256 



A. BERGSTRAND AND H. BUCHT 



protrusions. Thus, no disruption between basement 

 membrane and foot processes has taken place even 

 in the vicinity of large protrusions of the middle 

 layer, and the outer layer at least may indeed have a 

 cementing function as suggested by Pease (13). 

 Tangential or oblique sections through the capillary 

 wall can be distinguished easily from the protrusions 

 by the aspect of the endothelium and of the foot 

 processes (fig. 2). Within the protrusions of the 

 middle layer a finely spongy or felt-like structure 

 with interwoven filaments of about 30-40 A is 

 observed. Pores, however, were not found. A disrup- 

 tion between endothelium and inner layer of the 

 basement membrane by deposition of amyloid was 

 not yet detected. Sometimes the endothelium seemed 

 to be swollen. 



The parietal basement membrane measuring 1200- 

 1400 A in normal mice is thickened in animals with 

 amyloidosis. The mean width is 7400 A. The mem- 

 brane seems to be split into fine filaments but may 

 also appear homogeneous. 



The question arises whether the thickening and 

 the local protrusions of the osmiophilic middle layer 

 are due to the deposition of amyloid. Recent in- 

 vestigations (1, 2, 5) agree that amyloid is deposited 

 between endothelium and basement membrane. On 

 account of a comparative study with the light and 

 electron microscope (9) it is felt that the thickening of 

 the osmiophilic middle layer is not (or not exclu- 

 sively) due to an infiltration with amyloid. Since the 

 animals had a severe proteinuria it is probable that 

 the passage of pathologic proteins through the base- 

 ment membrane has resulted in a swelling of the 

 osmiophilic middle layer. This view is confirmed by 

 investigations of Mellors and Ortega (8). These 

 authors found by use of a microfluorescence method 

 that in human secondary amyloidosis globulins 

 were localized in the thickened glomerular capillary 

 walls before amyloid deposition was detected micro- 

 scopically. Randerath (17) also observed a swelling 

 of the glomerular capillary walls in human glomer- 

 ulonephrosis probably consecutive to a passage of 

 proteins. 



The observations reported in this study seem to 

 have some bearing, however, on the problem of 



structure and function of the glomerular basement 

 membrane. The basement membrane in mice with 

 amyloidosis has the same triple-layered structure as 

 in normal mice. The thickening of the osmiophilic 

 middle layer seems to indicate that the definite ultra- 

 filter is formed by this layer alone. 



Pores were not observed in the lamina densa although 

 it could be expected that they would become visible 

 in the swollen or bulging middle layer of mice with 

 amyloidosis rather than in the unaltered membrane 

 of normal animals. That pores do not exist cannot 

 be excluded with absolute certainty on the strength 

 of present information. The observations of Hall (3), 

 however, do not form a morphological basis for the 

 thesis of Pappenheimer (II, 12). 



References 



1. BoHLE, A. and Krecke, H.-J., Vlrchow's Arch. 327, 663 



(1955). 



2. Churg, J. and Grishman, E., Adi. J. Pathol. 29, 199 



(1953). 



3. Hall, B. V., Proc. V. Ann. Conf. Neplirotic Syndrome, 



New York. The National Nephrosis Foundation, 

 Inc., 1954, 1. 



4. — Proc. VI. Ann. Conf. Nephrotic Syndrome, New 



York. The National Nephrosis Foundation, Inc., 

 1955, 1. 



5. Jones, D. B.. Am. J. Pathol. 27, 991 (1951). 



6. Latvalahtl J., Experimental Studies on the Influence 



of Certain Hormones on the Development of Amy- 

 loidosis. Thesis. Helsinki, 1953. 



7. Letterer, E., Beitr. pathol. Aiiat. 75, 486 (1926). 



8. Mellors, R. C. and Ortega , L. G., Am. J. Pathol. 32, 



455 (1956). 



9. Miller, F. and Bohle, A., A7///. Wochschr. 34, 1204 



(1956). 



10. Palade, G. E., J. Exptl. Med. 95, 285 (1952). 



11. Pappenheimer, J. R., Physiol. Reviews 33. 387 (1953). 



12. — Klin. Wochschr. 32, 362 (1955). 



13. Pease, D. C, Anat. Rec. 121, 701 (1955). 



14. — /. Histochem. Cytochem. 3, 295 (1955). 



15. PiEL, C. F., Dong, L., Modern, F. W. S., Goodman, 



J. R., and Moore, R., /. Exptl. Med. 102, 573 (1955). 



16. PoLicARD, A., Collet, A., and Giltaire-Ralyte, L., 



Arch. anat. microscop. 44, 1 (1955). 



17. Randerath, E., Klin. Wochschr. 20, 281, 305 (1941). 



18. Rhodin, J., Exptl. Cell Research 8, 572 (1955). 



19. SiTTE, H., Mikroskopie (Wien) 10, 365 (1956). 



20. — personal communication (1956). 



21. Yamada, E., J. Biophys. Biochem. Cytol. 1, 551 (1955). 



Electron Microscope Investigation 



on Biopsy Material from Patients with Renal Diseases: 



A Case of Subacute Glomerulonephritis 



A. Bfrgstrand an<d H. Bucht 



Pathological Deparliiieni, Sahbatsbcvgs Hospital, Stockholm, ami lllrd Medical Service, St. Eriks Hospital. Stockholm 



In this paper a report is given on an electron though clear (proteinuria and haematuria), were 



microscope investigation of biopsy material from slight. Thus the morphological changes could be 



the kidneys of a patient suftering from mild subacute expected to be moderate and presumably easy to 



glomerulonephritis. The patient's clinical signs, al- compare to normal structure. 



