Paraoxonase activity in glomerulonephritic patients.

BACKGROUND: Cardiovascular disease is the most common cause of morbidity and mortality in patients with chronic renal failure. Glomerulonephritic patients have an increased risk for cardiovascular disease, but its etiology is unclear. It is known that an increase in oxidizability of apolipoprotein B-containing lipoproteins has a key role in the initiation of atherosclerosis, and paraoxonase enzyme activity particularly has a preventive role against atherosclerosis. The aim of the present study was to evaluate the oxidizability of apolipoprotein B-containing lipoproteins, serum, and urinary paraoxonase/arylesterase activities in glomerulonephritis patients who had normal lipid parameters and creatinine levels. METHODS: Thirty-two patients with glomerulonephritis and 22 healthy controls were included in this study. A total of 32 patients (including nine with membranous GN, eight with immunoglobulin A nephropathy, eight with mesangial proliferative GN, five with focal-segmental glomerulosclerosis, one with diffuse proliferative GN, and one with minimal chance disease having biopsy proven GN) were enrolled into the study. We compared serum and urinary paraoxonase, arylesterase, serum lipids, urea, creatinine, hemoglobin, total protein and albumin values between groups. RESULTS: Serum urea, creatinine, total protein, albumin, uric acid, hemoglobin, and lipid parameters were similar in the glomerulonephritis and control groups (p > 0.05). PON1 activity was significantly lower in GN group than controls, but there was no statistically significant difference on arylesterase activity between groups. Oxidizability of apolipoprotein B-containing lipoproteins was significantly higher in GN group than controls. CONCLUSION: Our study shows that the findings of normal serum levels of creatinine, lipids, and proteins increased the oxidizability of apolipoprotein B-containing lipoproteins, and any decrease in PON1 activity in patients diagnosed with GN should be considered important. Hence, the immediate commencement of preventive as well as curative treatment in other to avoid the risk of cardiovascular and renal problems would be a correct approach.

Effect of indomethacin and selective cyclooxygenase-2 inhibitors on proteinuria and renal function in patients with AA type renal amyloidosis.

AIMS: Because the cardiovascular system (CVS) side-effects of cyclooxygenase-2 (COX-2) selective inhibitors have recently been questioned, we aimed to compare the renal and haemodynamic effects of cyclooxygenase selective (celecoxib and rofecoxib) and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) (indomethacin) in patients with renal amyloidosis secondary to rheumatological diseases who required anti-inflammatory agents and are taking maximum tolerable dose of angiotensin-converting enzyme inhibitors. METHODS: The present study was performed on 11 patients with stable proteinuria who were diagnosed as AA amyloidosis secondary to rheumatological diseases confirmed by renal biopsies. The study had three consecutive stages (celecoxib 200 mg/day; indomethacin 100 mg/day; rofecoxib 25 mg/day.) Each was given for 4 weeks and a wash-out phase of 3 weeks was allowed between consecutive stages. RESULTS: Although the decrease of proteinuria in the celecoxib period was higher than in the rofecoxib and indomethacin periods, the difference was not statistically significant. No statistically significant differences were found between serum urea, creatinine, creatinine clearance and urinary sodium excretion. CONCLUSION: In this study, no differences were found between indomethacin and the two selective COX-2 inhibitors in respect to proteinuria and renal functions in 11 patients with renal amyloidosis secondary to rheumatological diseases with varying degrees of proteinuria. Routine doses of NSAIDs brought no additional benefit to the ACE inhibitor use in terms of proteinuria and renal functions. The use of selective COX-2 inhibitors should be limited to their anti-inflammatory and analgesic effects in this population.

Evaluation of the effect of the sublingually administered nifedipine and captopril via transcranial doppler ultrasonography during hypertensive crisis.

OBJECTIVE: This study was designed to show the effects of sublingually administered nifedipine and captopril on middle cerebral arterial blood flow during hypertensive crisis in the emergency department. METHODS AND RESULTS: Transcranial Doppler ultrasonography (TCD) was performed on the patients fulfilling the criteria (15 patients given captopril, 13 patients given nifedipine, mean (+/-SD) age 56 +/- 11 and 54 +/- 10 years, respectively). Then, patients were randomized into sublingually administered captopril or nifedipine groups and after the drug administration, TCD was repeated. Initial systolic and diastolic blood pressures were 200 +/- 21/125 +/- 21 mmHg in the captopril group and 199 +/- 17/ 123 +/- 20 mmHg in the nifedipine group. There was no significant difference between antihypertensive effects of the drugs after initiation of treatment. Before the treatment with captopril, middle cerebral artery (MCA) flow velocities (Vm) and pulsatility index (PI) were 76.74 +/- 6.38 cm/s and 1.18 +/- 0.09, respectively. The values after the treatment with captopril were 78.21 +/- 5.24cm/s (p < 0.05) and 0.92 +/- 0.08 (p < 0.001), respectively. Before the treatment with nifedipine, Vm and PIs were 64.73 +/- 5.11 cm/s and 1.14 +/- 0.18, respectively. After the treatment with nifedipine, Vm was 60.04 +/- 5.36 cm/s (p < 0.01) and PI was 1.21 +/- 0.09 (p < 0.01). CONCLUSION: After treatment with captopril, PIs were decreased to normal limits but in the group treated with nifedipine, PIs increased to more pathological values. These results showed that we should reconsider the use of nifedipine in the emergency departments as an antihypertensive agent in hypertensive attack treatment.