The use of chloroquine treatment for Plasmodium falciparum malaria was abandoned in China in 1979 because of widespread drug resistance. Subsequent studies found decreases in the prevalence of chloroquine-resistant strains. To evaluate these decreases and assess the current status of chloroquine sensitivity in Hainan, China, we determined the prevalence of the P. falciparum chloroquine resistance transporter (PfCRT) 76T marker in the DNA of blood samples collected from 1978 to 2001. Results showed the presence of PfCRT 76T in 101 of 112 samples (90%) from 1978 to 1981, 30 of 43 samples (70%) from 1986, 22 of 34 samples (65%) from 1997 to 1998, and 37 of 68 samples (54%) from 2001. The prevalence of PfCRT 76T thus progressively decreased after chloroquine was discontinued as a treatment for P. falciparum malaria (chi(2) = 5.2, P < 0.022 [1978-1981 versus 1986]; chi(2) = 7.4, P < 0.006 [1978-1981 versus 1997-1998]; and chi(2) = 28.8, P < 0.0001 [1978-1981 versus 2001]). Reduced prevalence of the PfCRT 76T marker is consistent with greater rates of chloroquine sensitivity from in vitro drug assays of blood samples in 1997 and 2001. Monitoring for continued decreases will provide valuable information for future drug-use policies in China.

Since 1979 several derivatives of artemisinin have been synthesized and studied in China. Artemisinin suppositories, artesunate (oral or parenteral), intramuscular artemether and dihydroartemisinin tablets have all proved rapidly effective. In all, 2352 patients (2150 with Plasmodium falciparum and 202 with P. vivax) have been included in clinical trials from our centre. All preparations have been well tolerated. These drugs have now replaced chloroquine and quinine for the treatment of malaria in China.

Many drugs can injure the kidneys, but they cause renal injury via only a few common mechanisms. Many patients who develop renal injury after drug exposure have identifiable risk factors that could be modified or that should preclude the use of these drugs in the first place. s KEY POINTS Pretreatment hydration can reduce the nephrotoxic potential of many drugs. Renal injury can present as acute renal failure, nephrotic syndrome, renal tubular dysfunction, or chronic renal failure. Early diagnosis is critical; therefore, physicians must be aware of the nephrotoxic potential of the medications they prescribe and the risk status of their patients. One must anticipate the problem and exclude drugs as possible causes of renal disease when no other obvious cause can be found. DRUG-INDUCED NEPHROTOXICITY GUO AND NZERUE Prophylaxis of druginduced renal failure Amphotericin B Adjust dosage Hydrate with normal saline infusion Use liposomal formulation Aminoglycosides Follow levels Correct potassium levels Give once-daily doses Adjust dosage for renal function Avoid use if possible in high-risk patients Possibly give calcium channel blockers Intravenous contrast Hydrate with normal saline infusion Possibly give acetylcysteine Cisplatin Hydrate with normal saline Possibly give thiosulfate ACE inhibitors Avoid in bilateral renal artery stenosis Use with caution in hypovolemia Acyclovir Avoid bolus doses Give intravenous fluids Adjust dose for renal function Lithium Monitor levels Amiloride may prevent nephrogenic diabetes insipidus Interleukin-2 Intravenous saline, albumin infusion Cyclosporine Follow levels Avoid drugs that raise levels (erythromycin, verapamil, ketoconazole) Indinavir Hydrate Establish high urine flow * ACE-angiotensin-converting enzyme COX-cyclo-oxygenase NSAID-nonsteroidal anti-inflammatory drug TTP-HUS-thrombotic thrombocytopenic purpura-hemolytic uremic syndrome

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