Mitsuru Hara

A PROLACTIN PRODUCING TUMOR ORIGINATED IN THE SPHENOID SINUS

The case presented is a prolactin producing tumor originated in the sphenoid sinus of a 40‐year‐old woman. Histologically this tumor is a typical chromophobe adenoma of the pituitary gland. Human prolactin was immunohistochemically detected in the cytoplasm of most tumor cells. The tumor invaded around the pituitary gland and in the nasal cavity without distant metastasis. Clinically the patient showed hyperprolactinemia and amenorrhea.

IgA nephropathy with subendothelial deposits

IgA nephropathy with subendothelial deposits in the capillary walls of the glomeruli (IgA type 2) was compared histometrically and clinically with IgA nephropathy without subendothelial deposits (IgA type 1) and membranoproliferative glomerulonephritis with subendothelial deposits (MPGN). Study cases consisted of 32 biopsies from 26 patients of IgA type 1, 25 biopsies from 20 patients of IgA type 2 and 31 biopsies from 27 patients of MPGN. Histological changes of the glomeruli consisted of an increase in the mesangial matrix and hypercellularity in the mesangium in both types of IgA nephropathy, and the degree of the changes was a little higher in IgA type 2 than in IgA type 1 (0.02<P<0.05). Mesangial changes of MPGN were marked as compared with IgA type 1 and IgA type 2 (P< 0.001). Histometry of the mesangium on the cases followed up showed that the degree of mesangial thickening increased with lapse of time in IgA type 2 and MPGN, whereas it remained unchanged up to 13 years in IgA type 1. Proteinuria tended to be mild in IgA type 1, moderate in IgA type 2, and marked in MPGN. The impairment of renal function was observed in 21.9% of IgA type 1, in 36.0% of IgA type 2 and in 58.1% of MPGN. IgA type 2 has been shown to be pathologically and clinically intermediate between IgA type 1 and MPGN. These results suggest that there is a clinicopathological overlap between IgA nephropathy and MPGN with IgA deposition.

Diffuse mesangial cell proliferation in focal sclerosing glomerulonephritis.

Morphometrical and clinical investigations were performed in 34 patients with the so-called hypercellular form of focal glomerulosclerosis (FGS), i.e., a form showing clear diffuse mesangial hypercellularity beside focal sclerosis with the light microscope. This form was compared with focal glomerulosclerosis without remarkable mesangial hypercellularity, with mild mesangioproliferative glomerulonephritis (gn), as well as with normal kidneys. The results were as follows: 1. Morphometrically both the increase in relative mesangial volume as well as in mesangial cell count is statistically significant in the hypercellular form compared with the nonhypercellular form and with controls. Comparison with mild mesangioproliferative gn shows no difference. 2. Even the so-called nonhypercellular form contains more mesangial matrix and mesangial cells than the controls. 3. The frequency of the hypercellular form is higher in males and in older patients. 4. All of our patients with hypercellular FGS had at the time of biopsy manifested nephrotic syndrome. The frequency of additional clinical symptoms (hematuria, hypertension, renal insufficiency) corresponds with the nonhypercellular form, but is different in mild mesangioproliferative gn. 5. Therapeutic response and prognosis is worse in the hypercellular form. Morphometrically both the increase in relative mesangial volume as well as in mesangial cell count is statistically significant in the hypercellular form compared with the nonhypercellular form and with controls. Comparison with mild mesangioproliferative gn shows no difference. Even the so-called nonhypercellular form contains more mesangial matrix and mesangial cells than the controls. The frequency of the hypercellular form is higher in males and in older patients. All of our patients with hypercellular FGS had at the time of biopsy manifested nephrotic syndrome. The frequency of additional clinical symptoms (hematuria, hypertension, renal insufficiency) corresponds with the nonhypercellular form, but is different in mild mesangioproliferative gn. Therapeutic response and prognosis is worse in the hypercellular form. The hypercellular form of FGS has to be separated from the nonhypercellular form as a defined entity.

Intrasellar gangliocytoma with multiple immunoreactivities

The authors report a rare case of intrasellar gangliocytoma without endocrinopathy. The tumor, removed by transsphenoidal surgery, exhibited immunoreactivities for VIP and galanin in the cytoplasm of several nerve cells, a-subunit, somatostatin, and serotonin in the cytoplasm of few nerve cells. Our case indicates that gangliocytomas can produce unusual combinations of peptides which, despite their known biologic activity, do not invariably cause clinical abnormalities.

The size of the juxtaglomerular apparatus in glomerulonephritis with the nephrotic syndrome

The juxtaglomerular apparatus was histoplanimetrically studied in renal biopsies of 65 cases of membranoproliferative glomerulonephritis and 64 cases of minimal proliferative intercapillary glomerulonephritis (MPI) (“minimal changes”). The juxtaglomerular cell complex (JGC complex) consisting of the epithelioid cells (granular cells) and the Goormaghtighs cells (agranular or lacis cells) was significantly enlarged in the nephrotic syndrome. 10 to 14 days duration of the nephrotic syndrome was shown to be sufficient to bring about an enlargement of the JGC complex. After a successful treatment of the nephrotic syndrome with steroids, there was no enlargement of the JGC complex. The enlarged JGC complex persisted despite steroid treatment in the steroid-resistant nephrotic syndrome, although a mild suppressive effect of steroids on the size of the JGC complex was observed. There was no significant relationship between hypertension and the size of the JGC complex. Creatinine retention tended to be associated with an enlargement of the JGC complex. The macula densa was not enlarged in the nephrotic syndrome, in contrast to the enlarged JGC complex. Morphometrische Untersuchungen zur Größe des juxtaglomerulären Apparates bei Glomerulonephritis wurden an Nierenbiopsien von 65 Fällen mit membranoproliferativer Glomerulonephritis und 64 Fällen mit minimal proliferierender intercapillärer Glomerulonephritis (MPI) (“minimal changes”) planimetrisch durchgeführt. Die aus den epitheloiden Zellen und Goormaghtigh-Zellen bestehenden juxtaglomerulären Zellkomplexe (JGZ-Komplexe) waren bei nephrotischem Syndrom statistisch signifikant vergrößert. Das Bestehen eines nephrotischen Syndroms über 10–14 Tage erwies sich als ausreichend, um eine Vergrößerung der JGZ-Komplexe hervorzurufen. Bei klinischer Besserung des nephrotischen Syndroms infolge einer Steroidbehandlung entsprach die Größe der JGZ-Komplexe den Kontrollen. Bei steroidresistentem nephrotischem Syndrom blieben die JGZ-Komplexe, trotz der Steroidbehandlung, vergrößert, jedoch ließ sich ein geringgradiger Hemmeffekt der Steroide auf die Größenzunahme der JGZ-Komplexe bei steroid-resistentem nephrotischem Syndrom feststellen. Ein Hypertonus hatte keinen statistisch signifikanten Einfluß auf die Größe der JGZ-Komplexe. Bei Kreatinin-Retention ergab sich eine Tendenz zur Hypertrophie der JGZ-Komplexe. Im Gegensatz zu den JGZ-KompIexen zeigten die Maculae densae keine signifikante Vergrößerung bei nephrotischem Syndrom.

The glomerular mesangium in hypertension

Glomerular changes were morphometrically studied in renal biopsies of 27 cases of nephrosclerosis showing clinically benign or malignant hypertension and of 15 cases of mild mesangioproliferative glomerulonephritis with hypertension. In nephrosclerosis, there was a mild increase in mesangial matrix without cell proliferation. The degree of the mesangial changes varied little despite a large variation in blood pressure and showed no significant difference between benign and malignant hypertension. In mild mesangioproliferative nephritis with hypertension, mesangial matrix, as well as the number of mesangial cells, showed an increase of varying degree. A quantitative assessment of the mesangium was proved effective in differentiating the glomerular changes in nephrosclerosis from those in mesangioproliferative nephritis with hypertension.