Introduction:
Cadmium is a rare, toxic trace element. Nowadays, cadmium is gaining more attention as an environmental pollutant. Human beings are being exposed to higher concentrations of cadmium due to the advancement in technology and industries. Although cadmium is important for growth in the sector of industrialization, the major issue about its health effect is its severe toxicity. Varied toxic clinical manifestations of cadmium involve the kidneys, liver, digestive tract, heart, testes, pancreas, bones, arteries, etc.
The half-life of cadmium metabolism is around 10 to 34 years or longer in the human body. The toxicological capacity of cadmium is therefore enhanced in man. Also, cadmium is known to strongly interact with other essential trace elements both at the absorption level and in the tissue. Some of these trace elements include copper, zinc, lead, etc. This results in the malfunctioning of the element-dependent enzyme activities. It also leads to a deficiency of essential minerals.
What Is the Epidemiology of Cadmium Nephropathy?
Human beings may be exposed to cadmium toxicity from their environment. Cadmium is a main compound in nickel-cadmium batteries, available as a pigment in the production of paint, in electroplating, and in manufacturing polyvinyl chloride plastic. Moreover, cadmium is also present in the majority of foodstuffs, and based on their dietary habits, the level of cadmium varies greatly. Cadmium exists in the environment in considerable amounts due to the use of fossil fuels, metal combustion, and harmful waste burning. The transfer of cadmium compounds to the agricultural soil by leakage of the sewage sludge may lead to its adsorption by plants that may play a pivotal role in the food chain and deposit in several human organs, including kidneys. Cigarette smoke is another great source of cadmium exposure.
What Happens to Cadmium in the Kidneys?
Kidneys are the primary target organs in both acute and chronic cadmium toxicity. The initial uptake of cadmium that is administered in the body is usually high in the liver. However, the metal will ultimately concentrate in the kidneys. A characteristic distribution pattern is followed by the cadmium in the kidneys. The concentration of cadmium is higher in the cortex than in the medulla. The cadmium is largely concentrated in the outer renal cortex as compared to the proximal tubules. The cadmium is not retained by the glomeruli to the same extent. The cadmium is continued to be accumulated by the renal cortex even when the other tissues reach their saturation levels long back. The cadmium concentration in the kidneys begins to level off as soon as the cadmium-induced renal changes start appearing. Hence, the renal accumulation of cadmium may be used as an indicator of cadmium toxicity.
What Are the Effects of Cadmium Toxicity on Kidneys?
Morphological Changes:
Pathological changes are developed in the kidneys due to cadmium intoxication, depending on the span of exposure. Multiple cadmium exposure in humans may result in severe necrosis of the convoluted renal tubules, poorly defined cells, and irregular cellular granulations.
The urinary sediment consists of casts that are composed of desquamating cells along with the creation of a few calcified casts. The renal glomeruli do not show apparent changes. The renal collecting tubules are not affected profoundly.
Ultrastructural Changes:
Ultrastructural alterations include extensive loss of the basal plasma membrane infoldings in the proximal renal tubules. There may be an alteration in the renal blood vessels. Moreover, the metal particles may also be accumulated in the tubule cells.
Functional Changes:
Chronic cadmium intoxication usually results in characteristic alterations of renal functions. The most common symptoms are aminoaciduria, enzymuria, and proteinuria.
-
Glycosuria (excessive sugar in the urine) is usually the first symptom of cadmium nephropathy in cadmium-exposed factory workers.
-
Polyuria (passing large amounts of urine).
-
Hypercalciuria (excess calcium in the urine) and increased urinary uric acid are also observed in cadmium-exposed workers.
-
Kidney stone formation may also be observed in some cases.
-
Aminoaciduria (an abnormal amount of amino acids in the urine) is one of the most common symptoms of cadmium nephropathy. The abnormal levels of amino acids reportedly present in the urine of cadmium nephropathy patients include alanine, glycine, lysine, citrulline, arginine, and proline.
-
The most significant feature of cadmium nephropathy is proteinuria (excessive levels of proteins in the urine). Urinary excretion of low molecular weight proteins in cadmium nephropathy is mainly derived from the serum.
-
Enzymuria (the presence of enzymes in the urine) is also a common manifestation of cadmium nephropathy. Enzymes that are usually detected in the urine of cadmium nephropathy patients include acid phosphatase, alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase etc. Enzymuria may be the earliest sign of renal abnormality in patients with cadmium nephropathy.
-
Hyperphosphaturia (increased amount of phosphates excreted in the urine).
How Is Cadmium Nephropathy Diagnosed?
Healthcare professionals should analyze the urine to diagnose this condition. The kidney is the major target organ that is affected by cadmium in chronic exposure. It has been reported that urinary cadmium levels equal to or greater than 1.1 pounds per 0.0022 pounds of creatinine are associated with renal damage. Also, cadmium levels of more than 4.4 pounds per 0.0022 pounds of creatinine may be attributed to extensive damage.
In addition, sensitive tests that can detect low molecular weight proteinuria and enzymuria may also be carried out to detect cadmium nephropathy.
What Is the Treatment for Cadmium Nephropathy?
The treatment for chronic cadmium nephropathy should be based on preventive measures. If the renal symptoms become apparent or the person is diagnosed with renal disease, the patient should be removed from further cadmium exposure. Various chelating agents have been used to treat cadmium poisoning in human beings. Ethylenediaminetetraacetic acid (EDTA) is the most commonly used chelating agent that is used to eliminate cadmium in the urine. However, British anti-lewisite (BAL), also known as dimercaprol, should not be used because the cadmium-BAL complex formed is known to be more toxic to the kidneys than cadmium alone.
Conclusion
Cadmium could cause toxicity in humans. The kidneys are the main target organs of cadmium intoxication. They affect the functions of the kidneys when the patient is exposed to cadmium for a very long time. Therefore, preventive measures should be taken to prevent chronic exposure to cadmium. Once the symptoms are diagnosed, immediate medical help should be taken to prevent further damage to the kidneys.
