Protocol design.

IgA nephropathy often progresses to endstage renal failure over a period of many years, and any therapy directed to IgA nephropathy will most likely have to be administered over an extended period of time. Therefore, optional therapy should be effective and free of long-term adverse effects. Besides fish oil, prednisone has also been investigated for treatment of IgA nephropathy, with a lack of consistent results; severe adverse effects are common with long-term use. Several studies have shown positive although not overly impressive results; therefore optimal therapy for slowing the progression of renal failure secondary to IgA nephropathy has not been established. Problematic issues with available studies included the following: (1) most of the clinical studies previously discussed were short-term, contained small numbers of patients, and most but not all were uncontrolled; (2) early reports involving fish oil therapy demonstrated conflicting results regarding its efficacy, including one study that observed increased progression of renal disease in patients treated with fish oil; however, recent studies have shown more promise for fish oil therapy for up to 2 years of treatment; and (3) since most of the studies were conducted over a short period of time, it is difficult to assess long-term effects and safety of oil treating IgA nephropathy, a disease that progresses to ESRD over 10-20 years. However, given the low number of adverse effects and apparent low risks associated with this relatively safe food supplement therapy observed in most clinical trials of up to 2 years duration, fish oil may slow the progression of renal failure in patients with IgA nephropathy. Therefore, with appropriate monitoring of renal function and blood tests, treatment with fish oil 6-12 g/d should be considered in patients with IgA nephropathy.

Anticonvulsants↗

PubMed1996

Quantitative determination of clonazepam in plasma by gas chromatography-negative ion chemical ionization mass spectrometry.

A gas chromatographic-negative ion chemical ionization mass spectrometric (GC-NCI-MS) method for the quantitative analysis of clonazepam in human plasma is described. Clonazepam (M(r) = 315) was derivatized by N,O-bis-(trimethylsilyl)trifluoroacetamide with 1% trimethylchlorosilane. A pre-conditioning procedure involving injection of a silyl-8 and ethyl acetate extraction solution from plasma reduces the interaction between clonazepam-TMS and the analytical system. The routine limit of quantification was set to be 0.25 ng/ml with an injection volume of 2 microliters and a sample volume of 1 ml. The signal-to-noise ratio was greater than five. The detection limit for clonazepam can reach 0.1 ng/ml. The isotope clonazepam-d5 was used as the internal standard.

Anticonvulsants↗