Angiotensin II receptor agonist antibodies are associated with microvascular damage in lupus nephritis

Angiotensin II type 1 receptor agonist antibodies (AT1R-AAs) have been associated with hypertension, atherosclerosis and vascular inflammation in human diseases. The aim of the study was to evaluate the prevalence of AT1R-AAs in active lupus nephritis (LN) patients and their association with vascular damage. One hundred and seven active LN patients underwent a complete clinical examination, measurement of AT1R-AAs, ambulatory blood pressure monitoring, carotid intima-media thickness measurement and morphometric analysis of subintimal fibrosis and medial hyperplasia of the vessels in the kidney tissue. Plasma AT1R-AAs were positive in 58 (54.2%) patients. The Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score, complement C3 and C4 levels and titers of anti-dsDNA antibodies were higher in the group with positive AT1R-AAs compared with those with negative AT1R-AAs. The AT1R-AA titers correlated with anti-dsDNA antibody titers and with complement C3 and C4 serum levels. In the kidney biopsy, the percentage of subintimal fibrosis and the area of medial hyperplasia were greater in the AT1R-AA-positive patients. No differences in arterial pressure, carotid intima-media thickness and response to therapy were detected. In conclusion, AT1R-AAs are prevalent in active LN patients and are associated with histologic features of microvascular damage.

Morphological changes in the Heart in unrelated deaths

Background: Cardiovascular diseases are the major cause of morbidity and mortality worldwide. In the Indian subcontinent, they account for more than 25% of deaths. Numerous studies have been conducted on the cardiovascular system in cases of sudden death; but there has been a major neglect to study the heart in cases of people who died of unrelated causes.In the present study, we have attempted to study the CVS in detail in those individuals who died of unrelated causes and have tried to assess the prevelance of atherosclerosis, conduction system lesions, inflammatory and valvular pathologies in them.Materials and Methods: The present study was a prospective one conducted from June 2007 to June 2009 in the department of Pathology, Kasturba Medical College, Mangalore. The hearts of persons who died of unrelated causes were studied.Results: Various lesions encountered in the heart were coronary artery disease (70.58%), medial hyperplasia of SAnode (38.23%) and AV node (55.88%), chronic inflammation of the conduction system (55.88%) and calcification (11.76%). Malarial myocarditis was seen in 5.88% and pulmonary stenosis was seen in 2.94% of the cases. No cardiac pathology was detected in 5.88% cases.Conclusion: Our study highlights the prevelace of atherosclerotic changes and conduction system abnormalities in the general population. Hence, we conclude that examination of the CVS is extremely important in cases of sudden death; but it should also be made mandatory in unrelated deaths too, as it can diagnose a lot of hidden pathology.

Morphological features of vasa vasorum in pathologically changed human great saphenous vein and its tributaries

Background: The question whether the primary increase of vasa vasorum (VV) of venous wall (i) plays an initial role in varicogenesis or (ii) is an expression of impairment of the nutritional conditions in superficial veins of lower extremities is not unambiguously solved yet. The aim of the study was to describe the arrangement of the VV within the wall of the human great saphenous vein (GSV) qualitatively, and of its tributaries at different stages of varicosis and in other pathological states like thrombophlebitis or phlebosclerosis. Material and methods: 22 patients deserving an aorto-coronary bypass surgery or GSV surgery were subdivided into three groups according to the staging of their varices and other pathology. The harvested GSV were prepared for light and scanning electron microscopy. One cadaverous specimen of GSV was injected with India ink. Results: In specimens from reticular and primary large varices local intimal hyperplasia was regularly found, partially accompanied with a mild increase of VV. Tortuosities and irregular dilations of adventitial veins were also found. In patients with recurrent primary varices or thrombophlebitis severe intimal and medial hyperplasia, thrombosis and a striking increase of VV were found. The intima remained avascular in all cases. Conclusions: Remarkable increase of VV accompanies the most severe forms of varices as well as all cases of the extreme grades of phlebosclerosis, medial hyperplasia and thrombosis. We hypothesize that this increase in VV is rather a secondary vascular reaction to the impaired metabolic conditions within the venous wall than a primary varicogenic factor.