Urinary N-acetyl-β-D-glucosaminidase in rheumatoid arthritis

Abstract

Excretion of urinary N-acetyl -D-g l u c o s a m i n i d a s e (NAG)and its isoenzyme patterns were studied in two groups of patients with rheumatoid arthritis (RA) and in normal control subjects. Urine samples were collected from 30 seropositive RA patients, 19 seronegative RA patients, and 15 normal healthy subjects. All the patients and normal subjects were assessed to have normal liver and kidney functions. A small portion of the urine sample was dialyzed against 0.01 M phosphate buffer, pH 7.0 and NAG activity was monitored. Mean ± SD values of urinary NAG in seropositive RA patients, in seronegative RA patients and in normal healthy subjects were found to be 4.20 ± 3.73 U/g creatinine, 2.96 ± 2.11 U/gm creatinine, and 1.71 ± 0.6 U/g creatinine, r e s p e c t i v e l y. The mean urinary NAG value in RA patients was found to be significantly higher (P < 0.05) in seropositive RA compared to the mean NAG value in normal healthy subjects and patients with seronegative RA when analyzed by one way ANOVA and Tukey-HSD test. The mean proportion of isoenzyme form B to isoenzyme form A in seropositive RA patients was also found to be significantly different (P < 0.05) from the mean proportion of these forms in normal healthy subjects and seronegative RA patients. There also appears to be a correlation between the concentration of urinary NAG and severity of the disease in seropositive RA.

Guidelines for treatment of renal injury during cancer chemotherapy 2016

“…However, urinary NAG activity is inhibited by many nephrotoxic substances, magnesium, and endogenous urea [ 61 ]. Furthermore, urinary NAG levels are increased not only in AKI, but also in rheumatoid arthritis [ 62 ], impaired glucose tolerance [ 63 ], and hyperthyroidism [ 64 ]; thus, the specificity of urinary NAG for AKI is considered low.…”

Biomarkers of nephrotoxic acute kidney injury

“…However, urinary NAG activity has been found to be inhibited by endogenous urea (Bondiou et al, 1985) as well as a number of industrial solvents and heavy metals . In addition, increased NAG levels have been reported in a variety of conditions in the absence of clinically significant AKI, including rheumatoid arthritis (Iqbal et al, 1998), impaired glucose tolerance (Fujita et al, 2002), and hyperthyroidism (Tominaga et al, 1989). As a result, insensitivity and nonspecificity may limit the use of NAG as a biomarker of nephrotoxicant induced AKI in some settings.…”

Symmetric dimethyl arginine and N-acetyl- β-D-glucosaminidase lysosimyria of proximal renal tubules as a target for nephrotoxicity in patients with rheumatoid arthritis treated with disease modifying antirheumatic drugs.

“…There are opposite results from the mutual interaction of co-administration of low dose of Methotrexate and other NSAIDs in patients suffering from RA. Some reports suggest that there is no significant interaction from the combined use of low dose Methotrexate with piroxicam, naproxen and sulindac, but others suggest possible interaction in patients who suffer from RA treated with naproxen and ibuprofen (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31), which needs the problem to be solved. Impairment of the renal function is noted in patients suffering from malignant diseases treated with high doses of Methotrexate, but it is unknown whether administration of low dose of Methotrexate could manifest similar effects.…”