia reported at least 99 pediatric deaths as a result of 'syrup medicines' that contained ethylene glycol and diethylene glycol.

On December 28, 2022, Uzbekistan reported the death of 18 children after they consumed India-made syrup that - you guessed it - contained ethylene glycol. According to the Uzbek Health Ministry, the syrups were manufactured by Indian drugmaker Marion Biotech. Again. Indians never learn.

On October 05, 2023, a report was published that syrups, for cough and allergic rhinitis, from two Indian manufacturers have been found to contain higher than permissible levels of contaminants – diethylene glycol and ethylene glycol. Cheating and corruption is endemic in India.

On 7 December 2023, the WHO reported that substandard (contaminated) syrup and suspension medicines, made in Pakistan by Pharmix Laboratories (PVT) LTD, were contaminated with ethylene glycol at levels ranging from 0.62 to 0.82% w/w relative to the accepted limit of not more than 0.10% w/w.

On 7 October 2025, news broke that at least 19 children, aged one to six, have died as a result of taking a common cough syrup. It contained 48.6% diethylene glycol. See here and here.

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Ethylene Glycol-Induced Chronic Kidney Disease.

[1] WHO: Medical Product Alert N°6/2022: Substandard (contaminated) paediatric medicines: Substandard (contaminated) paediatric medicines identified in WHO region of Africa – 5 October, 2022. See here.

Star Fruit-Induced Chronic Kidney Disease

Star fruit (Averrhoa carambola) is also known as carambola. It is the fruit of a species of tree that is native to tropical Southeast Asia. Nowadays, the tree is cultivated throughout tropical areas of the world.

The yellow fruit has distinctive ridges running down its sides. When cut in cross-section, the parts resembles a star, giving it the name of star fruit. The entire fruit is edible. It is usually consumened raw. It can also be cooked or made into relishes, preserves, garnish, and juices.

But star fruit has a bit of a dark side because it contains minute amounts of caramboxin (CBX), a potent neuroxin[1]. Individuals who already have some types of kidney disease are susceptible to adverse mild to severe neurological effects including intoxication, hiccups, vomiting, asthenia (abnormal physical weakness or lack of energy), mental confusion, seizures, coma, and death after eating star fruit.

Caramboxin has been identified as the neurotoxin responsible for these effects. It is a non-proteinogenic amino acid that stimulates the glutamate receptors in neurons. Its chemical structure is similar to the amino acid phenylalanine. Caramboxin is an agonist of both NMDA and AMPA glutamatergic ionotropic receptors with potent excitatory, convulsant, and neurodegenerative properties[1].

A possible interaction between caramboxin and oxalic acid, both present in starfruit can lead to both neurotoxic and nephrotoxic effects.

Consuming large amounts of starfruit or its juice on an empty stomach is not recommended, even for individuals with normal kidney function[2].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Star Fruit-Induced Chronic Kidney Disease.

[1] Garcia-Cairasco et al: Elucidating the neurotoxicity of the star fruit in Angewandte Chemie - 2009
[2] Moyses Neto et al: Star fruit: simultaneous neurotoxic and nephrotoxic effects in people with previously normal renal function in NDT Plus – 2009. See here.

PFAS-Induced Chronic Kidney Disease

Perfluoroalkyl and Polyfluoroalkyl Substances, better known by their acronym PFAS, are regarded as 'forever chemicals'. There are thousands of them.

PFAS molecules are made up of a chain of linked carbon and fluorine atoms. Because the carbon-fluorine bond is one of the strongest, these chemicals do not degrade in the environment. In fact, PFAS degrade so slowly (if at all) that scientists are unable to estimate an environmental half-life for PFAS, which is the amount of time it takes 50% of the chemical to disappear.

PFAS are widely used, long lasting chemicals. Variants of PFAS keep food from sticking to cookware, make clothes and carpets resistant to stains, and create firefighting foam that is more effective.

PFAS are used in industries such as aerospace, automotive, construction, electronics, and military. Because of their widespread use and their persistence in the environment, many PFAS are found in the blood of people and animals all over the world and are present at low levels in a variety of food products and in the environment.

It wouldn't be a problem if FPAS was 'just present' in the environment and in our body, but it has a detrimental effect on your kidneys[1]. Research shows that 'systemic changes were observed in the kidney, liver and testes, and histopathologic lesions such as renal tubular necrosis, hepatocellular necrosis, and germ cell degeneration were seen...'[2].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): FPAS-Induced Chronic Kidney Disease.

[1] Park et al: Perfluoroalkyl substances and cognitive function in older adults: Should we consider non-monotonic dose-responses and chronic kidney disease? in Environmental Research – 2021. See here.
[2] Han et al: Subacute dermal toxicity of perfluoroalkyl carboxylic acids: comparison with different carbon-chain lengths in human skin equivalents and systemic effects of perfluoroheptanoic acid in Sprague Dawley rats in Archives of Toxicology - 2020

Mycobacteria-Induced Chronic Kidney Disease

Mycobacterium tuberculosis
Tuberculosis (or TB) is an infectious disease usually caused by Mycobacterium tuberculosis bacteria. In South-East Asia and Western Pacific Regions, tuberculosis (or TB) is still a major public health issue and is expected to pose greater challenges with emergence of multi-drug resistance.

Spread of the mycobacterium to the kidney with a gradual, asymptomatic progression of the disease leads to delay in diagnosis. Involvement of urinary bladder and ureters leads to obstructive nephropathy. Extensive destructive caseous lesions, ulceration and dystrophic calcification involving renal parenchyma lead to CKD[1].

Involvement of the kidneys can also present as granulomatous interstitial nephritis that may be difficult to distinguish from sarcoidosis[2]. TB is the commonest cause of secondary amyloidosis in the Indian subcontinent[3]. Diagnosis of renal TB is usually unsatisfactory due to poor culture techniques, and poor sensitivity of nucleic acid based tests. In late disease, even with effective anti-tubercular drugs renal injury persists and leads to CKD[4].

Mycobacterium leprae
Leprosy caused by Mycobacterium leprae is another important mycobacterial infection of public health problem, which also involves the kidney. Despite reduction in its prevalence, leprosy remains endemic in many parts of the world particularly south Asia[5].

In a report of 122 cases from India, reduced creatinine clearance, and proteinuria were common. Autopsy studies revealed a wide spectrum of renal lesions, including renal amyloidosis, glomerulonephritis, tubulointerstitial nephritis and granulomatous disease[6].

We propose to call this Chronic Kidney Disease of non-Traditional causes (CKDnT): Mycobacteria-Induced Chronic Kidney Disease.

[1] Yadav et al: Genital tuberculosis: current status of diagnosis and management in Tranlational Andrology and Urology – 2016. See here.
[2] Oliveira et al: Single-centre experience of granulomatous interstitial nephritis—time for a new approach? in Clinical Kidney Journal – 2017. See here.
[3] Chugh et al: Pattern of renal amyloidosis in Indian patients in Postgraduate Medical Journal – 1981. See here.
[4] Lenk et al: Genitourinary tuberculosis in Current Opinion in Urology. – 2001
[5] Smith et al: The missing millions: a threat to the elimination of leprosy in PloS Neglected Tropical Diseases – 2015 See here.
[6] Silva et al: Leprosy nephropathy: a review of clinical and histopathological features in Revista do Instituto de Medicina Tropical de São Paulo. – 2015. See here.

Lithium-Induced Chronic Kidney Disease

Lithium is primarily used to treat and prevent episodes of mania (frenzied, abnormally excited mood) in people diagnosed with bipolar disorder, which is a manic-depressive disorder, a disease that causes episodes of depression, episodes of mania, and other abnormal moods[1]. Lithium decreases abnormal activity in the brain and can therefore be regarded as a mood-stabilizer.

In some cases lithium is also used to treat an episode of major depression, schizophrenia, disorders of impulse control, and certain mental illnesses in children.

Yes, Lithium has a documented positive effect on your brain, but beware of the side-effects. The problem of all medications is that, while you want it to have a positive effect in one part of your body, it also reaches those parts of the body you really do not want it to have effect.

A well-known complication of lithium is its detrimental effect on your kidneys. Research shows that the use of lithium seems to be related to a higher incidence of chronic kidney disease. Longer duration of lithium exposure significantly increased the risk of renal failure[2].

In the most extreme case your mood will have considerably improved, but you might die because your kidneys were so damaged that they stopped working altogether.

We would like to suggest to call this particular variant: Lithium-Induced Chronic Kidney Disease.

[1] Won, Kim: An Oldie but Goodie: Lithium in the Treatment of Bipolar Disorder through Neuroprotective and Neurotrophic Mechanisms in International Journal of Molecular Sciences - 2017
[2] Van Alphen et al: Chronic kidney disease in lithium-treated patients, incidence and rate of decline in International Journal of Bipolar Disorders - 2021

Soft Drinks-Induced Chronic Kidney Disease

Everybode knows (or should know) that consuming large amounts of sugary drinks will invariably increase your weight. The sugar in these drinks makes them high in calories.

But that's not all.

A scientific study revealed that a higher consumption of sugar-sweetened beverages was associated with an elevated risk of subsequent Chronic Kidney Disease in a study[1].

We would like to suggest to call this particular variant: Sugary Drinks-Induced Chronic Kidney Disease.

But that's not all.

Men who consume large amounts of carbonated or soft drinks are at higher risk of contracting gout than those who abstain, a study has concluded[2]. Researchers found that those who consumed five or six sweet beverages a week were nearly 30% more likely to suffer attacks of gout than those who drank less than one serving monthly. The risk rose to 85% for those drinking two or more a day. As well as sugar in drinks, the study found that natural fruit sugar, or fructose, posed a substantial risk for gout.

That means people who drank orange or apple juice or even ate those fruit regularly were prone to the illness. Meanwhile, diet soft drinks, which often contain sweetener rather than fructose, were not found to be associated with gout.

Gout is caused by a build-up of uric acid in the bloodstream and can cause joint swelling, inflammation and acute pain in the extremities. Women are less likely to suffer from the condition.

Fructose is often used as a substitute for sugar, especially in high-fructose corn syrup, which is cheaper than cane sugar. It is a common ingredient in fizzy drinks. The risk is such that researchers caution that patients who switch from purine-rich food to improve their gout could in fact make it worse if they start eating large amounts of fructose.

[1] Rebholz et al: Patterns of Beverages Consumed and Risk of Incident Kidney Disease in Clinical Journal of the American Society of Nephrology – 2019
[2] Choi, Curhan: Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study in British Medical Journal – 2008. See here.

Organic Solvent-Induced Chronic Kidney Disease

Organic solvents are carbon-based substances capable of dissolving or dispersing one or more other substances. Many classes of chemicals are used as organic solvents, including aliphatic hydrocarbons, aromatic hydrocarbons, amines, esters, ethers, ketones, and nitrated or chlorinated hydrocarbons.

They are used in paints, varnishes, lacquers, adhesives, glues, and in degreasing and cleaning agents, and in the production of dyes, polymers, plastics, textiles, printing inks, agricultural products, and pharmaceuticals.

The health effects associated with occupational exposure to organic solvents have long been recognised. Studies have shown both acute (short-term) and chronic (persistent) effects, particularly on the central nervous system, in workers exposed to solvents. Symptoms include neurological symptoms (including trembling of hands, tingling in arms and legs, dropping things by accident), mood (short temper, irritability) and memory and concentration problems.

A lesser known fact is that chronic exposure to organic solvents can also damage your kidneys. Scare research seems to show that the mechanisms behind organic solvents causing chronic kidney disease are obscure[1]. A direct toxic effect does not seem probable considering the frequent exposure to organic solvents in modern society and the fairly low incidence of this disease. The possibility of the solvents initiating, mediating or in some other way taking part in immunologic reactions appears more attractive. The general impression after reviewing the presented investigations is, that the possibility of a causal association between moderate hydrocarbon exposure and renal disease must be considered substantial. The indications are strong enough to state that individuals with signs of renal dysfunction or manifest renal disease should not be exposed to organic solvents.

So, would glue-sniffing (otherwise known as sniffing, huffing or bagging), a pathetic and cheap way to get high by inhaling organic solvents in (usually) glue, acetone, nitrous oxide (laughing gas) or butane, risk having kidney problems too? The answer, not surprisingly, is yes[2].

We would like to suggest to call this particular variant: Organic Solvent-Induced Chronic Kidney Disease.

[1] Askergren: Solvents and the Kidney in Progress in Clinical and Biological Research -1986
[2] Yurtseven et al: A 'glue sniffer' Teenager With Anuric Renal Failure and Hepatitis in Turkish Journal of Pediatrics - 2019

Schistosoma-Induced Chronic Kidney Disease

Schistosomiasis is a tropical disease, reported to occur in more than 70 countries, mainly in Africa, East Mediterranean and the Caribbean. From an estimated total of 200 million infected people – 85% of whom live in sub-Saharan Africa - approximately 120 million develop symptoms, 20 million have severe disease and 100,000 of them die each year.

Schistosomiasis is a parasitic disease caused by trematode worms of the genus Schistosoma. The five species that causes human schistosomiasis are Schistosoma haematobium, Schistosoma intercalatum, Schistosoma japonicum, Schistosoma mansoni and Schistosoma mekongi[1].

The parasites are released from infected freshwater snails. The disease is spread by contact with fresh water contaminated with the parasites.

The worms migrate to the veins around the bladder and ureters, leading to abdominal pain, diarrhea, bloody stool or blood in the urine. The late phase (chronic form) begins from the 6th month after infection and can last for several years. Over time, fibrosis can lead to obstruction of the urinary tract, hydronephrosis (swelling of a kidney due to a build-up of urine) and kidney failure.

Some studies show that renal lesions are irreversible because many cases have delayed diagnosis[2]. However, specific antiparasitic treatment can alter the renal disease development or progression when instituted in the initial phases. Patients with proliferative forms do not respond to antiparasitic treatment nor to immunosuppression, suggesting that this type of glomerular involvement has a progressive pattern.

We would like to suggest to call this particular variant: Schistosoma-Induced Chronic Kidney Disease

[1] Bezerra da Silva et al: Schistosomiasis-associated kidney disease: A review in Asian Pacific Journal of Tropical Disease – 2013. See here. 
[2] Martinelli et al: Envolvimento glomerular na esquistossomose mansônica in Jornal Brasileiro de Nefrologia – 1996

Silicone-Induced Chronic Kidney Disease

Silicones, sometimes known as polysiloxanes, are polymers that are used for a host of industrial and household purposes. These include sealants, adhesives, lubricants, medicine, cooking utensils, and thermal and electrical insulation. Silicones come in several forms, such as oil and grease.

You might wonder how silicone might end up in your body, but the answer is quite simple: a deluded quest for beauty and too little money to pay for it.

Reassuringly called injectables, unqualified people criminals use cheap over-the-counter silicone as filler for body contouring (lips, butt or breast plumping). The results are often disasterous. As the FDA warns 'injectable silicone can move throughout the body and cause serious health consequences, including death. Large-scale injectable silicone for body contouring and enhancement can also result in a painful and hard, gravel-like substance that stays permanently beneath the skin[1].

Silicone injections are particularly dangerous if used to give patients a bigger butt, according to the FDA. "When injected into areas with many blood vessels such as the buttocks ('butt'), silicone can travel through those vessels to other parts of the body and block blood vessels in the lungs, heart, or brain," the FDA said. "This can cause a stroke or even death."

The body wants to get rid of these foreign substance and it usually triggers an auto-immune reaction. Siliconosis, calcinosis cutis with hypercalcemia and chronic kidney disease have all been reported in association with silicone injection[2]. But it seems that your kidneys in particular are taking the brunt of the assault. Your kidneys can fail, even decades after the illegal silicone injections[3].

We would like to suggest to call this particular variant: Mercury-Induced Chronic Kidney Disease.

[1] FDA: The FDA Warns Against Injectable Silicone for Body Contouring and Enhancement: 14 November 2017. See here.
[2] Barilaro et al: ASIA syndrome, calcinosis cutis and chronic kidney disease following silicone njections. A case-based review in Immunologic Research – 2016
[3] d'Ythurbide et al: Reactive amyloidosis complicated by end-stage renal disease 28 years after liquid siliconeinjection in the buttocks in BMJ Case Reports – 2012

Mercury-Induced Chronic Kidney Disease

Mercury is a toxic metal as we well know from several recent environmental disasters, like Minamata in Japan[1]. We know from past experience that working with mercury or compounds containing mercury, such as methylmercury (ethylmercury is quite harmless) or cinnabar (mercury sulfide, once used as a pigment), will lead to health problems. Symptoms do depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. It will also create mental problems, as is shown in the Mad Hatter Syndrome.

But mercury poisoning will also have nefarious effects on your kidneys[2]. It accumulates readily in the renal tubular cells. To some extent, these tubular cells are able to regenerate, but prolonged exposure will surely lead to chronic kidney disease. Children's kidneys are particulary vulnerable to mercury poisoning[3].

Organic forms of mercury, which primarily affect the central nervous system, may also have serious toxicological effects in the kidneys.

Remember, you can inwittingly ingest mercury by consuming contaminated seafood, such as tuna. A study found that people, living in coastal regions of south-eastern Asia, the western Pacific and the Mediterranean, average biomarkers that approach the FAO/WHO references[4]. The Provisional Tolerable Daily Intake (PTDI) for inorganic mercury is set at 4 μg/kg body weight.

We would like to suggest to call this particular variant: Mercury-Induced Chronic Kidney Disease.

[1] Harada: Minamata disease: methylmercury poisoning in Japan caused by environmental pollution in Critical Reviews in Toxicology - 1995
[2] Orr, Bridges: Chronic Kidney Disease and Exposure to Nephrotoxic Metals in International Journal of Molecular Sciences – 2017. See here.
[3] Bose-O’Reilly, et al: Mercury Exposure and Children’s Health in Current Problems in Pediatric and Adolescent Health Care – 2011. See here.
[4] Sheehan et al: Global methylmercury exposure from seafood consumption and risk of developmental neurotoxicity: a systematic review in Bulletin of the World Heath Organisation - 2014. See here.