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Toxicology – Nephrotoxins and Acute Kidney Injury
Overview
Acute kidney injury (AKI) can be categorized into three major types based on the underlying cause: prerenal, intrinsic, and postrenal. Identifying the category helps guide diagnosis and management.
Prerenal Causes
These result from decreased renal perfusion. Common examples include hypotension, dehydration, and narrowing of the renal arteries.
Intrinsic Causes
These involve direct damage to kidney structures. Examples include glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis.
Postrenal Causes
These are due to obstruction of urine flow, such as kidney stones, tumors, benign prostatic hyperplasia (BPH), or other urinary tract blockages.
Toxic Acute Tubular Necrosis (ATN)
Chemical and Environmental Exposures
Pesticides, iodinated contrast agents, and organic solvents such as carbon tetrachloride and chloroform can directly damage renal tubules.
Pigment-Related Injury
Hemoglobin from hemolysis and myoglobin from rhabdomyolysis can accumulate in renal tubules, leading to kidney injury.
Toxic Alcohols
Substances like ethylene glycol and methanol can cause severe renal damage through toxic metabolites.
Heavy Metals
Metals such as mercury, arsenic, lead, chromium, gold, and cadmium are known nephrotoxins.
Paraproteinemia
Bence Jones proteins, often seen in multiple myeloma, can damage renal tubules and impair function.
Medications and Substances
Drugs such as aminoglycosides, acyclovir, cidofovir, indinavir, cisplatin, cyclosporine, tacrolimus, and NSAIDs are commonly implicated. Certain herbal toxins (e.g., aristolochic acid) and foods like star fruit have also been associated with nephrotoxicity.
Ischemic Acute Tubular Necrosis
This form of ATN results from reduced blood flow and oxygen delivery to the kidneys. Causes include shock, severe burns, trauma, sepsis, pancreatitis, liver cirrhosis, renal artery embolism, and disseminated intravascular coagulation. It may also occur with conditions such as hypercalcemia, tumor lysis syndrome (hyperuricemia), phosphate nephropathy, and exposure to medications like ACE inhibitors, ARBs, mannitol, and NSAIDs.
Overview
Acute kidney injury (AKI) can be categorized into three major types based on the underlying cause: prerenal, intrinsic, and postrenal. Identifying the category helps guide diagnosis and management.
Prerenal Causes
These result from decreased renal perfusion. Common examples include hypotension, dehydration, and narrowing of the renal arteries.
Intrinsic Causes
These involve direct damage to kidney structures. Examples include glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis.
Postrenal Causes
These are due to obstruction of urine flow, such as kidney stones, tumors, benign prostatic hyperplasia (BPH), or other urinary tract blockages.
Toxic Acute Tubular Necrosis (ATN)
Chemical and Environmental Exposures
Pesticides, iodinated contrast agents, and organic solvents such as carbon tetrachloride and chloroform can directly damage renal tubules.
Pigment-Related Injury
Hemoglobin from hemolysis and myoglobin from rhabdomyolysis can accumulate in renal tubules, leading to kidney injury.
Toxic Alcohols
Substances like ethylene glycol and methanol can cause severe renal damage through toxic metabolites.
Heavy Metals
Metals such as mercury, arsenic, lead, chromium, gold, and cadmium are known nephrotoxins.
Paraproteinemia
Bence Jones proteins, often seen in multiple myeloma, can damage renal tubules and impair function.
Medications and Substances
Drugs such as aminoglycosides, acyclovir, cidofovir, indinavir, cisplatin, cyclosporine, tacrolimus, and NSAIDs are commonly implicated. Certain herbal toxins (e.g., aristolochic acid) and foods like star fruit have also been associated with nephrotoxicity.
Ischemic Acute Tubular Necrosis
This form of ATN results from reduced blood flow and oxygen delivery to the kidneys. Causes include shock, severe burns, trauma, sepsis, pancreatitis, liver cirrhosis, renal artery embolism, and disseminated intravascular coagulation. It may also occur with conditions such as hypercalcemia, tumor lysis syndrome (hyperuricemia), phosphate nephropathy, and exposure to medications like ACE inhibitors, ARBs, mannitol, and NSAIDs.
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