Shuei Nakayama

Effect of Antibiotic Administration on Urinary Guanidinoacetic Acid Excretion in Renal Disease

It is known that there is a marked decrease in urinary guanidinoacetic acid (GAA) excretion in patients with uremia1–3. We have previously reported that urinary GAA (U-GAA) excretion is significantly decreased in experimental animals injected with 20 to 50 mg/kg of gentamicin4. Our further study also showed that such a reduction in GAA excretion is seen even in animals injected with 5 mg/kg, a relatively small dose of gentamicin5. These findings have led some to suggest that GAA would be useful for the early diagnosis of antibiotic-induced nephrotoxicity.

Reassessment of Selectivity Index in Nephrotic Syndrome with Special Reference to the Clinical Significance of a Small-Molecular IgG Fraction in the Urine

The selective index O and the transR IgG have been valuable in clinical use, but they do not appear to always correctly reflect the GBM sieving effect on plasma protein and thus do not correctly predict the response to steroids. We applied a new technique to 22 nephrotic patients with the following results. (a) Fragments of IgG molecules (M-IgG, MW 5-10 X 10(4); S-IgG, MW 1-5 X 10(4)) were present in the urine in addition to normal IgG (L-IgG). These fragments were immunologically identical with the intact IgG molecule and therefore, could falsely portray GMB permeability. (b) The data strongly suggest that the S-IgG fragment found in the nephrotic urine is the IgG-Fc fragment present in increased amounts in such urine. (c) IgG L/S shows a positive correlation with O and transR IgG and can be used as a new and better selectivity index of GBM permeability. This, in turn, may provide a more accurate means of predicting the response to steroid therapy. For example, in the cases we analyzed, the transR IgG and O were incorrect in 31.9% and 22.7%, respectively, whereas with our new method they were incorrect in only 13.6%.

Late Relapse in a Case of Mesangioproliferative Glomerulonephritis

A case of atypical proliferative glomerulonephritis (PGN) without mesangial immunoglobulin (Ig) A deposition (so-called non-IgA PGN) showing exacerbation of heavy proteinuria under long-term observation is reported. Examinations of first renal biopsy specimens revealed membranoproliferative glomerulonephritis (MPGN)-like findings. Urinary protein excretion completely disappeared after treatment with prednisolone (PSL) and an antiplatelet drug, i.e., dipyridamole. Negative reaction for urinary protein continued for more than 10 years. Fourteen and a half years after the first biopsy, the patient had heavy proteinuria again. Results of the second renal biopsy showed marked proliferation of glomerular mesangial cells. Under electron microscopy, lobulation and double contours of the glomerular capillary walls were also observed segmentally. Depositions of IgG, IgM, IgA, and C3 were observed mainly in the glomerular capillary walls, but not in the mesangial areas; however, these findings were not compatible with IgA nephropathy or MPGN. No hypocomplementemia was observed during the clinical course. The patient was treated with 30 mg of PSL and 75 mg of dipyridamole daily and showed a good response to such treatment. It appears that this patient had a rare case of atypical non-IgA PGN.