Nitric oxide and oxidative stress in atherosclerotic renovascular hypertension: Effect of endovascular treatment

WOS: 000184102500008PubMed ID: 12847196PURPOSE: Because activation of the renin-angiotensin system leads to an increase in oxidative stress, the authors investigated nitric oxide (NO; nitrite + nitrate), superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) levels and the effect of endovascular treatment on these parameters in patients with atherosclerotic renovascular hypertension. The relationship of NO with blood pressure and renal functional indexes was also investigated. MATERIALS AND METHODS: In this prospective cohort study, serum creatinine, NO, SOD, catalase, plasma MDA, urinary microalbumin, and NO levels, and blood pressure were determined in 21 patients with hypertension and unilateral renal artery stenosis caused by atherosclerosis at entry and after 24 hours, 2 weeks, and 6 weeks of endovascular treatment. RESULTS: MDA concentrations decreased 24 hours after intervention and remained low 2 and 6 weeks later. In addition, serum SOD and NO and urine NO levels were increased significantly 24 hours after endovascular treatment and decreased after 2 and 6 weeks. However, serum catalase levels did not differ after the intervention. Blood pressures decreased after treatment. There were no significant differences in urinary microalbumin levels, estimated glomerular filtration rates, and creatinine levels after endovascular treatment. CONCLUSIONS: Endovascular treatment decreases oxidative stress and may offer new benefits in the treatment of patients with hypertension associated with renal artery stenosis. The decrease in oxidative stress and/or the upregulation of SOD may increase the bioavailability of NO, which in turn may lead to the rapid hypotensive response

Spuriously elevated inorganic phosphate level in a multiple myeloma patient

WOS: 000184333200011PubMed ID: 12890170We report the case of a patient with IgG multiple myeloma and pseudohyperphosphatemia. The patient had no clinical features of hyperphosphatemia. Subsequent investigations demonstrated that this hyperphosphatemia was spurious and was caused by a high concentration of the paraprotein. Deproteinization of the serum samples by sulfosalicylic acid resulted in normalization of the elevated phosphate values. This pseudohyperphosphatemia resulted from an increase in optic density because of interference between monoclonal immunoglobulin and the molybdic reagent used to determine phosphate in serum. These data indicate that the finding of marked hyperphosphatemia in multiple myeloma patients should always prompt an assay carried out on a deproteinized sample. In addition, knowledge of this phenomenon may avoid confusion, unnecessary testing and obviate confusion in the clinical evaluation of patients with multiple myeloma

The urinary excretion of glycosaminoglycans and heparan sulphate in lupus nephritis

WOS: 000178303700004PubMed ID: 12189454Renal involvement in systemic lupus erythematosus (SLE) affects the disease outcome. In order to advance the diagnosis and the initiation of therapy, non-invasive diagnostic techniques are required. In this study, urinary glycosaminoglycans (GAG) and heparan sulphate (HS) were measured in 26 patients with biopsy-proven lupus nephritis and compared to 16 healthy controls. Uronic acid as a representative of GAGs in urine was determined spectrophotometrically with the meta-hydroxydiphenyl, following acid treatment. HS was determined as hexosamine by the method of Smith and Gilkerson. The median values of GAG (3.99 mg/g crea./day) and HS (2.41 mg/g crea./day) in patients were significantly (P = 0.001) higher than in the control group (1.98 and 0.87, respectively). There was a positive correlation between GAG and HS values (P = 0.000, r = 0.924) in SLE patients. There were no differences in HS excretion, microalbuminuria and SLE-DAI scores between different classes of lupus nephritis. However, GAG values in class 3 nephritis were significantly (P = 0.033) higher than from both class 2 and class 4 lupus nephritis. There were no differences in all the measured parameters between normoalbuminuric, microalbuminuric and macroproteinuric patients. Furthermore, there were no correlations between GAG, HS excretions and SLE-DAI scores or microalbuminuria. These results suggest that urinary GAG and HS may serve as useful, independent and non-invasive markers of lupus nephritis

Effect of enalapril on urinary glycosaminoglycan, heparan sulphate and microalbuminuria in type II diabetic patients

WOS: 000083179000004PubMed ID: 23902355Recent studies in diabetic humans have shown that angiotensin converting enzyme (ACE) inhibitors may provide additional renal benefit above and beyond conventional antihypertensive agents. We investigated the effect of enalapril on urinary glycosaminoglycans (GAG), heparan sulphate (HS) and microalbuminuria (MAU) in diabetic patients. Urinary GAG and HS levels were determined in controls (n = 16, 41.3 +/- 12.9 years old) and in type II diabetics (n = 18, 53 +/- 9.6 years old) who were not using ACE inhibitors. Four of these patients had also hypertension. The duration of diabetes was 5.5 +/- 3 years (mean +/- SD). Microalbuminuria was detected in seven patients. The subjects were treated with enalapril (5-10 mg day(-1)) for 6 weeks. The median values of GAG (n = 18, 2.8 mg uronic acid g(-1) crea. day(-1)) and HS (n =18, 1.36 mg glycosamine g(-1) crea. day(-1)) in the pre-treatment group were significantly (p < 0.01) higher than the control group (n = 16, 1.98 mg uronic acid g(-1) crea. day(-1) and 0.87 mg glycosamine g(-1) crea. day(-1)), respectively. Before treatment, GAG and HS levels seemed to be not different between microalbuminuric and normoalbuminuric as well as hypertensive and normotensive patients. Following enalapril treatment, the median values of GAG (n =18, 1.35 mg uronic acid g(-1) crea. day(-1)) and HS (n = 18, 0.99 mg glycosamine g(-1) crea. day(-1)) tended to decrease to the levels which were not significantly different from the control group. Following treatment, significant reduction in urinary albumin excretion (from 15.45 to 11.1 mg day(-1)) (p < 0.0005) was also observed. When considering the pre- and post-treatment concentrations, there were positive correlations between urinary GAG and HS values (p < 0.05, r = 0.6541 and p < 0.01, r = 0.5984). These results suggest that measurement of urinary heparan sulphate may be another useful predictor of clinical diabetic nephropathy; and enalapril causes marked reduction in HS and GAG values in all patients independently by the presence of hypertension