Asymmetric dimethylarginine (ADMA) and its enantiomer, Symmetric dimethylarginine (SDMA), are naturally occurring amino acids that were first isolated and characterized in human urine in 1970. ADMA is the most potent endogenous inhibitor of nitric oxide synthase (NOS), with higher levels in patients with end-stage renal disease (ESRD). ADMA has shown to be a significant predictor of cardiovascular outcome and mortality among dialysis patients. On the other hand, although initially SDMA was thought to be an innocuous molecule, we now know that it is an outstanding marker of renal function both in human and in animal models, with ESRD patients on dialysis showing the highest SDMA levels. Today, we know that ADMA and SDMA are not only uremic toxins but also independent risk markers for mortality and cardiovascular disease (CVD). In this review, we summarize the role of both ADMA and SDMA in chronic kidney disease along with other cardiovascular risk factors.

An affection of the ulnar nerve is not difficult to diagnose but may be difficult to localize. The study of peripheral nerve conduction velocity was brought to bear upon this problem by Simpson (1956), who found distal slowing in motor fibres in a deep palmar lesion of the ulnar nerve and local slowing in a chronic traumatic lesion at the elbow. Sensory conduction in clinically established lesions of the ulnar nerve at the elbow was investigated by Gilliatt and Thomas (1960); in none of nine could a sensory action potential be recorded at the wrist or a mixed nerve potential proximal to the elbow. Kaeser (1963), also using surface recording electrodes, found that when there was a lesion of the nerve at the elbow the sensory potential at the wrist was absent or too small to use for measurement. He was nevertheless able to localize 25 out of 29 lesions at the elbow by stimulating the nerve proximal and distal to the joint and demonstrating slowed motor conduction in the affected segment. Our experience of motor conduction studies was less favourable, and, since technical improvements now permit the investigation of sensory conduction, we decided to re-evaluate the means by which lesions of the ulnar nerve may be diagnosed and localized. PATIENTS AND NORMAL SUBJECTSLesions of 50 ulnar nerves (29 right, 21 left) were studied in 46 patients, 37 of whom were men. Nine patients were aged below 40 years, 34 were from 40 to 70 and three were above 70. The history was taken and the clinical examination conducted according to the scheme of Table I. AETIOLOGY (Table II) Three-quarters of the lesions fell into three groups, of which the largest comprised those without relevant history. SYMPTOMS (Table III) In three-quarters of the lesions the symptoms had lasted for a year or less; two-thirds gave rise to both sensory and motor symptoms.

Objective-To determine whether patients with the clinical phenotype of multifocal motor neuropathy but without the electrophysiological criteria for conduction block would respond to intravenous immunoglobulin (IVIg). Methods-Ten patients were selected with a slowly progressive, asymmetric, lower motor neuron disorder, and were treated prospectively with IVIg at a dose of 2g/kg over 5 days. All subjects had neurophysiological testing to look for evidence of conduction block before treatment. Muscle strength was assessed by MRC grades and hand held myometry, measuring pinch and grip strength. A 20% increase in both pinch and grip myometry was considered a positive response. Results-In no patient was conduction block detected. Four of the 10 patients showed a positive response to IVIg, with the best response occurring in two patients who presented with weakness but without severe muscle wasting. Three of the four responders have continued to receive IVIg for a mean period of 17 months (range 15-24 months), with continued eVect. The response to IVIg was not related to the presence of anti-GM1 antiganglioside antibodies, but responders had a selective pattern of muscle weakness and normal (>90% predicted) vital capacity. Conclusion-The findings suggest that a course of IVIg should be considered in patients with the clinical phenotype of multifocal motor neuropathy but without neurophysiological evidence of conduction block. (J Neurol Neurosurg Psychiatry 1999;67:15-19)

GLA had a beneficial effect on the course of diabetic neuropathy.

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