Renal toxicity of the nonsteroidal anti-inflammatory drugs

T he only important pathological condition that causes a significant increase in the serum creatinine level is damage to a large number of nephrons. Unlike the BUN, the serum creatinine level is not affected by hepatic protein metabolism. Tests to measure serum creatinine, urine creatinine, and creatinine clearance are all used only to evaluate renal function. Only renal dysfunction changes the results. The serum creatinine level does not rise until at least half of the kidney's nephrons are destroyed or damaged. Because creatinine levels rise and fall more slowly than BUN levels, creatinine levels are often preferred to monitor renal function on a long-term basis.

The use of molecular targeted therapies for the treatment of cancer has increased over the last decade. The benefits of these compounds in terms of efficacy are often relatively modest and counter balanced by the occurrence of significant toxicities. Many of these newer agents used in clinical practice lack specificity and selectivity and have a propensity to inhibit multiple targets. The biological consequences of multi-kinase activity are poorly defined and numerous class-specific toxicities have been described. The kidney is an organ where most of these targeted pathways are expressed. Preclinical data and human renal biopsies have generated an understanding of the mechanisms involved in how targeted agents can cause renal toxicity. This review article discusses the observed nephrotoxicity with this burgeoning class of therapeutics and reviews both the biological reasons for its occurrence and possible ways to prevent significant renal damage.

Some studies have suggested that patients with a very high degree of renal vascular resistance (which reflects permanent damage to the kidneys), even with a 75% or more stenosis of the renal artery, often have a poor response to the angioplasty procedures. (The tension of the blood vessels to the kidney, called renal vascular resistance, is measured by Doppler ultrasonography. A so-called resistive index over is considered very high). In these patients, angioplasty is usually not done and the high blood pressure or renal failure is managed only by the customary therapeutic measures for these problems as described previously.

Since we launched our website in 2014, there has been a significant amount of new research published that indicates that gadolinium is being deposited in the brain.  As a result of those findings, on July 27, 2015, the FDA released a new Safety Announcement regarding Gadolinium-Based Contrast Agents.   The FDA is investigating the risk of brain deposits of gadolinium following repeated use of GBCAs for magnetic resonance imaging (MRI).  While GBCAs are being investigated, they can still be administered; however, health care professionals have been cautioned to limit GBCA use to circumstances in which the use of contrast is deemed necessary.

Renal toxicity of the nonsteroidal anti-inflammatory drugs

renal toxicity of the nonsteroidal anti-inflammatory drugs

Since we launched our website in 2014, there has been a significant amount of new research published that indicates that gadolinium is being deposited in the brain.  As a result of those findings, on July 27, 2015, the FDA released a new Safety Announcement regarding Gadolinium-Based Contrast Agents.   The FDA is investigating the risk of brain deposits of gadolinium following repeated use of GBCAs for magnetic resonance imaging (MRI).  While GBCAs are being investigated, they can still be administered; however, health care professionals have been cautioned to limit GBCA use to circumstances in which the use of contrast is deemed necessary.

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