Brenner & Rector's The Kidney. 7th edition by Barry M. Brenner

The first edition of this highly esteemed textbook of nephrologydates back to 1976. Regular updates have taken into accountthe steady, remarkable progress made in this discipline of internalmedicine in the last quarter of the 20th century. The most recent,7th edition has became available this year. As previously, itlargely reflects the advances of the last few years and presentsthe state of the art in the field of interest.     

Different patterns of uremic polyneuropathy: clinicopathologic study

Ten patients with a uremic polyneuropathy were investigated. Chronic renal failure was associated with a variety of neuropathies, including an acute axonal neuropathy, a progressive axonal neuropathy with secondary segmental demyelination, and a predominantly demyelinative neuropathy. All patterns were associated with distal degeneration of fibers evidenced by axonal sprouting observed on single-fiber preparations. The etiology of such variations in pathology of uremic neuropathy is still not clearly understood.     

Optimal Treatment Strategies in End-Stage Renal Failure. Claude Jacobs (editor), Oxford University Press, Oxford, UK, 2002

This book by Claude Jacobs and other well known clinical nephrologistsfrom Europe and the US is a valuable contribution to availablemodalities and optimal strategies for the treatment of end-stagerenal disease (ESRD). The first part of the book includes generalchapters on extra-corporeal renal replacement therapy (RRT),peritoneal dialysis, renal transplantation and multi-organ transplantation.The second part     

When response inhibition is followed by response reengagement: An event‐related fMRI study

In the course of daily living, changing environmental demands often make our actions, once initiated, unnecessary or even inappropriate. Under such circumstances, the ability to inhibit the obsolete action and to update behavior can be of vital importance. Previous lesion and neuroimaging studies have shown that the right prefrontal cortex and the basal ganglia seem to play an important role in the inhibition of already initiated motor responses. The present study was designed to investigate whether the neural activity of inhibitory motor control was altered if the inhibition process was succeeded by an additional process, namely the reengagement into an alternative action. Therefore, cerebral blood oxygenation during performance of a stop‐change paradigm was registered in 15 male participants using event‐related functional magnetic resonance imaging. Data analysis showed, that during successful and failed stopping and changing (response inhibition and subsequent response reengagement) of initiated motor responses a very similar network was activated including primarily the right inferior frontal cortex (IFC). Besides, stopping‐related activation in right IFC was significantly greater for fast inhibitors than for slow ones. Results of the present study thus further underline the important role of right IFC in response inhibition and suggest that the inhibition process functions similarly regardless whether changing task demands require the complete suppression of an already initiated motor response or its suppression and a subsequent response reengagement into an alternative action. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.     

Dietary salt restriction accelerates atherosclerosis in apolipoprotein E-deficient mice

BACKGROUND: Whether a general reduction in salt intake reduces or actually enhances cardiovascular mortality in man remains an issue of controversy. Low sodium diets may lead to adverse side effects by stimulating the renin-angiotensin and sympathetic nervous systems. The present study was designed to investigate the effects of low dietary salt on atherosclerotic lesion progression in apolipoprotein E deficient (apoE(-/-)) mice. METHODS AND RESULTS: We fed 7-week-old apoE(-/-) mice on low (0.036% NaCl; n=28) or regular (0.64% NaCl; n=26) salt diets for 16 weeks. At the age of 23 weeks, the cross-section surface area of atherosclerotic plaques was measured in aortic root and thoracic aorta. Serum total cholesterol, triglycerides, plasma angiotensin levels and urinary protein/creatinine concentrations were assessed. Exposure to low salt caused significant increases in atherosclerotic lesion surface area in thoracic aorta, but did not alter lesion area in aortic root. Low-salt mice also had higher serum total cholesterol and higher plasma angiotensin II (ANG-II) concentrations. Atherosclerotic lesion area was correlated with ANG-II levels in low-salt but not in regular-salt animals, and with total cholesterol concentration in all mice. Mean arterial pressure was comparable in both groups. CONCLUSIONS: Dietary salt restriction accelerated atherosclerotic lesion formation in apoE(-/-) mice through a mechanism that is probably related to ANG-II formation. Whether these findings are relevant to human cardiovascular disease remains to be evaluated.     

Factors of increase in serum triglyceride-rich lipoproteins in uremic rats

The possible mechanisms of the increase in serum triglycerides (TG) and TG-rich lipoproteins were studied in chronically uremic (U) rats by comparison with either ad-lib fed control (C) rats or diet-restricted (DR), sham-operated pair-fed control rats. A first series of animals was studied in the fed state and a second series after a 16-hr fast. In U animals the concentration of serum TG and TG-rich particles was lower than that of C rats in the fed state but significantly higher than that of C and DR rats after a 16-hr fast. Serum glucose and lactate concentrations in the fed or fasted state were unchanged by uremia. Serum insulin concentration was significantly decreased in U rats as compared to C and DR rats in both series. The fast did not increase the concentration of serum nonesterified fatty acids (NEFA) in U or DR animals to the same extent as in C rats, whereas the serum concentration of beta-hydroxybutyrate (BOB), which was higher than that of C rats in the fed state, was significantly lower after a 16-hr fast. In U animals, as compared to control rats of either series, a significant decrease of epididymal lipoprotein lipase (LPL) activity was observed during both nutritional states when expressing the enzymic activity per number of cells. In conclusion, our data provide evidence against hepatic over-production of TG-rich lipoproteins in rats with chronic renal failure and strongly point to an LPL-mediated defect of their peripheral catabolism, probably related to the insulin deficiency state.     

Cost of treating predialysis patients with recombinant human erythopoietin

Treatment of the anaemia of predialysis patients with recombinanthuman erythropoietin (rHuEpo) is likely to become a widely acceptedpractice during the coming years. We estimated the impact onhealth care expenditures with the example of the French populationof end-stage renal disease patients. Using retrospective data,we calculated the percentage of predialysis patients with advancedchronic renal failure who would be eligible for treatment accordingto two different criteria based on haemoglobin and clinicalcondition, the total duration of treatment, and the total amountof rHuEpo delivered. We estimate that the total cost of treatingFrench predialysis patients could vary between 2.2 and 6.5 millionSwiss francs, or 50 000 to 140 000 Swiss francs per millionpopulation, using rHuEpo dosage from 50 to 150 IU/kg week.     

Duodenal calcium binding protein and active calcium transport in rats: are they functionally related?

The effects of calcitriol and a novel calcitriol analogue, 22-oxacalcitriol(OCT) on duodenal Ca transport, calbindin-D9k mRNA, and calbindin-D9kcontent were studied in two animal models reflecting commonhuman pathologies, namely arterial hypertension and chronicrenal failure, as well as in normal rats. The hormone or itsanalogue were administered intraperitoneally to vitamin-D-repleterats. Active Ca transport was increased in both spontaneouslyhypertensive rats (SHR) and in normotensive control WKY rats5 h after calcitriol dosing of either 60 and 600 ng per rat.In WKY, calbindin-D9k content was slightly increased after theinjection of 60 ng calcitriol, but not of 600 ng calcitriolwhereas calbindin-D9k mRNA stayed essentially unchanged. Incontrast, active Ca transport was significantly stimulated afterthe higher dose of 600 ng calcitriol. In SHR, while both dosesof calcitriol increased active Ca transport, they had no stimulatoryeffect on calbindin-D9k mRNA or protein. In chronically uraemicrats, active Ca transport, duo denal calbindin-D9k, and calbindin-D9kmRNA were stimulated after the injection of two subsequent dosesof 300 ng calcitriol per rat. OCT treatment at same dosage ledto a similar stimulation of calbindin-D9k and calbindin-D9kmRNA, but failed to induce an increase in active Ca transport.These results show that the stimulation of intestinal activeCa transport and calbindin-D9k can be entirely dissociated atthe protein synthesis and the mRNA expression level (1) aftercalcitriol administration to normal and hypertensive rats, and(2) after OCT administration to uraemic rats. Even though calbindinmay play a significant role in the regulation of Ca translocationacross the enterocyte, our work provides evidence that intestinalactive Ca transport can be enhanced independently of changesin calbindin-D9k and vice-versa, at least under the presentnon-steady-state conditions.