Renal Thrombotic Microvascular Disease Associated with Lupus Anticoagulant

Kincaid‐Smith, Priscilla; Nicholls, Kathy

doi:10.1159/000185881

Cited by 19 publications

(8 citation statements)

References 9 publications

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“…In our case, the absence of renal failure or urinary abnormal ities at the onset of the clinical picture make such a possi bility improbable. Furthermore, other conditions such as thrombotic microangiopathy or severe nephroangiosclerosis [22,24,25] were excluded by clinical and histologi cal findings.…”

Section: Discussionmentioning

confidence: 99%

Renal Infarction in a Severely Hypertensive Patient with Lupus erythematosus and Antiphospholipid Antibodies

Hernández

Dominguez²,

Diaz³

et al. 1996

Nephron

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Systemic lupus erythematosus (SLE) patients, specially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations. However, renal infarction has been rarely reported in these patients. The case of a young female with renal infarction, diagnosed by renal arteriography and scintigraphy, and arterial hypertension (AH) is described. In subsequent years she also suffered several cerebrovascular accidents with important neurological sequelae. No evidence of systemic disease was observed at this time. Fourteen years after the renal infarction a diagnosis of SLE was established. Despite therapy with prednisone, acetylsalicylic acid, azathioprine and antihypertensive drugs the progression of the neurological disease led to death. The sudden appearance of severe AH in a young woman with a renal infarction should alert the clinician about a possible underlying renal artery thrombosis in association with SLE and antiphospholipid antibodies.

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Section: Discussionmentioning

confidence: 99%

Renal Infarction in a Severely Hypertensive Patient with Lupus erythematosus and Antiphospholipid Antibodies

Hernández

Dominguez²,

Diaz³

et al. 1996

Nephron

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“…Rapidly progressive renal failure with mi croangiopathic hemolytic anemia and malignant hyper tension is frequent in the clinical context of scleroderma and is known as 'sclerodermal crisis'. Sometimes, as in the case we present, hypertension is only moderate and in a percentage of 10-40%, renal insufficiency is not accom panied by hypertension [8,9], Histologic findings in the acute form of scleroderma are impossible to distinguish from other forms of throm botic microangiopathy [9], Recently Kincaid-Smith and co-workers [4,5] have described this type of lesion in the renal biopsy of a group of 12 women with circulant LA and a high incidence of spontaneous abortion. This clini cal setting has been considered a postpartum malignant nephroangiosclerosis variant, described for the first time by Counihan and Doniach [10] in 1954.…”

Section: Discussionmentioning

confidence: 99%

“…It is not possible to establish a definite pathogenic relationship between both phenomena from only 1 case. Nevertheless, this association can be considered of inter est in view of the described coexistence of circulant LA with a pattern of thrombotic microangiopathy [2][3][4][5]11] and the importance of intravascular thrombosis as a trigger of the sclerodermal crisis. The frequent finding of microthrombosis at the small vessel and glomerular level is contemplated by some authors as the pathogenic basis of the rapidly progressive renal failure in scleroderma, having been considered the microangiopathic hemolytic anemia as the definite marker for the development of renal failure [9].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, thrombotic involve ment of small renal vessels and glomeruli has been re ported in patients with SLE and LA, these cases present ing a worse evolution of renal function [2,3). KincaidSmith et al [4] have described the occurrence of throm botic microangiopathic lesions in the kidneys of women with a circulating LA and, as it has been recently noted in an editorial of Nephron [5], this has been the first descrip tion of thrombotic lesions involving the microvasculature in LA patients not affected by SLE. The aim of this work is to present the case of a woman with an overlap sclero derma-polymyositis syndrome and a positive circulating LA who developed a scleroderma nephropathy, charac terized by rapidly progressive renal failure caused by thrombotic microangiopathy with widespread thrombi in small arteries and glomeruli.…”

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confidence: 99%

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Thrombotic Microangiopathic Nephropathy in Scleroderma and Lupus Anticoagulant

Quereda¹,

Pascual²,

Pardo³

et al. 1991

Nephron

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A 47-year-old woman with overlap scleroderma-polymyositis syndrome and positive circulating lupus anticoagulant developed scleroderma nephropathy, characterized by rapidly progressive renal failure caused by thrombotic microangiopathy with widespread thrombi in small arteries and glomeruli. The possible relationship between lupus anticoagulant and the development of thrombosis at the small renal vessels level with the triggering of the scleroderma crisis is discussed.

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“…It is noteworthy that intrarenal thrombosis occurring in association with LA is not confined to patients with SLE [8]. An earlier report documented 12 women with pregnancy-related acute renal failure (only 2 of whom had lupus nephritis) caused by thrombotic microangiopathy (TMA) occurring in association with LA [9].…”

Section: Introductionmentioning

confidence: 99%

Anticardiolipin Antibodies in South African Patients with Lupus Nephritis: A Clinical and Renal Pathological Study

Naiker¹,

Rughubar²,

Duursma³

et al. 2000

Am J Nephrol

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Aims: This study was conducted prospectively to ascertain the prevalence of anticardiolipin antibodies (ACAs) in patients with lupus nephritis and to determine whether this subgroup of patients differed clinically and histologically from patients without the antibody. Patients and Methods: 40 SLE patients (26 Blacks, 14 Indians, 37 females, 3 males) with evidence of renal involvement underwent clinical assessment and percutaneous renal biopsy. Special investigations included: urinary protein quantitation; radioisotope glomerular filtration rate (GFR); complement levels, and antinuclear antibodies and ACAs. Histology was reviewed by a single senior pathologist blinded to the ACA results. In addition to the standard WHO classification, specimens were examined for intrarenal thrombosis. Results: The prevalence of ACA was 45% (18 of 40 patients). Thrombocytopenia was more frequent in patients with ACA (33 vs. 13.6%, p = 0.015). Patients with ACA did not differ from controls with regard to the incidence of thrombosis, neurological disorders, recurrent fetal loss, active disease and hypertension. Mean GFR and 24-hour urine protein (ACA vs. controls) were 51.3 versus 67 ml/min (NS) and 2.4 versus 3.7 g (NS), respectively. Intrarenal microvascular thrombosis (glomerular and arteriolar) occurred in 27.7% of ACA patients versus 9% of controls (p = 0.025). Apart from a higher incidence of class-III nephritis in the controls, standard histology (WHO classification) did not differ between the 2 groups. Conclusion: The prevalence of ACA in our patients with lupus nephritis was 45%. This subgroup did not differ from patients without the antibody apart from a higher incidence of thrombocytopenia and intrarenal microvascular thrombosis.

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Renal Thrombotic Microvascular Disease Associated with Lupus Anticoagulant

Cited by 19 publications

References 9 publications

Renal Infarction in a Severely Hypertensive Patient with Lupus erythematosus and Antiphospholipid Antibodies

Renal Infarction in a Severely Hypertensive Patient with Lupus erythematosus and Antiphospholipid Antibodies

Thrombotic Microangiopathic Nephropathy in Scleroderma and Lupus Anticoagulant

Anticardiolipin Antibodies in South African Patients with Lupus Nephritis: A Clinical and Renal Pathological Study

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