- Email: [email protected]
Renal involvement in disseminated lupus erythematosus
SELECTED
647
ABSTRACTS
The demonstration of a calcified mitral valve is unequivocal evidence stenosis and also indicates its rheumatic etiology. Dilatation of the left auricle without general cardiac enlargement presumptive evidence of mitral stenosis. The diagnosis of mitral stenosis can be made amination, even in the absence of characteristic “ subclinical mitral disease. ”
at
times physical
by
of mitral is highly
roentgenologie signs herein
excalled
AUTROR. Altschule,
Valve.
Mark Arch.
D., and Budnitz, Path. 30: 7, 1940.
Edward:
Rheumatic
Disease of the Tricuspid
The clinical syndrome of rheumatic disease of the tricuspid valve is charaeterized by distention and increase in diameter of all visible veins, hepatomegaly, systolic (and in the absence of aurieular fibrillation, presystolic), venous and hepatic pulsations, cyanosis, jaundice, enlargement of the heart to the right, and The clinical evidence of cirrhosis murmurs over the area of the tricuspid valve. The special of the liver or of congestive heart failure may complicate the picture. pathologic condition causing this syndrome consists in insufficiency and variable degrees of stenosis of the tricuspid valve, dilatation of the right auricle and of the veins, and cirrhosis of the liver. The eardiae output is normal when congestive failure is not present. Nevertheless, the venous pressure is elevated, proving that the rise in pressure is due to mechanical obstruction to the heart’s inflow of blood. When cardiac decompensation occurs, the output of the heart diminishes and the venous pressure rises above its former high level. The relation of the pathologic and physiologic features of the syndrome to its clinical manifestations is discussed in detail. AUTHORS.
Stickney, J. Minott, and Keith, Lupus Erythematosus. Arch.
Norman Int.
Med.
M.: 66:
Renal InvoIvement 643,
in Disseminated
1940.
The visceral involvement in disseminated lupus erythematosus has been reviewed clinically. The pathologic changes in the kidneys in fifteen fatal cases have been studied. In eight of the fifteen cases there was no definite renal change except that seen terminally in debilitating disease. Without exception, the weight of the kidneys was normal or greater than normal. No contracted kidneys were found. The most definite lesion was a proliferation of the endothelial ceils of the gllomerular capillaries, Hyaline thickening of these capillary walls and an irregularity and -thickening of the basement membrane were also frequently present. These changes are somewhat similar to those which have been described in acute glomerulonephritis and the toxemias of pregnancy. In one case in this series (Case 15) there were pathologic changes characteristic of glomerulonephritis. The relationship of the changes noted to the lupus erythematosus is uncertain, since the renal disease preceded the cutaneous and the cutaneous lesions were inactive during the final illness. In one other instance (Case 4) there was some evidence of a subacute or early chronic glomerulonephritis. In this patient, too, the evidence of renal damage was known to have antedated the onset of the cutaneous lesions. The arteries and arterioles were normal in most of the cases. In several there was slight thickening of the intima, but no thromboses were seen. The changes in the tubules were of a minor nature. AUTHORS.
647
ABSTRACTS
The demonstration of a calcified mitral valve is unequivocal evidence stenosis and also indicates its rheumatic etiology. Dilatation of the left auricle without general cardiac enlargement presumptive evidence of mitral stenosis. The diagnosis of mitral stenosis can be made amination, even in the absence of characteristic “ subclinical mitral disease. ”
at
times physical
by
of mitral is highly
roentgenologie signs herein
excalled
AUTROR. Altschule,
Valve.
Mark Arch.
D., and Budnitz, Path. 30: 7, 1940.
Edward:
Rheumatic
Disease of the Tricuspid
The clinical syndrome of rheumatic disease of the tricuspid valve is charaeterized by distention and increase in diameter of all visible veins, hepatomegaly, systolic (and in the absence of aurieular fibrillation, presystolic), venous and hepatic pulsations, cyanosis, jaundice, enlargement of the heart to the right, and The clinical evidence of cirrhosis murmurs over the area of the tricuspid valve. The special of the liver or of congestive heart failure may complicate the picture. pathologic condition causing this syndrome consists in insufficiency and variable degrees of stenosis of the tricuspid valve, dilatation of the right auricle and of the veins, and cirrhosis of the liver. The eardiae output is normal when congestive failure is not present. Nevertheless, the venous pressure is elevated, proving that the rise in pressure is due to mechanical obstruction to the heart’s inflow of blood. When cardiac decompensation occurs, the output of the heart diminishes and the venous pressure rises above its former high level. The relation of the pathologic and physiologic features of the syndrome to its clinical manifestations is discussed in detail. AUTHORS.
Stickney, J. Minott, and Keith, Lupus Erythematosus. Arch.
Norman Int.
Med.
M.: 66:
Renal InvoIvement 643,
in Disseminated
1940.
The visceral involvement in disseminated lupus erythematosus has been reviewed clinically. The pathologic changes in the kidneys in fifteen fatal cases have been studied. In eight of the fifteen cases there was no definite renal change except that seen terminally in debilitating disease. Without exception, the weight of the kidneys was normal or greater than normal. No contracted kidneys were found. The most definite lesion was a proliferation of the endothelial ceils of the gllomerular capillaries, Hyaline thickening of these capillary walls and an irregularity and -thickening of the basement membrane were also frequently present. These changes are somewhat similar to those which have been described in acute glomerulonephritis and the toxemias of pregnancy. In one case in this series (Case 15) there were pathologic changes characteristic of glomerulonephritis. The relationship of the changes noted to the lupus erythematosus is uncertain, since the renal disease preceded the cutaneous and the cutaneous lesions were inactive during the final illness. In one other instance (Case 4) there was some evidence of a subacute or early chronic glomerulonephritis. In this patient, too, the evidence of renal damage was known to have antedated the onset of the cutaneous lesions. The arteries and arterioles were normal in most of the cases. In several there was slight thickening of the intima, but no thromboses were seen. The changes in the tubules were of a minor nature. AUTHORS.