Drug-induced nephropathies

Drug-induced renal disease is a common problem. Drugs cause several renal syndromes, such as prerenal azotemia, fluid and electrolyte abnormalities, acute tubular necrosis, acute interstitial nephritis, and chronic interstitial nephritis. Acute renal failure due to acute tubular necrosis is the most common syndrome and is most frequently caused by aminoglycoside antibiotics, radiographic contrast agents, and amphotericin B. Avoidance of these drugs in volume-depleted or hypotensive patients with preexisting renal disease or in those receiving multiple nephrotoxic drugs is the most effective way to reduce nephrotoxicity. Acute interstitial nephritis is an immune process that is most commonly caused by penicillins, diuretics, allopurinol, nonsteroidal anti-inflammatory drugs, cimetidine, and sulfonamides. Prompt recognition of the disease and cessation of the responsible drug are usually the only necessary therapy. Chronic interstitial nephritis is most often seen after prolonged use of several different types of analgesic agents, including aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs. These patients develop recurrent papillary necrosis and eventually chronic renal failure. They are also at risk of developing transitional cell carcinomas of the urinary collecting system. Some patients who are receiving cyclosporine also develop chronic renal failure due to interstitial fibrosis.     

Drug-induced psychoses

Major causes of drug-induced psychoses include cocaine, amphetamines, phencyclidine, cannabinoids, LSD, mescaline, the so-called designer drugs, anticholinergic compounds, and steroids. Most drug-induced psychoses are managed with general supportive measures, reassurance, minimizing patient stimulation, and benzodiazepines as needed; however, specific antidotes such as physostigmine for anticholinergic poisoning or urinary acidification to enhance excretion of amphetamines or phencyclidine may be indicated in some patients. Any patient with a drug-induced psychosis must be evaluated carefully for evidence of other toxic effects of the drug in question.     

Drug-induced edema

It is well known that there are many drugs which induce edema. Drug-induced edema can be divided into three types by the mechanism as follows, 1) sodium overload, 2) renal dysfunction and 3) hyperpermeability of blood vessel. In the category of sodium overload, edema is induced by much fluid replacement and antibiotics which contain large amount of sodium and sodium bicarbonate. As the category of renal dysfunction, NSAIDs, antihypertensive drugs, anticancer drugs and so on induce edema in patients with renal dysfunction. In the category of hyperpermeability of blood vessel, edema is induced by calcium antagonist, insuline and so on. In order to diagnose drug-induced edema early, it is important that we interrupt or reduce the quantity of suspicious drug.     

Drug-induced nephrotoxicity

Drugs are a common source of acute kidney injury. Compared with 30 years ago, the average patient today is older, has more comorbidities, and is exposed to more diagnostic and therapeutic procedures with the potential to harm kidney function. Drugs shown to cause nephrotoxicity exert their toxic effects by one or more common pathogenic mechanisms. Drug-induced nephrotoxicity tends to be more common among certain patients and in specific clinical situations. Therefore, successful prevention requires knowledge of pathogenic mechanisms of renal injury, patient-related risk factors, drug-related risk factors, and preemptive measures, coupled with vigilance and early intervention. Some patient-related risk factors for drug-induced nephrotoxicity are age older than 60 years, underlying renal insufficiency (e.g., glomerular filtration rate of less than 60 mL per minute per 1.73 m2), volume depletion, diabetes, heart failure, and sepsis. General preventive measures include using alternative non-nephrotoxic drugs whenever possible; correcting risk factors, if possible; assessing baseline renal function before initiation of therapy, followed by adjusting the dosage; monitoring renal function and vital signs during therapy; and avoiding nephrotoxic drug combinations.