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These studies suggest that kidney damage can be caused by nephrotoxicity from drugs and pollutants, acute kidney injury from various sources including environmental toxins, and chronic kidney disease due to fibrosis, inflammation, and immune dysfunction.
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Extrinsic factors such as cardiovascular disease, obesity, and diabetes are significant contributors to kidney damage. These conditions can lead to chronic kidney disease (CKD) and acute kidney injury (AKI) by causing systemic hypertension and metabolic imbalances that strain the kidneys. Infections and hypovolemic shock are also predominant causes of AKI, especially in low-income and middle-income countries.
Intrinsic factors include conditions like glomerular nephritis and polycystic kidney disease, which directly affect the kidney's structure and function. These conditions can lead to renal fibrosis and tubular cell death, further exacerbating kidney damage. Chronic kidney disease (CKD) is characterized by progressive scarring that affects all kidney structures, often resulting from a self-perpetuating cycle of fibrosis activated after initial injury.
The kidney is highly susceptible to damage from various nephrotoxic drugs and environmental pollutants. Drugs such as certain cancer therapeutics, antibiotics, and radiocontrast agents are known to be nephrotoxic. Environmental pollutants like cadmium, mercury, arsenic, and lead also pose significant risks to kidney health . These substances can induce renal cell death through mechanisms similar to those caused by intrinsic and extrinsic factors.
Oxidative stress plays a crucial role in kidney damage. The kidneys, particularly the renal proximal tubules, are highly susceptible to oxidative stress due to their high mitochondrial content and energy demands. Free radicals and prooxidants produced during acute or chronic kidney injury can further aggravate the disease and contribute to subsequent complications.
Inflammation is a common feature in both AKI and CKD. It can be a direct contributor to kidney injury or a result of the injury itself. Inflammatory responses often involve renal cell death through apoptosis or necrosis, leading to further kidney damage. The immune system also plays a role, with pathogenic immune responses against renal autoantigens and systemic autoimmunity contributing to kidney disease. Endothelial damage and the activation of innate immunity further link inflammation and kidney damage.
Kidney damage can result from a complex interplay of extrinsic and intrinsic factors, nephrotoxic substances, oxidative stress, and inflammatory responses. Understanding these mechanisms is crucial for developing effective prevention and treatment strategies for both acute and chronic kidney diseases. Early detection and management of these risk factors are essential to mitigate long-term kidney damage and improve patient outcomes.
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