As. Devriese et al., RIFAMPICIN-ASSOCIATED ACUTE-RENAL-FAILURE - PATHOPHYSIOLOGIC, IMMUNOLOGICAL, AND CLINICAL-FEATURES, American journal of kidney diseases, 31(1), 1998, pp. 108-115
A 71-year-old woman was treated for a relapsing pulmonary tuberculosis
with reinstitution of rifampicin after a medication-free interval of
2 years. After ingestion of the second dose, she developed severe hemo
lytic anemia and acute renal failure (ARF) necessitating dialysis. We
demonstrated the presence in the patient's serum of rifampicin-depende
nt immunoglobulin G (IgG) and IgM antibodies, which caused red blood c
ell lysis through interaction with the I antigen on the erythrocyte su
rface. A review of the literature yielded 48 cases of rifampicin-assoc
iated renal failure. A subgroup of 37 patients could be distinguished,
which, analogous to our case, suddenly developed ARF and frequently a
lso developed hemolytic anemia and/or thrombocytopenia during intermit
tent or interrupted treatment. Regarding the pathogenesis of the ARF,
renal biopsy consistently revealed tubular lesions. Although intravasc
ular hemolysis with hemoglobinuria may play a role, it is not uniforml
y present. Our demonstration of an antibody with anti-I specificity pr
ovides a possible explanation. The I antigen is also expressed on tubu
lar epithelium and may, therefore, be the target structure through whi
ch rifampicin-antibody complexes lead to tubular cell destruction. The
other cases of rifampicin-associated ARF were unrelated to this subgr
oup: two cases of rapidly progressive glomerulonephritis, five cases o
f acute interstitial nephritis, and four cases of light chain proteinu
ria were recorded. (C) 1998 by the National Kidney Foundation, Inc.