Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

Dragun, Duska; Müller, Dominik N.; Bräsen, Jan Hinrich; Fritsche, Lutz; Nieminen-Kelhä, Melina; Dechend, Ralf; Kintscher, Ulrich; Rudolph, Birgit; Hoebeke, Johan; Eckert, Diana; Mazák, István; Plehm, Ralph; Schönemann, Constanze; Unger, Thomas; Budde, Klemens; Neumayer, Hans‐Hellmut; Luft, Friedrich C.; Wallukat, Gerd

doi:10.1056/nejmoa035717

Cited by 777 publications

(736 citation statements)

References 37 publications

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“…Furthermore, because our data support the clinical relevance of AMR diagnostic criteria during LT with regard to HLA DSAs, the relationship between AMR and non-HLA-Ab (of either allo-or autoimmune nature) (44) may be further characterized, analogous to what has occurred in kidney transplantation (45)(46)(47). Our data indicate the presence of RAS exclusively during AMR.…”

mentioning

confidence: 49%

Antibody-Mediated Rejection in Lung Transplantation: Clinical Outcomes and Donor-Specific Antibody Characteristics

Roux

Lan

Holifanjaniaina

et al. 2016

American Journal of Transplantation

121

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mentioning

confidence: 49%

Antibody-Mediated Rejection in Lung Transplantation: Clinical Outcomes and Donor-Specific Antibody Characteristics

Roux

Lan

Holifanjaniaina

et al. 2016

American Journal of Transplantation

121

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“…In preeclampia, diminished placental perfusion could alter the AT 1 receptor expression in an aberrant fashion, thereby permitting autoantibody production (6). And in allograft renal-rejection subjects, posttransplantation reperfusion injury may alter the intragraft expression of AT 1 receptor, change its density, or cause conformational changes; a permissive environmental phenomenon might enhance local intragraft immunoreactivity owing to an activated innate immune response (33). It seems that both of the speculations could not explain the AT 1 -AAs phenomenon in hypertension.…”

Section: Discussionmentioning

confidence: 99%

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

et al. 2008

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Agonistic AT 1 receptor autoantibodies (AT 1 -AAs) have been described in the patients with malignant hypertension or preeclampia. Furthermore, AT 1 -AAs were highly associated with refractory hypertension. Function of vascular smooth muscle cells (VSMCs) is important in the regulation of blood pressure. We investigated and compared the ability of angiotensin II (Ang II) and AT 1 -AAs to stimulate the intracellular calcium mobilization and cellular proliferation of rat VSMCs. Twenty-two patients with refractory hypertension, 24 patients with non-refractory hypertension and 37 normotensives were recruited. The serum of each patient was detected for the presence of

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“…These autoantibodies against AT 1 receptors lead to a stimulation of the receptor (18). Some renal transplant patients who have chronic allograft failure without classic HLA antibodies have such agonistic antibodies against the AT 1 receptor, and they were involved in vasculitis with destruction of the renal allograft (18).…”

Section: Angii Receptorsmentioning

confidence: 99%

Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

Rüster

Wolf

2006

Journal of the American Society of Nephrology

413

320

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Inhibition of the renin-angiotensin-aldosterone system (RAAS) is one of the most powerful maneuvers to slow progression of renal disease. Angiotensin II (AngII) has emerged in the past decade as a multifunctional cytokine that exhibits many nonhemodynamic properties, such as acting as a growth factor and profibrogenic cytokine, and even having proinflammatory properties. Many of these deleterious functions are mediated by other factors, such as TGF-␤ and chemoattractants that are induced in the kidney by AngII. Moreover, understanding of the RAAS has become much more complex in recent years with the identification of novel peptides (e.g., AngIV) that could bind to specific receptors, elucidating deleterious effects, and non-angiotensin-converting enzyme (ACE)-mediated generation of AngII. The ability of renal cells to produce AngII in a concentration that is much higher than what is found in the systemic circulation and the observation that aldosterone may be engaged directly in profibrogenic processes independent of hypertension have added to the complexity of the RAAS. Even renin has now been identified to have a "life on its own" and mediates profibrotic effects via binding to specific receptors. Finally, drugs that are used to block the RAAS, such as ACE inhibitors or certain AngII type 1 receptor antagonists, may have properties on cells independent of AngII (ACE inhibitor-mediated outside-inside signaling and peroxisome proliferatoractivated receptor-␥ stimulatory effects of certain sartanes). Although blockade of the RAAS with ACE inhibitors, AngII type 1 receptor antagonists, or the combination of both should be part of every strategy to slow progression of renal disease, a better understanding of the novel aspects of the RAAS should contribute to the development of innovative strategies not only to completely halt progression but also to induce regression of human renal disease.

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Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

Cited by 777 publications

References 37 publications

Antibody-Mediated Rejection in Lung Transplantation: Clinical Outcomes and Donor-Specific Antibody Characteristics

Antibody-Mediated Rejection in Lung Transplantation: Clinical Outcomes and Donor-Specific Antibody Characteristics

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

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