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

Cannabis and Chronic Kidney Disease

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.

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.

Kidney Stones and Gout

Kidney stones
Kidney stones are hard deposits made of minerals and salts that form inside your kidneys. Kidney stones have many causes and can affect any part of your urinary tract — from your kidneys to your bladder. Kidney stones form when your urine contains more crystal-forming substances — such as calcium, oxalate and uric acid — than the fluid in your urine can dilute. At the same time, your urine may lack substances that prevent crystals from sticking together, creating an ideal environment for kidney stones to form.

Kidney stones form due to a combination of genetics and environmental factors. Risk factors include high urine calcium levels, obesity, certain foods, sodium (salt), some medical conditions or medications, calcium supplements, gout, not drinking enough fluids and soft drinks containing phosphoric acid (typically colas).

Gout
Gout occurs when urate crystals accumulate in your joint, causing the inflammation and intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in your blood.

Gout is a common and complex form of arthritis. It is characterized by sudden, severe attacks of pain, swelling, redness and tenderness in the joints, often the joint at the base of the big toe. The affected joint is hot, swollen and so tender that even the weight of the sheet on it may seem intolerable.

Gout forms due to a combination of genetics and environmental factors. Risk factors include foods rich in purine (steak, organ meats and seafood), alcoholic beverages (especially beer), and drinks sweetened with fruit sugar (fructose).

New research
The underlying etiology of kidney stones is thought to be multifactorial with an environmental (notable dietary), hormonal, and genetic component. The heritability of kidney stones has been estimated at 56%[1].

According to a recent study, the belief that these environmental factors are the primary cause of gout is mostly untrue[2]. Some foods may slightly increase the risk of developing gout (beer, wine, spirits, potatoes and meat), while others (cheese, eggs, peanuts and brown bread) may decrease that risk. However, a comparison of healthy and unhealthy diets shows there is only an 0.3% impact. Adhering to a Mediterranean diet reduced that impact even further to 0.06%. In comparison, the heritability explained by common genetic variants, was estimated to be 23.9%.

This suggests that both kidney stones and gout may share a common etiology.

[1] Halbritter et al: Update on Hereditary Kidney Stone Disease and Introduction of a New Clinical Patient Registry in Germany in Frontiers in Pediatrics - 2018
[2] Major et al: Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts in British Medical Journal – 2018. See here.

Fluoride-Induced Chronic Kidney Disease

Today, almost all toothpastes contain fluoride. It is well recognised that the decline in the prevalence of dental caries over the past 30 years can be attributed mainly to the widespread use of toothpaste that contain fluoride. Sodium fluoride, the most commonly used fluoride compound is considered safe and effective.

Fluoride naturally occurs in the environment. Concentrations in surface waters depend on location but are generally low and usually do not exceed 0.3 mg fluoride per liter. Groundwater can contain much higher levels.

There is no evidence of increased incidence of renal disease or renal dysfunction in humans exposed to up to 8 mg fluoride per liter in drinking water[1].

Usually fluoride is removed from your body via the kidneys. Too much fluoride may damage your kidneys beyond repair.

What happens if you happen to live in an area that has a natural water supply that is high in fluoride? Research from El Qued (southern Algeria) indicates that kidney damage occured in patients, who were living in an area with a high level of fluoride in their drinking water, had kidney damage proporional to their age[2]. Which means: the older you are, the more fluoride you have ingested during your lifetime, the more damage to your kidneys can be observed.

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

[1] Wong et al: Topical fluoride as a cause of dental fluorosis in children in Cochrane Databases of Systematic Reviews – 2010
[2] Reggabi et al: Renal function in residents of an endemic fluorosis area in southern Algeria in Fluoride - 1984

Air Pollution-Induced Chronic Kidney Disease

We all know that air pollution is detrimental to your health. In large parts of the world the environment is so polluted with continued air pollution that incidences of cardiovascular diseases are rising sharply.

Air pollution depends on the size of the pollutants you inhale. Usually two sizes, called Particle Matter (PM) are studied: PM₁₀ and PM_2.5. PM₁₀ are inhalable particles, with diameters that are generally 10 micrometers and smaller. PM_2.5: fine inhalable particles, with diameters that are generally 2.5 micrometers and smaller.

Science has studied the effects on your lungs and found positive associations between cardiorespiratory diseases and different air pollutants. Worldwide studies showed statistical significance for all pollutants, suggesting that variables in particle size influence the average cardiorespiratory disease risk and may explain the varying effects of air pollution[1].

But your lungs are not the only organ that is diseased in the long run. Your kidneys are also at risk for Chronic Kidney Disease. Now, a study has used a database of 2,482,737 United States veterans and liked their possible exposure to air pollution (PM_2.5) with satellite data. Which answered the question where these veterans were at a given moment in time and wat the air pollution was at that moment.

The study found that an increase in PM_2.5 concentration was associated with similarly increased risk of Chronic Kidney Disease[2]. We would like to suggest to call this particular variant: Air Pollution-Induced Chronic Kidney Disease.

Air pollution is also linked to kidney, bladder, and colorectal cancer, a new study finds. Researchers observed 43,320 non-lung cancer deaths. PM_2.5 was significantly positively associated with death from cancers of the kidney[3]

[1] Requia et al: Global Association of Air Pollution and Cardiorespiratory Diseases: A Systematic Review, Meta-Analysis, and Investigation of Modifier Variables in American Journal of Public Health – 2017 
[2] Bowe et al: Particulate Matter Air Pollution and the Risk of Incident CKD and Progression to ESRD in American Society of Nephrology – 2017 
[3] Taylor et al: Ambient Air Pollution and Cancer Mortality in the Cancer Prevention Study II in Environmental Health Perspectives -2017

Salt-Induced Chronic Kidney Disease

Nowadays there are people who dispute that salt intake increases blood pressure. These people are clearly wrong and can probably be included into the anti-vaxxers movement. But the real question is: does a higher blood pressure as a result of higher salt intake eventually results in damaged kidneys?

Research indicates that healthy kidneys can disperse of salt quickly, but if the salt intake suddenly increases humans do usually not excrete this salt more rapidly, but they undergo substantial salt retention[1]. This process is done by the kidneys, but this is likely to damage the kidneys in the long term and is exacerbated by the higher blood pressure in the veins in the kidneys.

While, restriction of sodium intake is an important preventive and therapeutic measure in patients with chronic renal diseases or at risk of renal damage, such as hypertensive or diabetic patients, it still doesn't explain if salt itself can result in a chronic kidney disease[2].

We know that people who consume too much salt on a chronic basis cause the kidneys to struggle with electrolyte balance continually. Meanwhile, high blood pressure places vascular stress on the kidneys. In this compromised state, the damage to small blood vessels in the nephrons, the parts of the kidney that filter toxins and wastes from digested food for excretion, decreases normal kidney function. This loss of function, known as chronic kidney disease, may progress little by little for years or decades.

Chronic kidney disease is incurable, so controlling your salt intake throughout life is an important preventive measure. People with chronic kidney disease also have greater risks for potentially fatal heart attacks and strokes.

I would like to propose the term Salt-Induced Related Chronic Kidney Disease for this specific Chronic Kidney Disease.

[1] Kurtz et al: An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension in Kidney International – 2016
[2] Boero et al: Salt intake and kidney disease in Journal of Nephrology - 2002

Colistin-Induced Chronic Kidney Disease

Antibiotics were true life-savers when they became widely available after 1945. Almost criminal overuse and misuse of these medications has led to the rapid emergence of resistant bacteria is occurring worldwide. Many decades after the first patients were treated with antibiotics, bacterial infections have again become a threat.

What happens if all other antibiotics fail, you might ask. The answer is that doctors are forced to use colistin, a decades-old drug that fell out of favor in human medicine due to its kidney toxicity. However, it remains one of the last-resort antibiotics for some types multidrug-resistant bacteria.

Colistin is a nephrotoxic antibiotic. Nephrotoxicity is the concerning adverse effect of this drug. The mechanism of nephrotoxicity is via an increase in tubular epithelial cell membrane permeability, which results in cation, anion and water influx leading to cell swelling and cell lysis. There are also some oxidative and inflammatory pathways that seem to be involved in colistin nephrotoxicity. Risk factors of colistin nephrotoxicity can be categorized as dose and duration of colistin therapy, co-administration of other nephrotoxic drugs and patient-related factors such as age, sex, hypoalbuminemia, hyperbilirubinemia, underlying disease and severity of patient illness[1]. Another viewpoint says that periodic assessment of serum creatinine levels, modification of the colistin dose according to renal function, avoidance of coadministration of other nephrotoxic agents (if possible), shortening the duration of antimicrobial treatment, and attention to overall patient care, including hydration status, will minimize the potential for nephrotoxic effects of this valuable old antibiotic[2].

I would like to propose the term Colistin-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

But we cannot win the arms race with nature, because animals and humans are finding ways to circumvent colistin and several MCR (Mobilized Colistin Resistance) genes have been reported since 2015 in all corners of the world.

[1] Ordooei Javan et al: A review on colistin nephrotoxicity in European Journal of Clinical Pharmacology – 2015
[2] Falagas, Rafailidis: Nephrotoxicity of Colistin: New Insight into an Old Antibiotic in Clinical Infectious Diseases - 2009

Fipronil-Induced Chronic Kidney Disease

Fipronil is a slow-acting potent poison kill compat pests and is marketed under brand names as Frontline. It is typically used to kill fleas, mites and ticks on cats and dogs. All fleas are usually dead within 24 hours, all ticks within 48 hours. In other environments and under a variety of trade names, fipronil is used against rats (Fipronil), grasshoppers and locusts (Regent, Adonis), cockroaches (Goliath, Nexa), termites and Rasberry crazy ants (Termidor, Ultrathor, Taurus), wasps (Fipronil), etc. Furthermore, fipronil is highly toxic to aquatic life, even in minute doses[1].

Because of its effectiveness against insects, fipronil is probably the main cause of the colony collapse disorder in bees. Remember, without bees there are no flowers and witout flowers there are no plants which supply the vast majority of foods.

Suppose you inhale, ingest or absorb (through your skin) fipronil. Once may not constitute a problem, but you might be at seriuos risk if you're a commercial pet groomer or veterinarian. Symptoms of acute toxicity include sweating, nausea, vomiting, headache, abdominal pain, dizziness, agitation, weakness and seizures that affect the entire brain. Clinical signs of exposure to fipronil are generally reversible and resolve spontaneously.

The key word in the previous sentence is 'generally', because not all symptoms are reversible. Research suggest that prolonged exposure to fipronil may cause Chronic Kidney Disease[2][3]. I would like to propose the term Fipronil-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

News: Eggs recalled after banned pesticide found on Dutch poultry farms. See here. 

[1] Qureshi et al: Exposure to sub-acute doses of fipronil and buprofezin in combination or alone induces biochemical, hematological, histopathological and genotoxic damage in common carp (Cyprinus carpio L.) in Aquatic Toxicology – 2016
[2] Fipronil: Third Reevaluation - Report of the Hazard Identification Assessment Review Committee - 2000
[3] Katheek, David: Assessment of Renal Toxicity in Rats Exposed to Commercial Formulations of Fipronil in International Journal of Pharmaceutical, Chemical and Biological Sciences - 2017. See here.

Silica-Induced Chronic Kidney Disease

Silica, a chemical compound found in abundance in nature, is comprised of quartz, a constituent of rock, and makes up 90-95% of sand. Prior research suggests that silica exposure is associated not only with silicosis, lung disease, rheumatoid arthritis, small vessel vascultitis and other autoimmune diseases, but also with kidney damage[1].

Still, some think that the connection between silica dust and Chronic Kidney Disease hasn't been proven enough. New research has now proven without any doubt that there is a direct relation between silica dust and Chronic Kidney Disease[2].

Approximately 3 million workers in USA and Europe are exposed to crystalline silica. Evidence suggests that there are a myriad of occupational and environmental exposures that may contribute to the development of and progression of Chronic Kidney Disease. Recent reports have highlighted silicon-containing compounds as being particularly damaging to the renal system, particularly for individuals who experience intense and prolonged exposure, such as miners, sandblasters, glass-makers, brick and grain workers.

America's 'dust bowl', also known as the 'Dirty Thirties', was the period of severe dust storms that eroded the soils as a result of severe drought during the 1930s. It is returning with a vengeance. Climate change will bring higher temperatures and less precipitation. It shall turn the Midwest into dust again and dust storm will create havoc to lungs and kidneys of millions of Americans.

I would like to propose the term Silica-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

[1] Hogan et al: Silica exposure in anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and lupus nephritis in Journal of the American Society of Nephrology = 2001
[2] Vupputuri et al: Silica exposure and chronic Kidney disease in Renal Failure - 2012

Glyphosate-Induced Chronic Kidney Disease

Glyphosate - beter known as RoundUp - is a broad-spectrum systemic herbicide and crop desiccant. It is used to kill weeds, especially annual broadleaf weeds and grasses that compete with crops.

Monsanto, its producer, claimed that glyphosate is harmless to humans and most scientific reviews agree with that statement and think that there's no 'support for a causal relationship between glyphosate exposure and the risk of on-Hodgkin’s lymphoma or of multiple myeloma'[1].

Still, other studies and case reports say that glyphosate causes toxicity not only after (accidental) ingestion but also after dermal exposure by inhalation route and on eye exposure[2].

We know Sri Lankan Agricultural Nephropathy as Phosphate Fertiliser-Induced Chronic Kidney Disease. Several reports claim that multiple heavy metals and glyphosate may play a role in its pathogenesis. Heavy metals, excessively present in the urine samples of patients with Phosphate Fertiliser Related Chronic Kidney Disease, are capable of causing damage to kidneys. Synergistic effects of multiple heavy metals and agrochemicals may be nephrotoxic[3].

I would like to propose the term Glyphosate-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

You could easily imagine that the positive scientific reports about glyphosate are 'paid for by Monsanto', but that didn't stop California from deciding to ban the substance: it added glyphosate to their list of chemicals known to cause cancer. See here.

[1] Acquavella et al: Glyphosate epidemiology expert panel review: a weight of evidence systematic review of the relationship between glyphosate exposure and non-Hodgkin’s lymphoma or multiple myeloma in Critical Reviews of Toxicology – 2016
[2] Indirakshi et al: Toxic Epidermal Necrolysis and Acute Kidney Injury due to Glyphosate Ingestion in Indian Journal of Critical Care Medicine – 2017
[3] Jayasumana et al: Simultaneous exposure to multiple heavy metals and glyphosate may contribute to Sri Lankan agricultural nephropathy in BMC Nephrology - 2015

Iodine-Induced Chronic Kidney Disease

Ah, you might wonder, I do not consume too much iodine. That can be true if you do not like seafoods because those regularly contain high amounts of iodine. That doesn't constitute a problem because iodine is an essential element for life. Yes, our life too.

The problem not your beloved seafood, but iodine-containing contrast mediums such as those injected for an anginogram or radiology dye studies.

[Anginogram of the heart using iodine contrast medium]

Contrast-Induced Nephropathy (CIN) is a Chronic Kidney Disease of non-Traditional (CKDnT) causes is a form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury. Despite technological advances, Contrast-Induced Nephropathy remains responsible for a third of all hospital-acquired acute kidney injury (AKI)[1][2].

The mechanism of Contrast-Induced Nephropathy is still not entirely understood, but it is thought to include direct damage from reactive oxygen species, contrast-induced increase in urine output, increased oxygen consumption, changes in dilation and narrowing of the blood vessels to the kidneys or changes in urine viscosity[3]. While the exact cause remains unknown, exposure to medical imaging contrast material is known to damage the kidneys.

I would like to propose the term Iodine-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

Other non-Traditional causes of Chronic Kidney Disease have already been discussed on this website, and they include – using my new nomenclature Medication Related Chronic Kidney Disease, Mycotoxin Related Chronic Kidney Disease, Silica Dust Related Chronic Kidney Disease, Aristolochic Acid Related Chronic Kidney Disease, Cadmium Related Chronic Kidney Disease, Radiation Related Chronic Kidney Disease, Sugar Cane Worker Chronic Kidney Disease, Phosphate Fertiliser Related Chronic Kidney Disease and High Altitude Related Chronic Kidney Disease.


[1] Hou et al: Hospital-acquired renal insufficiency: a prospective study in American Journal of Medicine – 1983
[2] Nash et al: Hospital-acquired renal insufficiency in American Journal of Kidney Diseases – 2002 
[3] Fernandes et al: Impact of Iodinated Contrast on Renal Function and Hemodynamics in Rats with Chronic Hyperglycemia and Chronic Kidney Disease in BioMed Research International – 2016

Medication-Induced Chronic Kidney Disease

The cause of several Chronic Kidney Disease (CKD) isn't always known, but the traditional causes of chronic kidney disease are diabetes (high blood sugar levels caused by diabetes damage blood vessels in the kidneys) and high blood pressure (uncontrolled high blood pressure damages blood vessels, which can lead to damage in the kidneys).

Diabetes or high blood pressure may also speed up the progression of Chronic Kidney Disease in someone who already has the disease.

Other non-Traditional causes of Chronic Kidney Disease have already been discussed on this website, and they include – using my new nomenclature Mycotoxin Related Chronic Kidney Disease, Silica Dust Related Chronic Kidney Disease, Aristolochic Acid Related Chronic Kidney Disease, Cadmium Related Chronic Kidney Disease, Radiation Related Chronic Kidney Disease, Sugar Cane Worker Chronic Kidney Disease, Phosphate Fertiliser Related Chronic Kidney Disease and High Altitude Related Chronic Kidney Disease.

Another non-Traditional causes of Chronic Kidney Disease is the long-term use of certain medicines that can damage the kidneys. Examples include over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs)[1], such as celecoxib andibuprofen, and certain antibiotics, such as erythromycin, clarithromycin and azithromycin[2].

However, some scientists beg to differ and think that there isn't a relationship between NSDAIDs and kidney disease[3]. Tell that to vultures who have died in their hundreds after they ate carcasses of livestock that were 'pre-treated' with diclofenac.

I would like to propose the term Medication-Induced Chronic Kidney Disease for this specific Chronic Kidney Disease.

[1] Ungprasert et al: Individual non-steroidal anti-inflammatory drugs and risk of acute kidney injury: A systematic review and meta-analysis of observational studies in European Journal of Internal Medicine – 2016
[2] Ma et al: Clinical manifestation of macrolide antibiotic toxicity in CKD and dialysis patients in Clinical Kidney Journal - 2014
[3] Yaxley, Litfin: Non-steroidal anti-inflammatories and the development of analgesic nephropathy: a systematic review in Renal Failure – 2016