Malignant Nephrosclerosis in Women Post Partum

Scheer, Robert; Jones, David B.

doi:10.1001/jama.1967.03130080042009

Cited by 34 publications

(10 citation statements)

References 10 publications

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“…3 We designed this trial to compare the efficacy of and tolerance to diclofenac sodium, a potent inhibitor of prostaglandin synthetase, with those of the commonly prescribed narcotic pethidine in the management of acute renal colic.…”

Section: Resultsmentioning

confidence: 99%

Lack of difference between malignant and accelerated hypertension.

Ahmed¹,

Walker²,

Beevers³

et al. 1986

BMJ

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Section: Resultsmentioning

confidence: 99%

Lack of difference between malignant and accelerated hypertension.

Ahmed¹,

Walker²,

Beevers³

et al. 1986

BMJ

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“…37 These observations accord better with MHA as a cause than as a consequence of the malignant phase.…”

Section: Features Of Mha and Malignant Hypertensionmentioning

confidence: 56%

“…40 -41 In some of these instances, fibrinoid necrosis appears to have developed while the blood pressure was normal or only slightly increased. 37 ' 40 Luminal fibrinoid, often extending into the glomerulus, together sometimes with glomerular infarction, is a more common finding in these states than fibrinoid necrosis. 10 -13 ' 35 ' 40~*8 Intimal hyperplasia or proliferation has also been described.…”

Section: Fibrinoid Lesions and The Coagulation Defectmentioning

confidence: 99%

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

Gavras¹,

Brown²,

Brown³

et al. 1971

Circ Res

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Evidence of microangiopathic hemolytic anemia (MHA) was found in 14 of 22 patients with malignant phase hypertension, and in one of these, a patient with proliferative glomerulonephritis, MHA and malignant hypertension developed together during a three-month period of observation.Among 61 rats subjected to unilateral nephrectomy, injected with DOCA, and given 1% saline to drink, 42 developed evidence of MHA, Eighty-four per cent of these also had fibrinoid necrosis and/ or plasmatic vasculosis in the remaining kidney at autopsy. Blood pressure rose to 150 mm Hg or more in 72% of these DOCA-injected animals. In 29 control rats subjected to unilateral nephrectomy only, blood pressure rose to 150 mm Hg or more in 2135, MHA developed in 14%, and fibrinoid lesions were found in none.The significance of these observations is discussed in relation to the possibility that MHA is either a consequence of malignant hypertension or a contributory factor in its pathogenesis. KEY WORDSmicroangiopathic hemolytic anemia DOCA malignant hypertension fibrinoid lesions bilateral nephrectomy renal failure intravascular coagulation glomerulonephritis• An association between malignant phase hypertension and microangiopathic hemolytic anemia (MHA) is now well recognized. 1 " 5Since the association appears relatively common and since MHA, when it occurs in other states, is characterized by features similar to those of malignant hypertension, it seemed possible to us that MHA might at least contribute to the development of the malignant phase. 6 If this is so, MHA should be demonstrable when (or before) the malignant phase appears. Our earlier studies threw little light on this particular question since, by the time most patients presented, both the conditions were well established.

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“…Postpartum hemolytic-uremic syndrome (PPHUS) was first reported some 20 years ago [1][2][3]. Its picture was then described as including acute renal failure (ARF) following uncomplicated pregnancy and uneventful de livery, toghether with ingravescent hypertension, micro angiopathic hemolytic anemia (M HA) and thrombocyto penia, classic histological evidence of thrombotic micro angiopathy (double contour, fluffy translucent subendothelial deposits, mesangiolysis), vascular lesions and a very poor prognosis in terms of both renal function and mortality [4][5][6][7].…”

Section: Sirmentioning

confidence: 99%