Skeletal muscle wasting is common and insidious in patients who receive maintenance hemodialysis treatment for the management of ESRD. The objective of this study was to determine whether 12 wk of high-intensity, progressive resistance training (PRT) administered during routine hemodialysis treatment could improve skeletal muscle quantity and quality versus usual care. Forty-nine patients (62.6 ؎ 14.2 yr; 0.3 to 16.7 yr on dialysis) were recruited from the outpatient hemodialysis unit of the St. George Public Hospital (Sydney, Australia). Patients were randomized to PRT ؉ usual care (n ‫؍‬ 24) or usual care control only (n ‫؍‬ 25). The PRT group performed two sets of 10 exercises at a high intensity (15 to 17/20 on the Borg Scale) using free weights, three times per week for 12 wk during routine hemodialysis treatment. Primary outcomes included thigh muscle quantity (cross-sectional area [CSA]) and quality (intramuscular lipid content via attenuation) evaluated by computed tomography scan. Secondary outcomes included muscle strength, exercise capacity, body circumference measures, proinflammatory cytokine C-reactive protein, and quality of life. There was no statistically significant difference in muscle CSA change between groups. However, there were statistically significant improvements in muscle attenuation, muscle strength, mid-thigh and mid-arm circumference, body weight, and C-reactive protein in the PRT group relative to the nonexercising control group. These findings suggest that patients with ESRD can improve skeletal muscle quality and derive other health-related adaptations solely by engaging in a 12-wk high-intensity PRT regimen during routine hemodialysis treatment sessions. Longer training durations or more sensitive analysis techniques may be required to document alterations in muscle CSA.

.-Increased cardiac output in pregnancy is associated with cardiac remodeling and possible reduction in contractility, which may worsen in preeclampsia. Left ventricular (LV) geometry and function were compared between nonpregnant controls (n ϭ 12) and normotensive (n ϭ 44) and preeclamptic (n ϭ 15) pregnant women using echocardiography. Loadindependent comparisons of LV systolic function compared end-systolic stress (ESS) and rate-corrected velocity of circumferential fiber shortening (V CFC). Mean arterial pressures were 101 Ϯ 14 mmHg in preeclampsia, 76 Ϯ 6 mmHg in normotensive pregnancy, and 78 Ϯ 6 mmHg in controls (P Ͻ 0.005 vs. preeclampsia). LV mass increased during normotensive pregnancy (66 Ϯ 13 to 76 Ϯ 16 g/m 2 ; P Ͻ 0.05; controls, 65 Ϯ 10 g/m 2 ; P Ͻ 0.05) and was greater in preeclampsia (90 Ϯ 18 g/m 2 ; P Ͻ 0.05). In normotensive pregnancy, ESS decreased (59 Ϯ 9 to 52 Ϯ 11 g/cm 2 ; P Ͻ 0.05; controls, 66 Ϯ 14 g/cm 2 ; P Ͻ 0.005). ESS was greater in preeclampsia (60 Ϯ 14 g/cm 2 ; P Ͻ 0.05). In controls, there was an inverse relationship between ESS and V CFC (r ϭ Ϫ0.78). The ESS-V CFC relationships in normotensive and preeclamptic pregnancy were unchanged from controls. We conclude that LV hypertrophy in normotensive and preeclamptic pregnancy matches changes in cardiac work, and LV contractility is preserved. preeclampsia; echocardiography; ventricular function; myocardial contractility; hypertension PREGNANCY IS ASSOCIATED WITH hemodynamic and hormonal changes that can affect the heart. From the first trimester, there is an increase in cardiac output that places a volume load on the heart. Hormonal changes include increased circulating estrogen and relaxin, which may directly or indirectly affect the heart. During pregnancy, the heart undergoes remodeling similar to that observed in athletes (9, 13) with increases in chamber dimensions, left ventricular (LV) wall thickness, and mass (2, 13, 24) that is consistent with a process of eccentric hypertrophy (15).More controversial is whether myocardial contractile function also changes in pregnancy. Ejection-phase indices of LV function, including systolic fractional shortening (FS) and mean velocity of circumferential fiber thickening (V CFC ), have been variously reported to increase (26), remain constant (15), or decrease (24) during pregnancy. The use of these indices is limited by the changes in ventricular loading conditions that occur during pregnancy. The inverse relationship between ventricular end-systolic stress (ESS) and V CFC has been described as a load-independent measure of contractility (5). The results of one study (21) that used the ESS-V CFC relationship suggest that myocardial contractility is actually reduced during pregnancy. There are even less data about changes in LV diastolic function during pregnancy. Hypertrophy of the left ventricle may result in reduced diastolic compliance (20), whereas hormonal influences such as nitric oxide may have the opposite effect (22).A change in myocardial contractility during pregnancy has impo...

No abstract

Ageing, poor nutritional status and elevated interleukin-8 are factors potentially contributing to the loss of muscle quality and quantity in ESRD. These deficits can predict functional impairments, with intramuscular lipid accumulation most closely related to decline of submaximal musculoskeletal performance (walking), and low muscle CSA most closely related to decline of maximal performance (peak isometric strength).

We reported that feeding rats 8% protein for 4 wk induces two new urea transport processes in initial inner medullary collecting ducts (IMCD); neither is present in rats fed 18% protein. In this study, we measured the time course of induction of these transporters in perfused initial IMCD segments from rats fed 8% protein. Net urea flux was induced after 3 wk, whereas vasopressin-stimulated passive urea permeability (P(urea)) was induced after 2 wk. 8-Bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) significantly increased P(urea)); adding vasopressin did not increase P(urea) further. In fact, there was no difference in vasopressin-stimulated cAMP production in initial or terminal IMCD segments from rats fed 18% or 8% protein, suggesting that the adaptive response was not due to increased cAMP production. Glucagon did not change cAMP production or P(urea). Specificity of the response was suggested because neither aldose reductase nor sorbitol dehydrogenase activity changed with feeding 8% protein. Thus 1) in initial IMCD segments, vasopressin-stimulated P(urea) is induced after 2 wk, but net urea flux requires 3 wk of feeding 8% protein; 2) this adaptation is not solely due to a higher rate of cAMP production; and 3) specificity of the adaptive response is suggested because activities of enzymes responding to decreases in concentrating ability are unchanged. These results suggest that two distinct urea transporters may be involved in the adaptation to a low-protein diet.

A retrospective study evaluated the influence of sex and age on plasma biochemistry and haematology parameters in a captive-bred colony of baboons. Over 1,140 ETDA and heparin blood samples were obtained from 160 clinically normal baboons between the ages of 11 months and 11 years. Data for these blood tests were analysed for the effects of sex, age and sex age interactions. Sex, age and sex age interactions were detected for many plasma biochemistry and haematological parameters. The reference range values for platelets, white-blood cells and mean corpuscular volume and plasma chloride, glucose, total protein and iron were higher (P < 0.01) and red blood cell, plasma sodium, potassium, total CO2, creatinine, urea, total bilirubin, albumin, alkaline phosphate, gamma glutamyl transpeptidase and phosphate were lower (P < 0.01) in the female compared to the male population. Sex age interactions (P < 0.05) were seen with haemoglobin, white blood cells, haematocrit, mean corpuscular volume, sodium, creatinine, urea, calcium, phosphate, total bilirubin, total protein alkaline phosphatase, the liver enzymes and triglycerides. Plasma alkaline phosphatase was highest ( > 800 micro/l) in young juveniles of both sexes; creatinine was higher in older ( > 4 years) compared to younger baboons of the same sex (P < 0.05). Plasma cholesterol and triglycerides were greater (P < 0.01) in young baboons compared to older animals.

The purpose of this study was to evaluate the effect of a 12-week intradialytic progressive resistance training (PRT) regimen on circulating pro- and anti-inflammatory cytokines. Forty-nine patients (62.6 ± 14.2 years) were recruited from the outpatient hemodialysis unit of the St. George Public Hospital, Sydney, Australia. Patients were randomized to: PRT + usual care (n = 24) or usual care control (n = 25). The PRT group performed two sets of 10 exercises at high intensity using free-weights, 3 times per week for 12 weeks during dialysis, while the control group did not exercise. Tumor necrosis factor-alpha, interleukin-1b, interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10, and interleukin-12 were measured in serum before and after the intervention period. Muscle cross-sectional area (CSA), intramuscular lipid, intermuscular adipose tissue, and subcutaneous and total thigh fat, evaluated via computed tomography of the non-dominant mid-thigh, were also collected at both time points. All cytokines were significantly elevated in the total cohort at baseline compared with normative data. There were no cytokine changes over time or between groups (p > 0.05). In secondary analyses pooling the groups, changes in logIL-6 and IL-8 were inversely related to changes subcutaneous thigh fat (p < 0.05) while changes in logIL-6 were also inversely related to changes in thigh muscle CSA, and total thigh fat (p < 0.03). These data suggest that 12 weeks of intradialytic progressive resistance training does not improve circulating pro- and anti-inflammatory markers. Further research is required to elucidate the implications and mechanisms of the relationships between IL-6 and IL-8 and body composition in ESRD.

BACKGROUNDLow protein diets have been recommended as a treatment for retarding renal failure progression for over 50 years. The objective of the current guideline was to evaluate the available clinical evidence pertaining to the effect of protein-restricted diets on the progression of CKD. SEARCH STRATEGYDatabases searched: Medline (1999 to November Week 2, 2003. MeSH terms for kidney diseases were combined with MeSH terms and text words for dietary protein restriction. The results were then combined with the Cochrane highly sensitive search strategy for randomised controlled trials and MeSH terms and text words for identifying meta-analyses and systematic reviews. The Cochrane Renal Group Specialized Register of Randomised Controlled Trials was also searched for relevant trials not indexed by Medline. Date of search: 16 December 2003. WHAT IS THE EVIDENCE?The relationship between dietary protein restriction and non-diabetic renal failure progression has been examined by 4 meta-analyses, 1-4 11 randomised controlled trials (RCTs), 5-12 1 prospective double-blind cross-over study, 13 8 prospective controlled trials, 14-21 13 prospective noncontrolled trials, 22-34 and 7 retrospective observational cohort studies. [35][36][37][38][39][40] In view of the potential for serious bias in the non-randomised studies, this review will be restricted to the RCTs and meta-analyses.The Modification of Diet in Renal Disease (MDRD) study by Klahr et al 5 is the largest and best-designed prospective RCT to date. Patients were included in the study if their GFR was 25-55 mL/min/1.73 m 2 (Study A) or 13-24 mL/min/1.73 m 2 (Study B), their mean arterial pressure was less than 125 mmHg and their dietary protein intake was greater than or equal to 0.9 g/kg body weight/day (Study A only). Patients with body weight extremes (< 80% or > 160% of standard body weight), dubious compliance, insulin-dependent diabetes mellitus or heavy proteinuria (> 10 g/day) were excluded.Study A patients (n = 585) were randomly assigned (with adequate allocation concealment) to a usual protein diet (1.3 g/kg/day) or a low protein diet (0.58 g/kg/day), while Study B patients (n = 255) were randomised to a low protein diet (0.58 g/kg/day) or a very low protein diet (0.28 g/kg/day). An open-label design was used. The groups were similar at the start of the trial. Only 3% of the patients had non-insulin-dependent diabetes mellitus and 24% of the patients had polycystic kidney disease. ACE GUIDELINES a. A protein-controlled diet consisting of 0.75-1.0 g/kg/day, is recommended for adults with chronic kidney disease (CKD). The administration of a low protein diet (≤ ≤ ≤ ≤ 0.6 g/kg/day) to slow renal failure progression is not justified when the reported clinically modest benefit on glomerular filtration rate (GFR) decline is weighed against the concomitant significant declines in clinical and biochemical parameters of nutrition. (Level I evidence) b. For children, reduction of dietary protein intake to the lowest safe amounts recommended by the World Health Orga...