Nephropathy, drug-induced,

Tubular and interstitial diseases (e.g., analgesic nephropathy, drug-induced nephritis, oxalate nephropathy, radiation nephritis, acute tubular necrosis, and sarcoidosis)... 

Lupus erythematosus Certain patients will develop a positive antinuclear antibody (ANA) test and some may show a lupus erythematosus-like syndrome similar to other drug-induced lupus, but it is not associated with hypocomplementemia and may be present without nephropathy. A positive ANA test does not mandate drug discontinuance however, a lupus erythematosus-like syndrome may develop later. Sensitivity reactions Once instituted for Wilson s disease or cystinuria, continue treatment with penicillamine on a daily basis. Interruptions for even a few days have been followed by sensitivity reactions after reinstitution of therapy. 

Fillastre JP, Mery JP, Druet P [Drug-induced glomerular nephropathies]. Nephrologie 1983 4 1-9. 

A drug-induced systemic lupus erythematosus (SEE) with proliferative glomerulonephritis has also been described in patients treated with D-penicillamine [111, 157]. Systemic lupus erythematosus syndrome is induced in approximately 2% of patients treated with D-penicillamine [112,158]. Unlike other forms of drug-induced systemic lupus erythematosus, anti-double-strand DNA anhbodies and/or hypocomplementemia are seen in D-penicillamine-induced systemic lupus erythematosus syndrome [111, 156]. Nephropathy is rare in D-penicillamine-induced systemic lupus erythematosus syndrome [111]. Walshe [112] reported that 8 patients developed the serological change of systemic lupus erythematosus of 120 patients with Wilson s disease treated with D-penicillamine, but none of them showed nephropathy. 

Heroin nephropathy/clinical course Amyloidosis associated with intravenous drug abuse HIV nephropathy and its relationship to heroin nephropathy Acute kidney injury due to drug-induced rhabdomyolysis Cocaine-induced renal disease 598 599 601 603 605... 

Despite a good overall safety profile, anti-TNF antibodies can induce a number of adverse effects, including autoimmunity and infections. A trial in the treatment of Crohn s disease noted infusion reactions, transient increased of anti-dsDNA antibodies, and serum sickness-like delayed hypersensitivity with retreatment. Induction of human-antichimeric-antibodies was suggested as the cause of some of the infusion reactions [90]. A prospective study in 35 patients with Crohn s disease showed induction of ANA and anti-dsDNA autoantibodies in 53% and 35% of infliximab-treated patients [91]. A single patient showed clinical features consistent with drug-induced lupus, including the presence of ANA and anti-dsDNA autoantibodies, which quickly resolved after discontinuation of infliximab. Reports on renal adverse effects of anti-TNF antibodies are very rare. Saint Marcoux described the occurrence of crescentic GN in as few as 2 patients out of a cohort of 39 patients, treated with an anti-TNF antibody for rheumatoid arthritis [92]. A case report by Chin et al. [93] described the case of a 29-year-old Australia-born Vietnamese who presented with nephrotic syndrome. A renal biopsy showed membranous nephropathy. Symptoms attenuated after discontinuation of infliximab therapy. 

The last three years have expanded insight as to how lymphocytes respond to antigens or xenobiotics, and also the knowledge of the pathophysiology of renal diseases. This provides new clues on the mechanisms by which chemically induced immune responses trigger kidney lesions. First, we will discuss the general mechanisms that could be responsible for drug-induce immune nephropathies. The role of Thl and Th2 CD4+ T-cell subsets in the development of nephropathies will be also debated. Then, we will describe the types of immune nephropathy than can be induced by xenobiotics in patients. Finally, we will focus on experimental models of chemical-induced systemic... 

Stachura I, Jayakumar S, Bourke E. T -F B lymphocyte subsets in fenoprofen nephropathy. Am J Med 1983 75 9-16. Shibasaki T, Ishimoto F, Sakai O, Joh K, Aizawa S. Clinical characterization of drug-induced allergic nephritis. Am J Nephrol 1991 11 174-180. 

Olyaei AJ, de Mattos AM, Bennett WM. Immunosuppressant-induced nephropathy. Drug Safety 1999 21 471 88. 

Compared with previously available therapy, the adverse effects associated with cyclosporine are much less severe but still worthy of concern. Nephrotoxicity, which can occur in up to 75% of patients, ranges from severe tubular necrosis to chronic interstitial nephropathy. This effect is generally reversible with dosage reduction. Vasoconstriction appears to be an important aspect of cyclosporine-induced nephrotoxicity. Hypertension occurs in 25% of the patients and more frequently in patients with some degree of renal dysfunction the concomitant use of antihypertensive drugs may prove useful. Hyperglycemia, hyperlipidemia, transient liver dysfunction, and unwanted hair growth are also observed. 

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