To find the clinical meanings of serum sialic acid (SA) in glomerulonephritis and nephrosis, it was estimated in 94 patients with diffuse glomerulonephritis, in 8 patients with nephrosis, in patients with other diseases and in healthy subjects and its relationships to the clinical andd pathohistological findings were studied. The method used was the Ehrlich's direct reaction using p-dimethylaminobenzaldehyde reported by Werner and Odin. Results were as follow: 1) Normal level of serum SA ranges from 32.5 to 71.0 mg/100ml with a mean of 52.7 mg/ 100ml. In the patients with rheumatism, tuberculous pleurisy, cancer, inflammations, nephrosis, glomerulonephritis and hypertension, SA levels were significantly elevated, whereas in liver cirrhosis they were lower. 2) In glomerulonephritis, in general, serum SA was higher than normal at its initial stage, once decreased towards 10 days after the onset of the disease, and gradually elevated again from one month after the onset to a second peak situating about 3rd month which was followed by a declining to normal level at 4-6th month. On an average, SA level was highest (68.3 mg/100ml) in subacute stage, in acute and chronic stage being somewhat lower (64.9 mg/100ml, and 61.8 mg/ 1OOml, respectively). 3) The first peak of this trend of serum SA level in glomerulonephritis is supposed to be associated with the preceding infection, the second with repair of renal tissues. 4) Roughly saying, serum SA levels were generally higher in the cases with severe histolic renal damages, especially in subacute stage. 5) Considering from the feature of serum SA and histological and clinical findings, acute and excerbated glomerulonephritis should be regarded active and be managed as such for 6 months at least. 6) Markedly elevated levels of SA were found in 8 cases of lipoidnephrosis with a mean of 82.3mg/100ml. They were especially higher when edema and marked albuminuria existed. 7) In 45 hypertensive patients, too, serum SA levels were significantly higher than normal (mean 62.Omg/1OOml), especially so in patients with albuminuria. 8) In general, serum SA level was higher with the impairment of renal functions. 9) In glomerulonephritis, serum SA level ran almost parallel with blood sedimentation rate, but the former was more sensitively correlated to the clinical course. Anti-streptolysine-O titer was also in parallel to SA level in rheumatism, but in glomerulonephritis the curves crossed each other. 10) There were significant positive correlations between serum SA level and blood pressure in glomerulonephritis and hypertension. 11) In inflammatic diseases the serum SA tends to decrease in convalescence.

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In the previous paper the clinical meanings of serum sialic acid (SA) in glomerulonephritis and nephrosis were reported. In this paper similar researches were made on the urinary SA. Estimations of the urinary SA were carried out by a method modified by the author. 1) By using cation resin (DAWX W50 X 8) column in the preliminary procedure of urine, most parts of urochromogen which interfere with the reaction were almost completely excluded. This procedure can afford a useful clinical method to determine the urinary SA. The urinary SA determined by this method was supposed to be a polymer different from that in sera. 2) Urinary SA concentration was not always high in glomerulonephritis, and was not in any direct correlation with the stages or degrees of histological damage. However, its urinary daily output was often greater in severe cases of acute and subacute stages. 3) It seems to be very important to investigate the urinary SA outputs along with the clinical course. In every stage, acute, subacute or chronic of glomerulonephritis, the daily output was greater in the early phase of treatment and was gradually decreased, though not continuously. In chronic stage, it was relatively small, especially smaller in fatal cases. After tonsillectomy some cases showed increased outputs. 4) In nephrosis, compared with glomerulonephritis, both urinary concentration and daily output of SA were strikingly greater. They were remakably increased in edematous stage and decreased with clinical healing. 5) In the cases of marked albuminuria (above 20mg/dl) in glomerulonephitis and nephrosis, the concentration and output of urinary SA were roughly correlated to those of protein in the urine, respectively. 6) In nephrosis and glomerulonephritis with marked albuminuria, excretion of SA into urine seems to be effected mainly by the leak of sialoprotein accompanying to albumin. It is suggested, however, that the SA clearance and its local discharge from the renal lesions must come into further consideration.

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