We like to introduce our Enzyme linked Immunosorbent assay (ELISA) kit for the quantitative determination of autoantibodies to aquaporin-4 (AQP4) in serum. This is a new reliable and convenient method to measure AQP4 autoantibodies, which are a specific marker for Neuromyelitis Optica (NMO), also known as Devic’s syndrome.

Measurement of AQP4 autoantibodies can be of considerable value in distinguishing NMO from Multiple Sclerosis when full clinical features may not be apparent and early intervention may prevent or delay disability. Total assay time is ~3 hours only. The ELISA method is an easy assay format for use in the routine clinical laboratory and suitable for automated systems.

The ELISA is manufactured under licence to US patent 7,101,679B2, European patent 1700120 and related patents and patents pending in other countries.

Literature: “A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis”; V.A. Lennon et al.; Lancet 2004 364 (9451): 2106-2112

“IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel”  V.A. Lennon et al.; The Journal of Experimental Medicine 2005 202: 473-477

“Neuromyleitis optica IgG predicts relapse after longitudinally extensive transverse myelitis”  B.G. Weinschenker et al.; Annals of Neurology 2006 59: 566-569

We modified our Plasma Nor-/Metanphrine ELISA kit that uses now common sample preparation of 400 µl plasma and acylation in liquid phase. The kit contains 6 Standards, 2 Controls, ready for use and a Metanephrine/ Normetanephrine standard range 20 - 3,000 pg/ml.
The ELISA kit contains common reagents for parallel testing and allows the parallel measurement of the catecholamine metabolites in large series. The correlation between the modified ELISA test and the RIA method (see literature below) shows excellent results.

Unger et al. (2006.) Diagnostic value of various biochemical parameters for the diagnosis of pheochromocytoma in patients with adrenal mass. European Journal of Endocrinology 154, 409-417
 

Dosing of most drugs must be adapted in renal insufficiency, making accurate assessment of renal function an essential component of diagnostics in clinical medicine. Furthermore, even modest impairment of renal function has been recognized as a cardiovascular risk factor. As the most commonly used marker of renal excretory function, serum creatinine concentration, does not adequately respond to mild to moderate impairment of renal function, more sensitive markers for renal excretory function are urgently seeked, especially in mild stages of renal impairment. SDMA is a methylated derivative of the amino acid L arginine (symmetric dimethylarginine). SDMA is eliminated from the body exclusively by renal excretion; therefore SDMA plasma concentration is tightly related to renal function. Thus, quantification of plasma SDMA is an adequate means to assess renal function, as could be demonstrated in a series of recent clinical trials: In 18 clinical studies involving more than 2,100 patients systemic SDMA concentrations were highly correlated with inulin clearance as well as with various clearance estimates and better corresponded to mild renal function impairment than serum creatinine.
Thus, SDMA exhibits properties of a reliable marker of renal function. Furthermore, there is evidence showing that elevated SDMA levels, as they may occur in renal function impairment, may prospectively indicate future risk of cardiovascular disease and mortality independently of the level of renal impairment.

Our new developed competitive SDMA-ELISA uses the microtiter plate format. SDMA is bound to the solid phase of the microtiter plate. SDMA in the samples is acylated and competes with solid phase bound SDMA for a fixed number of rabbit anti-SDMA antiserum binding sites. When the system is in equilibrium, free antigen and free antigen-antiserum complexes are removed by washing. The antibody bound to the solid phase SDMA is detected by anti-rabbit / peroxidase. The substrate TMB / peroxidase reaction is monitored at 450 nm. The amount of antibody bound to the solid phase SDMA is inversely proportional to the SDMA concentration of the sample.
 

You will find further information in the instruction for use for our new SDMA-ELISA including actual literature also.

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of the synthesis of NO. NO has been named an "endogeneous anti-atherogenic molecule" due to its diverse regulatory functions in vascular homeostasis.

The effects of ADMA on NO synthesis and NO-mediated pathophysiological processes have been described in numerous experimental studies. Moreover, elevated ADMA levels in plasma have been found in clinical studies including patients with hypercholesterolemia, hypertension, chronic heart failure, chronic renal failure, erectile dysfunction and in pregnant women who subsequently develop pre-eclampsia.

Recent prospective and cross-sectional studies indicated that elevated ADMA levels ar a risk factor for future cardiovascular events and total mortality. The higher morbidity and death rate can be counteracted by providing L-Arginin.

The measurement of ADMA is done with HPLC/MS or GCMS, both very expensive and time consuming methods and not suitable for clinical routine diagnosis.

We developed a competitive ADMA-ELISA using the microtitre plate format. The correlation of the ELISA method to HPLC-MS and GCMS is exceptionally good. No interference with any therapeutic drugs are observed. The ELISA method allows the measurement of large series of patient samples.