Intravenous gammaglobulin-associated acute renal failure

Gupta, Nitin; Ahmed, Iftikhar; Nissel-Horowitz, S.; Patel, Dilip; Mehrotra, Bhoomi

doi:10.1002/1096-8652(200102)66:2<151::aid-ajh1035>3.0.co;2-q

Cited by 32 publications

(6 citation statements)

References 7 publications

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“…22 Our data raise the possibility that IVIG may be beneficial in preventing or treating sickle cell vaso-occlusion. Caution is necessary, however, because IVIG administration has been associated with both renal toxicity 23,24 and thrombosis, 25 including an estimated 0.6% risk of stroke, 26 and there is reason to believe that patients with sickle cell disease may be predisposed to such toxicities. For personal use only.…”

Section: Resultsmentioning

confidence: 99%

Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes

Turhan

Jenab

Bruhns

et al. 2004

Blood

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Section: Resultsmentioning

confidence: 99%

Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes

Turhan

Jenab

Bruhns

et al. 2004

Blood

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“…Acute renal failure is a rare complication with approximately 150 cases reported in the literature 10 and has been associated with diabetes, preexisting renal disease, advanced age, and administration of intravenous immunoglobulin in saccharose-based solutions. Adverse thrombotic events have also been reported, such as acute myocardial infarction and stroke.…”

Section: Discussionmentioning

confidence: 99%

Insuficiência renal aguda após uso de imunoglobulina intravenosa para tratamento de miocardite

Pordeus¹,

Tostes²,

Mesquita³

et al. 2005

Arq. Bras. Cardiol.

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The patient is a 60-year-old female with functional class III/ IV (NYHA) heart failure of an immunomediated etiology (autoimmune myocarditis). After unsuccessful therapeutic attempts, intravenous immunoglobulin was used, leading to deterioration in renal function, a rare complication of that therapy. After hemodialysis, the patient's renal function was restored, and the chronic heart failure improved to functional class I.Myocardites constitute a group of diseases characterized by immuno-inflammatory aggression against the myocardium. The anatomicopathological substrate of this aggression has been classically described as a cellular infiltration of lymphocytes, macrophages, and other leukocytes, with destruction of cardiomyocytes, myocytolysis (Dallas criteria) 1 . In past years, advances in understanding of the complex pathophysiology of the disease and low sensitivity of the histopathological criteria have forced us to widen the model of aggression to beyond the immune response of the classical cellular type (Th1). Currently, we believe that an immunomediated aggression against the myocardium occurs, even when the infiltration of immunologic cells is absent. The characterization of pathogenic autoantibodies specific for more than a dozen autoantigens has led us to a new model 2 . The etiology of those diseases is still obscure. Activation of the immunologic system is known to occur, resulting in different forms of myocardial injury. The pathogenic stimuli that lead to the development of that cardiospecific aggression are yet to be elucidated.The current major hypothesis is based on the model of viral infection as the promoter of the immune reaction directed against the heart. Different types of viruses, such as coxsackievirus, parvovirus, adenovirus, cytomegalovirus, Epstein-Barr virus, and parvovirus B19, have often been implicated. However, most clinical studies have shown great variability and low positivity in evidencing the viruses 1 . Other clinical phenomena, such as skin diseases (eg, psoriasis and vitiligo), systemic autoimmune diseases, and even intestinal diseases, such as celiac disease, have been significantly associated with myocardites, suggesting, therefore, a wide and complex pathophysiological model 3 .The clinical findings of myocardites are highly varied. Their symptoms may range from fever and malaise to cardiac symptoms, such as palpitation, dyspnea, and chest pain. The physical examination, and laboratory and radiological findings are not specific, making the diagnosis difficult, which requires an elevated clinical suspicion.The most accurate noninvasive diagnostic method is indium-111 antimyosin myocardial scintigraphy 4 . This technique is not available in our country. However, another technique of nuclear medicine that uses gallium 67, a marker of inflammation, has been used despite its lower sensitivity and specificity.The endomyocardial biopsy, using Dallas histopathologic criteria, has been the standard diagnostic method, despite its low sensitivity. That technique has been boosted...

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“…In the 3 other cases, IVIgG was beneficial in the treatment of post-transfusion hyperhemolysis in sickle cell patients and no sickle crisis or other side effects were reported (18,92). Because IVIgG administration can produce serious dysfunction of the kidney (13,42), an organ targeted by sickle cell disease, its use in this patient population should be carefully evaluated through a well-designed prospective clinical trial.…”

Section: Effects Of High-dose Intravenous Gammaglobulinsmentioning

confidence: 99%

Sickle Cell Vasoocclusion: Heterotypic, Multicellular Aggregations Driven by Leukocyte Adhesion

Frenette

2004

Microcirculation

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Homozygous expression of sickle beta-globin alters the function of blood cells and the endothelium, producing a wide spectrum of clinical manifestations. Intravital microscopy studies in sickle cell mice suggest that vasoocclusion is a complex, sequential, multistep phenomenon involving (1) endothelial activation by sickle erythrocyte (SSRBC), (2) leukocyte (WBC) adhesion to the endothelium, and (3) the direct interaction between SSRBCs and adherent WBCs, which leads to reduced blood flow and tissue ischemia. Each of these steps represents a potentially useful therapeutic target. The identification of molecular determinants mediating vasoocclusion will provide new strategies for the prevention and treatment of this debilitating illness.

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Intravenous gammaglobulin-associated acute renal failure

Cited by 32 publications

References 7 publications

Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes

Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes

Insuficiência renal aguda após uso de imunoglobulina intravenosa para tratamento de miocardite

Sickle Cell Vasoocclusion: Heterotypic, Multicellular Aggregations Driven by Leukocyte Adhesion

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