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*Shefali Jayantibhai Chaudhary and Dr. Archana N. Paranjape


Nephrotoxicity is one of the most common kidney problems and occurs when the body is exposed to a drug or toxin that causes damage to the kidneys. When kidney damage occurs, we are unable to rid our body of excess urine, and wastes. Your blood electrolytes (such as potassium, and magnesium) all becomes elevated. Nephrotoxicity can be temporary with a temporary elevation of lab values (BUN and/or creatinine). If these levels are elevated, these may be due to a temporary condition such as dehydration or may be developing renal (kidney failure). If the cause of the increased BUN and/or creatinine levels is determined early, and healthcare provider implements the appropriate intervention, permanent kidney problems may be avoided. Nephrotoxicity may also be referred to as renal toxicity. Drugs are a common source of acute kidney injury. Compared with 30 years ago, the average patient today is older, has more co morbidities, and is exposed to more diagnostic and therapeutic 0-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 pre-emptive 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. Drug-induced nephrotoxicity (DIN) occurs in all settings in which drugs are ingested or administered. It is a significant source of morbidity and mortality in the acute care hospital setting. DIN accounts for nearly7% of all drug toxicity and from 18% to 27% of all cases of acute renal failure in hospitals. Overall, in-hospital drug use may contribute to 35% of all cases of acute tubular necrosis (ATN), most cases of allergic interstitial nephritis (AIN), as well as to nephropathy due to alterations in renal hemodynamics and post renal obstruction. The incidence and characteristics of outpatient or community acquired DIN are less well understood since mild toxicity is often unrecognized. However, the pharmacoepidemiology of these effects have become more important as care increasingly shifts to the outpatient setting. Although as many as 3% to 6% of hospital admissions have been attributed to adverse drug effects during outpatient therapy, 20%of hospital admissions due to acute renal failure have been attributed specifically to community-acquired DIN.(1)Manifestations of drug-induced nephrotoxicity include acid-base abnormalities, electrolyte imbalances, urine sediment abnormalities, proteinuria, pyuria, hematuria and most commonly, a decline in the glomerular filtration rate. The mechanisms of drug-induced nephrotoxicity may differ between various drugs or drug classes, and they are generally categorized based on the histological component of the kidney that is affected. Aminoglycoside antibiotics, radiocontrast media, conventional nonselective nonsteroidal anti-inflammatory drugs, and selective cyclooxygenase-2 inhibitors, amphotericin B, and angiotensin-converting enzyme inhibitors have been frequently implicated. For several thousands of years, natural products have played an important role in treating and preventing human diseases. Natural product medicines have come from various sources including terrestrial plants, terrestrial microorganisms, marine organisms, terrestrial vertebrates and invertebrate. The importance of natural products in modern medicine has been discussed in many recent reviews and reports. The sophistication of herbal remedies used around the world varies with the technological advancement of countries that produce and use them. These remedies range from medicinal teas and crude tablets used in traditional medicine to concentrated standardized extracts produced in modern pharmaceutical facilities and used in modern medical systems under a physician's supervision. Many drugs, including strychnine, vincristine, taxol, curare, ergot etc., are of herbal origin evolved as a result of ethnomedical research. About one-quarter of the prescription drugs dispensed by community pharmacies in the United States contain at least one active ingredient derived from plant material. Some known herbal plants used as nephroprotective drugs are Harungana madagascariensis, Acorus calamus, Ficus religiosa L, Indigofera barberi L., Achyranthes aspera L., Kigelia africana. Many herbal plants have proved to be nephroprotective agent by many preclinical and clinical studies and are widely used in renal diseases including nephrotoxicity. One another plant is said to be used as nephroprotective agent, known as Trichosanthes dioica. It contains many chemical constituents which exhibits protective actions against nephrotoxicity. This plant also contains anti-inflammatory, antioxidant and immunomodulator activity which are helpful to exhibit its nephroprotective activity. But it does not contain any scientific evidence about its safety and efficacy. So the present study was undertaken to evaluate nephroprotective activity of Trichosanthes dioica on gentamicin induced nephrotoxicity.

Keywords: Trichosanthes dioica, Gentamicin, Serum creatinine, Blood Urea Nitrogen, Phospholipids

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