Renal failure drug-induced

Lomaestro BM. Fluoroquinolone-induced renal failure. Drug Saf. 2000 22 479M85. 

Gallelli L, Gallelli A, Vero G, Roccia F, Pelaia G, De Sarro G, et al. Acute renal failure probably induced by prulifloxacin in an elderly woman a first case report. Clinical drug investigation. 2006 26(1 ) 49-53. 

In studies of the etiology of acute renal failure, medication-induced renal injury is reported as a major cause. In an analysis of over 2000 hospitalized patients, almost 100 experienced renal insufficiency and seven episodes were attributed solely to aminoglycoside therapy [11]. A high percentage of neonatal patients are treated with aminoglycosides and in the involvement of drugs in neonatal acute renal failure has increased up to 8-fold in the last 10 years [12]. 

Izuwa, Y, Kusaba, J., Horiuchi, M., Aiba, T., Kawasaki, H., and Kurosaki, Y. (2009) Comparative study of increased plasma quinidine concentration in rats with glycerol and cisplatin induced acute renal failure. Drug Metab. Pharmacokinet. 24, 451-157. 

Although there is a common belief that natural herbs do no harm, emergent cases reported that renal failure was associated with chronic use of certain herbal preparations. Another important issue is the interaction between herbs and Western medication. There is a tendency, from that assumption, to neglect the possible side effects induced by the combination of both medications. Drug-drug interactions are listed in the following examples. 

During periods of acute psychosis, some patients exhibit so much muscular activity that they develop muscular destruction with the muscle product myoglobin in urine, which produces acute renal failure (16). Some muscle destruction may be due to involuntary muscle activity induced by the drug, while some may be due to the struggles of the agitated patient. In the latter case, the use of restraints may worsen the situation. 

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

Paracetamol is a widely used analgesic, which causes liver necrosis and sometimes renal failure after overdoses in many species. The half-life is increased after overdoses because of impaired conjugation of the drug. Toxicity is due to metabolic activation and is increased in patients or animals exposed to microsomal enzyme inducers. The reactive metabolite (NAPQI) reacts with GSH, but depletes it after an excessive dose and then binds to liver protein. Cellular target proteins for the reactive metabolite of paracetamol have been detected, some of which are enzymes that are inhibited. Therefore, a number of events occur during which ATP is depleted, Ca levels are deranged, and massive chemical stress switches on the stress response. 

Nakahama H, Nakamura H, Kitada O, Sugita M. Chronic drug-induced tubulointerstitial nephritis with renal failure associated with propylthiouracil therapy. Nephrol Dial Transplant 1999 14(5) 1263-5. 

Shin J, Lee E, Kwon Y, Lee J, Cho S, Park C, Lee D, Kim M-S, Pyo H-J (1997) Exercise-induced acute renal failure associated with nonsteroidal anti-inflammatory drugs report of 2 cases (in Korean with English abstract). Korean J Nephrol 16 607-611... 

Pharmacokinetics Slow intravenous infusion is employed for treatment of systemic infections or for prophylaxis. Because vancomycin is not absorbed after oral administration, this route is only employed for the treatment of antibiotic-induced colitis due to Q difficile. Inflammation allows penetration into the meninges. Metabolism is minimal 90-100 % is excreted by glomerular filtration. [Note Dosage must be adjusted in renal failure since the drug will accumulate. Normal half-life is 6-10 hours compared to over 200 hours in end-stage renal disease.]... 

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