Renal injury in patients with rheumatoid arthritis treated with gold.

While severe nephrotoxicity is uncommon during gold therapy of rheumatoid arthritis (RA), the prevalence of mild nephrotoxicity has not been investigated. To study this, levels of leucine aminopeptidase (LAP) and N-acetyl-beta-glucosaminidase (NAG) (nmole/hr/mg urinary creatinine), and beta 2-microglobulin (beta 2M) (microgram/mg urinary creatinine) were measured in urine samples from 33 patients with RA receiving gold and 28 patients with various musculoskeletal diseases not receiving gold. Each patient had a normal urinalysis and blood urea nitrogen or serum creatinine. LAP was above 30 in 55% of RA patients and 7% of controls (p < 0.01). NAG was above 100 in 70% of RA patients and 14% of controls (p < 0.01). In 8 RA patients, NAG was over 200; LAP was over 100 in 4, but in none of the controls. Beta 2M was above 0.32 in 7 of 23 female RA patients and in none of 12 female controls (p = 0.012) and none of the male patients. Patients who excreted high levels of beta 2M also excreted high levels of NAG and LAP. These data show that gold in therapeutic doses affects renal tubular cells, cauing the release of NAG and LAP from lysosomes and brush borders of the cells. This may represent the mildest stage of nephrotoxicity. Elevated beta 2M in the urine of some patients indicate a degree of nephrotoxicity sufficient to cause renal tubular dysfunction.