Chronic kidney disease

Indoxyl sulfate might be involved in vascular disease in patients with chronic kidney disease, and higher serum levels of this protein-bound uremic toxin might be associated with increased mortality in this patient group, according to researchers in Europe. In a study that enrolled 139 patients with chronic kidney disease, Barreto and colleagues found that baseline serum indoxyl sulfate levels were inversely associated with renal function and were directly related to aortic calcification and pulse wave velocity. A serum indoxyl sulfate level in the highest tertile was a strong predictor of overall and cardiovascular mortality.

Barreto, F. C. et al. Serum indoxyl sulfate is associated with vascular disease and mortality in chronic kidney disease patients. Clin. J. Am. Soc. Nephrol. 4, 1551–1558 (2009).

Hypertension

Patients with resistant hypertension should reduce their dietary salt intake as excessive dietary sodium contributes to resistance to antihypertensive treatments. These were the conclusions of a randomized, crossover study that compared low-sodium and high-sodium diets in 12 individuals with resistant hypertension. Blood pressure decreased with the low-sodium diet but not with the high-sodium diet; the mean change between high-sodium and low-sodium groups was 22 mmHg for systolic blood pressure and 9.1 mmHg for diastolic blood pressure. The reduction in blood pressure associated with the low-sodium diet seemed to be associated with intravascular volume reduction.

Pimenta, E. et al. Effects of dietary sodium reduction on blood pressure in subjects with resistant hypertension: results from a randomized trial. Hypertension 54, 475–481 (2009).

Cystic kidney disease

The pathogenetic mechanisms involved in cystic kidney disorders such as nephronophthisis and autosomal recessive and dominant polycystic kidney diseases are unclear. A study reported in Nature Medicine has now shown, however, that these disorders could be caused by impairments in Wnt–β-catenin signaling causing interference with renal homeostasis. Lancaster and colleagues found that mice lacking the Ahi1 gene, which encodes jouberin protein and is mutated in Joubert syndrome, show pathology consistent with nephronophthisis as a result of a decrease in endogenous Wnt activity. The researchers also showed that, in vivo, jouberin is needed for a Wnt pathway response to injury and renal tubule repair; without jouberin, cystogenesis occurs.

Lancaster, M. A. et al. Impaired Wnt–β-catenin signaling disrupts adult renal homeostasis and leads to cystic kidney ciliopathy. Nat. Med. 15, 1046–1054 (2009).