Factors predictive of renal involvement in patients with primary Sjogren's syndrome

Aim: To identify clinical and immunological risk factors underlying the development of renal involvement in primary Sjogren's syndrome (pSS). Subjects and methods: Seventy-eight patients (75 females, 3 males) with pSS were carefully inter-viewed and clinical and laboratory data from the time of diagnosis recorded. The baseline data on patients shown to have either latent or overt distal renal tubular acidosis (dRTA), mild proteinuria or increased urinary excretion of alpha-1 microglobulin (alpha (1)m) after a mean disease duration of 9 +/- 4 years, were compared to the baseline data on those who did not have these manifestations at follow-up. Results: Patients with subsequent latent or overt dRTA were found to have significantly higher baseline levels of serum total gamma -globulin (24 +/- 7 vs. 19 +/- 6 g/l, p = 0.011) and serum protein (84 +/- 7 vs. 79 +/- 7 g/l, p = 0.024) compared to those with normal renal acidification capacity. The baseline levels of serum beta-2 microglobulin (beta M-2) were higher in patients with an acidification defect than in those with normal acidification capacity (3.1 +/- 1.1 vs. 2.6 +/- 0.8 mg/l, p = 0.072). In those with subsequent proteinuria the levels of serum beta M-2 were almost significantly higher at baseline as compared to those with normal urinary protein excretion (3.1 +/- 1.4 vs. 2.5 +/- 0.8 mg/l, p = 0.052). The subgroup of pSS patients who had increased urinary alpha (1)m excretion as a sign of tubular proteinuria, had higher baseline levels of ESR (55 +/- 27 mm/h vs. 40 +/- 23 mm/h, p = 0.076) and significantly higher baseline levels of serum beta (2)m (4.6 +/- 1.8 vs. 2.6 +/- 0.8 mg/l, p = 0.029) as compared to those with normal urinary alpha (1)m excretion. Conclusions: High levels of serum total gamma -globulin, serum protein and serum beta (2)m were the best predictors of the development of dRTA in pSS patients. High baseline levels of serum beta (2)m were also associated with the subsequent occurrence of mild proteinuria and increased urinary alpha (1)m excretion in patients with pSS.