Antiphospholipid syndrome presenting as unilateral renal artery occlusion: case report and literature review.

The objective of this study is to report a case of primary antiphospholipid syndrome (APS) presenting as complete renal artery occlusion, and to review the literature on the subject. We describe the clinical presentation, course and outcome of one patient who presented with resistant hypertension later found to be due to thrombosis and complete occlusion of the left renal artery. We review the medical literature registered in the Medline PubMed database from 1966 to 2004 using keywords: antiphospholipid, Hughes syndrome, kidney, renal, renal artery thrombosis. We describe one patient and analyzed ten well-documented cases of renal artery thrombosis due to APS. Most of the patients were women, at a mean age of 32 years. All but one case had primary APS. The presenting symptom was hypertension in ten cases. Most patients had both lupus anticoagulant and anticardiolipin antibodies. Arterial occlusion was left sided in 55%, right sided in 27% and bilateral in 18%. Renal artery thrombosis is an uncommon presentation of APS. This entity should be considered in the differential diagnosis of severe hypertension.

Large aorta and narrow arteries: two short stories of too long diagnostic delay.

The diagnosis of Takayasu arteritis requires a high degree of clinical suspicion. We herein present two cases of Takayasu arteritis that demonstrate two important aspects of the disease, which leaded to a significant delay in the diagnosis. The first case presented with an indolent disease with a clinical course of 20 years until clinical diagnosis was finally established while the second case shows the commonly unrecognised aspect of severe renovascular hypertension in these patients.

Fucoidin, an inhibitor of leukocyte adhesion, exacerbates acute ischemic renal failure and stimulates nitric oxide synthesis.

OBJECTIVES: To lessen renal ischemic injury caused by fucoidin, a substance capable of reducing tissue infiltration by neutrophils, and to seek a possible interrelationship with the nitric oxide system which may also modulate leukocyte infiltration. MATERIAL AND METHODS: Acute ischemic renal failure was induced in rats by uninephrectomy followed by 60 min of clamping of the renal artery. The rats were injected with fucoidin (25 mg/kg) or fucoidin+nitroprusside (2.5 mg/kg) before reperfusion, and urine was collected for 24 h afterwards. Serum and urine were examined for creatinine sodium and protein; creatinine clearance and fractional excretion of sodium (FENa) were calculated. The renal tissue of the sacrificed animals was examined histologically for tissue damage and histochemically for myeloperoxidase, a marker of neutrophil infiltration. The nitric oxide system was evaluated by measuring urinary nitrates and inducible nitric oxide synthase messenger RNA (iNOs mRNA). RESULTS: Renal failure was more severe in the fucoidin group than the nitroprusside group (creatinine clearance 0.11+/-0.08 ml/min for ischemia+fucoidin versus 0.26+/-0.11 ml/min for ischemia only; p<0.002). Adding nitroprusside to fucoidin lessened the decline in creatinine clearance (0.13+/-0.13 ml/min; p=NS). Fucoidin was associated with greater tubular damage, as evidenced by increased FENa (7.2%+/-2.8% vs 1.51%+/-1.96% for ischemia only; p<0.001). Nitroprusside weakened this trend. Fucoidin caused an increase in the fractional excretion of nitrates, a response accompanied by increased iNOS mRNA. CONCLUSIONS: Fucoidin failed to protect the kidney from ischemic damage and was even nephrotoxic. It also stimulated the formation of iNOS RNA.

Acute myeloid leukemia presenting as obstructive jaundice.

A 36-year-old man presented with abdominal pain and jaundice. Ultrasound examination of the abdomen showed dilatation of the intrahepatic bile ducts and a normal common bile duct. No calculi were demonstrated. A computerized tomography scan did not show any masses. A peripheral blood smear was diagnostic of acute myeloid leukemia. After remission-inducing chemotherapy, there was a complete regression of the jaundice, which had not recurred at the 12-month follow-up.

A lipid emulsion reduces mortality from clomipramine overdose in rats.

Tricyclic antidepressants are a common cause of self poisoning. Since these drugs are highly lipid soluble, we examined the interaction between imipramine and a lipid emulsion. Rats were given an iv dose of imipramine with either normal saline or a lipid emulsion as vehicle. The rats who received the lipid emulsion had a significantly lower mortality. The role of lipid emulsions poisoning therapy is reviewed.

Heparin-induced thrombocytopenia with thrombotic sequelae: a review.

Heparin-induced thrombocytopenia (HIT) occurs in 1-5% of patients treated with heparin. The pathogenesis involves the formation of antibodies to heparin-platelet factor 4 complexes, and the major clinical sequelae are thrombotic. Diagnosis is based on a combination of clinical and laboratory data. Treatment consists of stopping heparin, but, insofar as the risk of thrombosis remains high, treatment by alternative antithrombotic agents is indicated. Most clinical experience has been with danaparoid sodium and hirudin. The use of low-molecular-weight heparins (LMWH) in subsequent HIT episodes has been described, but is not recommended, especially with the introduction of new agents, such as oral thrombin inhibitors and pentasaccharides, which are hoped to reduce the use of heparins and the occurrence of HIT.