The clinical usefulness of serial assays of urinary N-acetyl-β-D-glucosaminidase (NAG), γ-glutamyltransferase (GGT) and β₂-microglobulin (β₂M) were tested to evaluate and follow up the nephrotoxicity resulting from the prolonged administration of ciclosporin (CS). Three groups of patients were studied for 18 months: group A: functioning renal transplant patients (n = 13) on maintenance therapy from 12-31 months with CS and prednisone; group B: functioning renal transplant patients (n = ll) treated with prednisone and azathioprine; group C: patients (n = 10) affected by autoimmune steroid-unsensitive uveitis, free from previous renal disorder and treated with CS (for 8-16 months) at progressively decreasing doses. In groups A and B, the urinary enzymes and β₂M underwent overlapping increases, so that these parameters cannot be considered reliable indices of CS-induced nephrotoxicity. This is due to the fact that transplanted kidneys are already altered by concomitant or preexisting affections, or by persistent immunologic injury. Conversely, in patients with uveitis, the serial assays of such urinary parameters prove to be quite reliable to evidence clinically yet unrecognizable kidney involvement due to prolonged CS administration. High enzymuria has been shown to be an earlier marker of nephrotoxicity only in nephropathy-free patients; on the other hand, the regression of elevated β₂Muria into normal ranges indicates complete tubule cell recovery.

The recovery of tubules after relief of obstructive nephropathy may be investigated through serial assessment of the urinary excretion of tubular enzymes alpha-glucosidase, gamma-glutamyl-transferase and N-acetyl glucosaminidase as well as of the microprotein beta-2-microglobulin. We studied 21 patients in whom obstructive nephropathy was relieved by operative or nonoperative methods. Anuria persisted from 2 to 14 days. In these patients urinary excretion of alpha-glucosidase, gamma-glutamyl-transferase, N-acetyl glucosaminidase and beta-2-microglobulin, as well as the serum creatinine were assessed weekly. Serum creatinine was the earliest index to return to normal (within 9 to 26 days). Enzymuria returned to normal within 35 to 45 days, whereas normal urinary excretion of beta-2-microglobulin occurred more than 100 days after relief of obstructive nephropathy. N-acetyl glucosaminidase and gamma-glutamyl-transferase proved to be more reliable than alpha-glucosidase in detecting recovery of the luminal membrane of the proximal tubule. The return to normal of urinary beta-2-microglobulin levels has been shown to occur later, since more specific and complex intracellular functions underlie this index. The pathophysiological aspects of recovery of obstructive nephropathy may be considered similar to those observed in ischemic acute renal failure, since in both instances hemodynamic changes are involved.

The post-exercise urine samples from 122 long-distance runners showed evident abnormalities upon microscopic examination in 95% of all subjects. Proteinuria, alone or with microscopic hematuria, was frequently found. Macroscopic hematuria was a rare occurrence. The urine samples collected in 30 runners before, immediately after the race, and 6, 12, 24, 36, and 48 h later showed a significant post-race decrease in the osmolarity and a significant increase in gamma-glutamyl transferase and N-acetyl-beta-glucosaminidase enzyme activity. Plasma renin activity and plasma aldosterone, determined before and after the race in nine runners, showed a significant increase in the post-race samples. The abnormal urinary findings disappeared in all cases within 24-36 h. It can be concluded that urinary abnormalities are very common after exercise. These abnormalities are most often of a "renal" origin, probably due to a temporary hemodynamic impairment, partially of glomerular but principally of tubular function.

The authors present a case of Henoch-Schönlein purpura in a young soldier (19 years old) which they consider important for its etiology and the length of its oligoanuric phase. The syndrome followed a Salmonella hirschfeldii infection, and a protracted oligoanuric phase was followed by nephrotic syndrome and selective glomerular proteinuria which lasted for 1 year. The young man recovered after the eradication of the Salmonella. It seems possible that there was an overall anomalous regulation of the ‘lymphoid system of the mucosa’, perhaps dependent on a genetic predisposition.

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