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Bidirectional interactions exist between the kidneys and the gut. These interactions are commonly referred to as the gut-kidney axis. Chronic kidney disease (CKD) leads to disturbances of the gut ecosystem. Key features include the increase of protein fermentation at the expense of carbohydrate fermentation and a disrupted epithelial barrier. A disturbed gut ecosystem may contribute to the high burden of cardiovascular disease in patients with CKD. The present review discusses the impact of CKD on the gut microenvironment and provides an update as to how gut dysbiosis and a leaky gut may be linked to accelerated cardiovascular disease and hypertension. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is highly prevalent in chronic kidney disease, suggesting that molecules retained in uremia might contribute to this increased risk. We explored the relationship between p-cresol, a protein-bound uremic retention solute, and CVD by comparing the strength of this relationship relative to traditional and novel cardiovascular risk factors. Univariate Cox proportional hazard analysis showed that the free serum p-cresol concentration was significantly associated with CVD when the primary end point was the time to the first cardiovascular event. In multivariate analysis, free p-cresol was significantly associated with CVD in non-diabetics. In diabetic patients, however, a significant relationship between p-cresol and cardiovascular events could not be demonstrated despite their having significantly higher p-cresol levels. Our study shows that free p-cresol is a novel cardiovascular risk factor in non-diabetic hemodialysis patients.Kidney International (2008) 73, 1174–1180; doi:10.1038/ki.2008.31; published online 27 February 2008 [ABSTRACT FROM AUTHOR]

Describes a case of a male patient with juvenile myotonic dystrophy (MD) or Steinert's disease and early development of a megarectum. Health condition of the patient during his childhood; Psychological problems of the patient; Pathophysiological mechanisms behind gastrointestinal involvement in MD.

The article presents a letter to the editor commenting on a paper suggesting that the decreased antioxidant capacity of plasma ultrafiltrate is related to the removal of protein-bound uremic toxins.

Pulmonary-renal syndrome is a common and serious disorder with a broad differential diagnosis. We describe a case of a middle-aged man presenting with interstitial pulmonary disease and severe renal impairment caused by a hypocomplementemic immune-complex-mediated interstitial nephritis. Serum levels of IgG4 were elevated, and renal biopsy specimens revealed the presence of interstitial IgG4(+) plasma cells. There was a rapid improvement of both pulmonary and renal abnormalities after the initiation of corticosteroids. To our knowledge, this report is the first to show interstitial pulmonary disease in association with interstitial kidney disease as the predominant and presenting symptoms of IgG4-related disease. [ABSTRACT FROM AUTHOR]

The mechanism responsible for the selective vulnerability of motor neurons in amyotrophic lateral sclerosis (ALS) is poorly understood. Several lines of evidence indicate that susceptibility of motor neurons to Ca2+ overload induced by excitotoxic stimuli is involved. In this study, we investigated whether the high density of Ca2+-permeable AMPA receptors on motor neurons gives rise to higher Ca2+ transients in motor neurons compared to dorsal horn neurons. Dorsal horn neurons were chosen as controls as these cells do not degenerate in ALS. In cultured spinal motor neurons, the rise of the cytosolic Ca2+ concentration induced by kainic acid (KA) and mediated by the AMPA receptor was almost twice as high as in spinal neurons from the dorsal horn. Furthermore, we investigated whether increasing the motor neuron''s cytosolic Ca2+-buffering capacity protects them from excitotoxic death. To obtain motor neurons with increased Ca2+ buffering capacity, we generated transgenic mice overexpressing parvalbumin (PV). These mice have no apparent phenotype. PV overexpression was present in the central nervous system, kidney, thymus, and spleen. Motor neurons from these transgenic mice expressed PV in culture and were partially protected from KA-induced death as compared to those isolated from nontransgenic littermates. PV overexpression also attenuated KA-induced Ca2+ transients, but not those induced by depolarization. We conclude that the high density of Ca2+-permeable AMPA receptors on the motor neuron''s surface results in high Ca2+ transients upon stimulation and that the low cytosolic Ca2+-buffering capacity of motor neurons may contribute to the selective vulnerability of these cells in ALS. Overexpression of a high-affinity Ca2+ buffer such as PV protects the motor neuron from excitotoxicity and this protective effect depends upon the mode of Ca2+ entry into the cell. [Copyright &y& Elsevier]