A family with familial combined hyperlipidaemia in which affected members had nonsymmetric subcutaneous lipomatosis (NSSCL) is described. Affected members had high serum levels of total cholesterol, low density lipoprotein (LDL) cholesterol and high density lipoprotein (HDL) cholesterol. By contrast, family members without NSSCL had normal lipid levels. There was also a correlation between the degree of hyperlipidaemia and the amount of subcutaneous lipomas. The occurrence of hyperlipidaemia in family members with NSSCL suggests the existence of a genetic linkage between these two characteristics, but did not show any association with HLA haplotyping. To our knowledge this association between lipid abnormalities and NSSCL has not been previously reported.

A seventy-six-year-old man with ischemic heart disease, peripheral vascular disease, and chronic renal failure developed bilateral cyanotic toes, which upon muscle biopsy, were shown to be caused by atheromatous emboli. The probable source was atheromatosis of the abdominal aorta. The toes became gangrenous, but surgical therapy was deferred because the patient was considered a high risk. With lovastatin therapy there was complete healing and except for transient cyanosis related to temporary cessation of therapy, there has been no recurrence for the past thirty months. The possible role of lovastatin in the conservative treatment of this disorder is discussed.

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.

Changes in nitric oxide (NO) levels were determined in ischaemic acute renal failure in streptozotocin-induced diabetes mellitus rats. Two weeks after streptozotocin administration and immediately after right nephrectomy, the left renal artery was occluded for 60 min. Similar procedures were carried out in non-diabetic rats. The nitrite (NO2) + nitrate (NO3) levels were measured in plasma and urine. The effects of chronic oral supplementation with L-arginine and an NO synthase inhibitor (N-omega-nitro-L-arginine) were also studied in both diabetic and non-diabetic rats before and after renal artery clamping. The rats with diabetic acute renal failure had a much lower creatinine clearance (90 +/- 22 microliters.min-1. 100g body weight-1, p < 0.005), and higher fractional excretion of sodium (FENa)% (10.90 +/- 4.2, p < 0.001) and protein excretion (2078 +/- 69 micrograms/ml creatinine clearance, p < 0.001) compared with the respective values in the non-diabetic groups (163 +/- 30; 1.46 +/- 86; 453.3 +/- 31). The plasma and urine NO2 + NO3 levels were significantly higher in the untreated diabetic rats compared with the untreated normal rats before ischaemia (p < 0.001). The ischaemic acute renal failure in non-diabetic rats increased the plasma and urinary NO2 + NO3 excretion after ischaemia. The urinary excretion of these metabolites decreased significantly and their plasma levels remained unchanged in the ischaemic diabetic rats. The L-arginine administration resulted in a small but significantly higher creatinine clearance after clamping in the non-diabetic rats. The NO synthase inhibitor caused deterioration in renal function in all ischaemic and non-ischaemic groups. In summary, the greater vulnerability to ischaemia of the diabetic kidney seems to be associated with both impaired response to and impaired production of NO.

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.