The kidneys can be damaged by a large number of therapeutic agents. The aim of this article is to discuss the pathological features of drug-induced renal disease as diagnosed by kidney biopsy. The literature is reviewed and cases seen by the authors that have a known drug association are analysed. Mechanisms of injury are varied and all renal structures may be affected. The tubulointerstitial compartment is most frequently involved, but glomerular and vascular lesions are seen in a significant proportion of cases.
Humans ; Kidney Diseases ; chemically induced ; pathology

Aristolochic Acids ; adverse effects ; Humans ; Kidney Diseases ; chemically induced

Melamine (Tripolycyanamide) and its derivatives have recently become a public concern on food safety. To better understand melamine and its major derivative cyanuric acid.literature on their chemical properties, metabolism, biological effects, relevant toxicology studies, and the detection methods is reviewed. Studies indicate that the acute toxicity of melamine and cyanuric acid is low. In mammalian, these compounds are hardly metabolized in vivo and are rapidly eliminated in the urine. When used in large dosage,these compounds demonstrate marked renal toxicity,as well as toxic effect towards heart. The renal toxicity is exemplified by the calculi formation, acute renal failure, and subsequently induced carcinomas of the urinary bladder. Among the tested species, male cats and rats are more prone to be affected by the compounds. The HPLC/MS/MS is becoming the mainstay of the detection methods. Despite of the achieved knowledge on melamine and cyanuric acid, further research is warranted to unveil the mechanism of underlying susceptibility of kidney, to develop better analytic methods,and to explore possible biomarkers for better clinical diagnosis.
Animals ; Carcinogens ; toxicity ; Cats ; Female ; Kidney Diseases ; chemically induced ; Male ; Rats ; Species Specificity ; Triazines ; toxicity ; Ureteral Calculi ; chemically induced

Angiotensin II ; metabolism ; Cisplatin ; adverse effects ; Humans ; Kidney ; drug effects ; Kidney Diseases ; chemically induced ; metabolism

OBJECTIVETo lessen the occurrence of contrast-induced nephropathy (CIN), the preventive measures of CIN were reviewed.

DATA SOURCESThe data used in this review were from PubMed with relevant English articles and from Chinese Knowledge Information (CNKI) published from 1989 to 2009. The search terms were "contrast medium", "contrast-induced nephropathy" and "prevention". Articles involved in prevention of CIN were selected.

STUDY SELECTIONCIN is the third most common cause of acute kidney injury and is associated with an unfavorable prognosis. The best treatment is prophylaxis because CIN can not be reversed or ameliorated.

RESULTSThirty articles were included. Among various preventive measures, pericatheterization hydration is almost universally accepted as an appropriate and safe measure to prevent CIN, although there is no agreement as to composition, amount, and timing of hydration. Based on the use of concomitant nephrotoxic agents or high doses of contrast medium (CM) is one of risk factors for CIN, discontinuation of potentially nephrotoxic drugs 2 - 3 days before and after the procedure until renal function recover, and using the lowest possible dose of CM can decrease the risk of CIN. It is promising that removing the majority of CM from the coronary sinus, before it enters the systemic circulation, during coronary angiography can reduce the risk for CIN in animal studies and in limited clinical trials. Inconsistent data exist with respect to application of some vasodilators (endothelin antagonists and adenosine antagonists) and antioxidants (N-acetylcysteine and statins) in preventing CIN in high-risk patients, and new vasodilators and antioxidants continue to be tested.

CONCLUSIONSPericatheterization hydration, discontinuation of nephrotoxic drugs, and using the lowest possible dose of CM are effective measures to lessen the risk for CIN. Other prophylactic strategies and some drugs are promising, but further confirmation is required.

Contrast Media ; adverse effects ; Humans ; Iodine ; adverse effects ; Kidney Diseases ; chemically induced ; prevention & control

Anti-Bacterial Agents ; adverse effects ; Humans ; Integrative Medicine ; Kidney Diseases ; chemically induced ; therapy

Drug-induced nephrotoxicity is very common in both new drug development and clinic practice. Various drugs can induce kidney injuries, including tubulointerstitial, glomerular and renal vascular disease. To investigate the mechanism of drug induced nephrotoxicity is important for risk reduction of new drug development, reasonable drug usage, early discovery and effective prevention/treatment of adverse effects in clinics.
Acute Kidney Injury ; chemically induced ; Animals ; Anti-Infective Agents ; adverse effects ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; Antineoplastic Agents ; adverse effects ; Humans ; Immunosuppressive Agents ; adverse effects ; Kidney Diseases ; chemically induced ; Kidney Tubular Necrosis, Acute ; chemically induced ; Nephritis, Interstitial ; chemically induced ; Renal Insufficiency ; chemically induced

OBJECTIVETo investigate the nephrotoxic effects of methyl cantharidimide tablets on urinary protein and enzymes in Beagle dogs.

METHODBeagle dogs were randomly divided into negative control group(blank tablet), methyl cantharidimide tablets group (6.11,12.21, 24.42 mg x kg(-1)), continuously 30 days of oral adminiStration, once a day. The drug and control group were collected and determined fresh urine in 1, 2, 3 and 4 weeks of the administration; Serum urea nitrogen (BUN), creatinine (Crea), total protein (TP) and albumin (ALB) as well as sodium, potassium, chloride electrolyte were determined on 15 and 30 days of the administration; Urine albumin (mAlb), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin( NGAL), N-acetyl-beta-D-glucosaminidase (NAG), clusterin, beta2-microglobulin (beta2-MG), alpha1-microglobulin (alpha1-MG), alanine aminopeptidase( AAP) and im- munoglobulins IgG were tested on 15 and 30 days of the administration.

RESULTCompared with the control group, urine protein and white blood cells was significantly increased in each dose group. On 15 days of the administration, mAlb were higher in each dose group, KIM-1, NGAL, clusterin, NAG and AAP were significantly higher in high-dose group, while the middle and low dose group had no significant difference, as well as blood SCr and BUN no obvious abnormalities. On 30 days, mAlb, KIM-1, clusterin, NAG, AAP were increased in each dose group, appearing dose-effect relationship, beta2-MG and NGAL levels were significantly increased in high-dose group. Contents above indicators were increased with significant dose and time relationship, and serum BUN, Scr were correlated, suggesting that urine mAlb, KIM-1, clusterin, NAG and AAP indicators that can sensitively respond the changes of proteins and enzymes in urine.

CONCLUSIONMethyl cantharidimide tablets has a renal toxicity, urine mAlb, KIM-1, clusterin, NAG and AAP can be used as the early nephrotoxic biomarkers of methyl cantharidimide tablets.

Animals ; Biomarkers ; urine ; Dogs ; Female ; Kidney ; drug effects ; Kidney Diseases ; chemically induced ; Male ; Proteins ; metabolism ; Tablets ; adverse effects ; Urine ; chemistry

Adult ; Female ; Humans ; Ketamine ; adverse effects ; Kidney ; drug effects ; physiopathology ; Kidney Diseases ; chemically induced ; complications ; Substance-Related Disorders ; complications

OBJECTIVESTo determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia.

METHODSSD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+.

RESULTSWith increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01).

CONCLUSIONTMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.

Animals ; Female ; Hypokalemia ; chemically induced ; veterinary ; Injections, Intraperitoneal ; Kidney Diseases ; chemically induced ; veterinary ; Lethal Dose 50 ; Male ; Rats ; Rats, Sprague-Dawley ; Severity of Illness Index ; Trimethyltin Compounds ; pharmacology ; poisoning