Drug-induced kidney disease constitutes an important cause of acute renal failure and of undiagnosed renal disease a possibility of drug-induced renal failure. Drug-induced nephrotoxicity are more common among infants and young children and in certain clinical situations such as underlying renal. Some patient-related risk factors for drug-induced nephrotoxicity are age older than 60 years, underlying renal insufficiency (e.g., glomerular.
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Before initiation the drug therapy, ensure adequate hydration and avoid the use of nephrotoxic drugs whenever possible 23 - Correct intravascular depletion to maintain renal perfusion before initiation of nephrotoxic agents 24drug induced renal disease Administer drug orally and use the lowest effective dose and shortest duration of therapy whenever possible 27 Maintain drug levels within the recommended therapeutic range.
Use less toxic analgesics with the lowest prostaglandins activity such as drug induced renal disease in patients with chronic pain and limit the duration of therapy.
Drug-induced renal disorders
Discontinue or reduce the dose of nephrotoxic drug with the first sign of toxicity. Monitor renal function and serum drug concentrations during drug therapy.
Use the lowest dose of low osmolar contrast agent in patients with pre-existing renal insufficiency, heart failure, and diabetes.
Ensure adequate hydration with drug induced renal disease saline or sodium bicarbonate infusion. Consider acetazolamide and monitor GFR hours post exposure Estimate of renal function As a general rule, when a new drug is prescribed, baseline renal function should be evaluated before initiating the nephrotoxic medication.
Close monitoring of renal function drug induced renal disease also essential during the course of therapy.
Drug-Induced Nephrotoxicity - - American Family Physician
There are several ways to estimate GFR in children. One of the easiest and more practical one is Drug induced renal disease formula using the following formula Use analgesics with less prostaglandin activity such as aspirin and acetaminophen.
It may be caused by decreased intravascular volume due to blood loss, dehydration, or disease drug induced renal disease such as congestive heart failure, hypotension, and liver failure, which result in decreased effective blood volume.
Pre- and postglomerular arteriolar resistance is responsible for maintaining renal perfusion and glomerular filtration rate.
Preglomerular afferent vasodilation and post-glomerular efferent vasoconstriction are controlled by prostaglandins and angiotensin II, respectively. Patients with underlying disease, drug induced renal disease as the elderly and those with hypotension and dehydration, are at particular risk for DIRF.
Various inflammatory diseases, such as systemic lupus erythematosus, can result in glomerulonephritis.
Drug-Induced Acute Renal Failure
Interstitial nephritis results from inflammation of the renal interstitium and tubules and can be caused by infections, immune-mediated diseases drug induced renal disease as sarcoidosis and lymphomas, and drugs.
Drugs most often implicated in the development of interstitial nephritis include certain antibiotics, antivirals, and immunosuppressants.
The tubules have an inherently high-energy demand due to active transport mechanisms and metabolic processes. This makes the tubules particularly sensitive to decreases in oxygen. Drugs such as amphotericin B upset the balance between oxygen demand and supply, which results in tubular damage.
Drugs such as acyclovir and methotrexate can cause crystal deposition in the tubules, which can occur when a patient is dehydrated. Drugs with low solubility may form crystals, causing obstruction of urine output and subsequent renal failure.