Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury. Although sepsis is a major triggering factor, acute kidney injury predisposes to confusion by causing generalised inflammation, leading to increased permeability of the blood–brain barrier, exacerbated by hyperosmolarity and metabolic acidosis due to the retention of products of nitrogen metabolism potentially resulting in increased brain water content. Downregulation of cell membrane transporters predisposes to alterations in neurotransmitter secretion and uptake, coupled with drug accumulation increasing the risk of encephalopathy. On the other hand, acute brain injury can induce a variety of changes in renal function ranging from altered function and electrolyte imbalances to inflammatory changes in brain death kidney donors.

Although more convenient for both patients and staff to undertake bioimpedance measurements pre dialysis, overhydration over estimates muscle mass and under estimates fat. For more reliable and reproducible assessments of nutritional status, we suggest that bioimpedance measurements of body composition should be made when patients are closer to their target weight than when overhydrated.

Although there have been many advancements in the treatment of patients with chronic kidney disease (CKD) over the last 50 years, in terms of reducing cardiovascular risk, mortality remains unacceptably high, particularly for those patients who progress to stage 5 CKD and initiate dialysis (CKD5d). As mortality risk increases exponentially with progressive CKD stage, the question arises as to whether preservation of residual renal function once dialysis has been initiated can reduce mortality risk. Observational studies to date have reported an association between even small amounts of residual renal function and improved patient survival and quality of life. Dialysis therapies predominantly provide clearance for small water-soluble solutes, volume and acid-base control, but cannot reproduce the metabolic functions of the kidney. As such, protein-bound solutes, advanced glycosylation end-products, middle molecules and other azotaemic toxins accumulate over time in the anuric CKD5d patient. Apart from avoiding potential nephrotoxic insults, observational and interventional trials have suggested that a number of interventions and treatments may potentially reduce the progression of earlier stages of CKD, including targeted blood pressure control, reducing proteinuria and dietary intervention using combinations of protein restriction with keto acid supplementation. However, many interventions which have been proven to be effective in the general population have not been equally effective in the CKD5d patient, and so the question arises as to whether these treatment options are equally applicable to CKD5d patients. As strategies to help preserve residual renal function in CKD5d patients are not well established, we have reviewed the evidence for preserving or losing residual renal function in peritoneal dialysis patients, as urine collections are routinely collected, whereas few centres regularly collect urine from haemodialysis patients, and haemodialysis dialysis patients are at risk of sudden intravascular volume shifts associated with dialysis treatments. On the other hand, peritoneal dialysis patients are exposed to a variety of hypertonic dialysates and episodes of peritonitis. Whereas blood pressure control, using an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), and low-protein diets along with keto acid supplementation have been shown to reduce the rate of progression in patients with earlier stages of CKD, the strategies to preserve residual renal function (RRF) in dialysis patients are not well established. For peritoneal dialysis patients, there are additional technical factors that might aggravate the rate of loss of residual renal function including peritoneal dialysis prescriptions and modality, bio-incompatible dialysis fluid and over ultrafiltration of fluid causing dehydration. In this review, we aim to evaluate the evidence of interventions and treatments, which may sustain residual renal function in peritoneal dialysis patients.

Background: Muscle weakness is a risk factor for mortality in haemodialysis (HD) patients; we wished to determine whether measuring the composition of the arm with bioimpedance was associated with arm muscle strength. Methods: We measured pinch strength (PS) and hand grip strength (HGS) in 250 adult HD patients with corresponding post-dialysis multifrequency bioelectrical assessments with segmental body analysis. Results: Mean age 64.0 ± 15.6, 66% male and 45.6% diabetic. The maximum HGS in the dominant or non-fistula arm was 18.9 ± 9.2 kg and PS 4.09 ± 1.96 kg respectively, with a correlation of r = 0.80, p < 0.001. HGS was associated with body cell mass (β 0.37, p < 0.001) and PS with appendicular muscle mass (β 0.06, p < 0.001). Both HGS and PS were independently associated with the ratio of extracellular water (ECW) to total body water (TBW); β -139.5, p = 0.024, β -44.8, p < 0.001 in the arm. The presence of an arterio-venous fistula increased the ECW/TBW ratio in the arm from 0.383 ± 0.009 to 0.390 ± 0.012, p < 0.05. Conclusion: Muscle strength measured by HGS and PS was associated with both markers of whole body and segmental body composition within the arm, particularly ECW/TBW. Bioimpedance measurements and assessment of muscle strength should be measured in the non-fistula arm.

Introduction: Increased natriuretic peptides are associated with increased cardiovascular and all-cause mortality for haemodialysis (HD) patients. However, debate continues whether these biomarkers are increased by extracellular water (ECW) excess and can be used to aid clinical assessment of volume status and help determine target weight. Methods: We measured N terminal probrain natriuretic peptide (NT-proBNP) predialysis in 375 stable haemodialysis outpatients with corresponding pre and postdialysis multifrequency bioelectrical impedance assessments (MFBIA) of (ECW)/total body water (TBW). Results: Median age 64 (51-75), 63.9% male, 42.9% diabetic, 43.2% Caucasoid, 14.4% with a history of myocardial infarction, 8.4% coronary artery bypass surgery, dialysis vintage 28.2 (12.3-55.5) months. Median predialysis NT-proBNP 283 (123-989) pmol/l, and predialysis ECW/TBW ratio 0.397 ± 0.029. On multivariate analysis, predialysis log NT-proBNP was associated with predialysis systolic blood pressure (β 0.007, p = 0.000), weight (β −0.008, p = 0.001), valvular heart disease (β 0.342, p = 0.015, ECW/TBW (β 1.3, p = 0.019) and log CRP (β 0.145, p = 0.037). Dividing patients into NTproBNP quartiles, %ECW/TBW and relative ECW overhydration were significantly greater for the highest quartile vs. lowest (40.5 ± 4.1 vs. 39.0 ± 1.1, and 1.51 ± 1.24 vs. 0.61 ± 0.69 l, respectively, p < 0.001). Conclusion: In this study, predialysis NTproBNP values were associated with direct assessments of the extracellular volume excess measured by MFBIA and systolic arterial blood pressure. This suggests that predialysis NTproBNP values can potentially be used to aid clinical assessment of volume status in dialysis patients to determine target weight.

No abstract

Zinc is an essential trace element which plays many vital roles in cellular metabolism, growth, tissue repair, neurotransmitter production, and inflammation (1). Zinc deficiency has major clinical effects, particularly in children, ranging from poor appetite, weight loss, growth retardation, delayed healing of wounds, to loss of taste and mental slowness (2). Generally, zinc intake correlates well with dietary protein intake, as the major dietary sources of zinc are meats, dairy products, legumes, and whole grains. Nevertheless, zinc may bind to phytates, oxalate, iron, or medicines such as phosphate binders prescribed to chronic kidney disease (CKD) patients, leading to the formation of less absorbable insoluble complexes in the small intestine. Once absorbed from the gastrointestinal tract, zinc is transported in the plasma predominately by albumin, and stored intracellularly. Zinc is largely excreted in the feces, with urinary excretion accounting for less than 10% of daily losses. As zinc excretion is principally through the gastrointestinal tract, dialysis patients are at no greater risk of zinc toxicity than the general population. However, in dialysis patients, several factors may contribute to altered body zinc storage. Poor appetite and restriction of dietary protein may lower zinc intake. Many medicines, including ion exchange resins, may interfere with zinc absorption. As such, several studies have measured plasma zinc levels in hemodialysis (HD) patients (3), reporting no effect with HD (4), although a meta-analysis reported HD patients were more likely to have low plasma zinc levels (5). In theory, peritoneal dialysis (PD) patients are more likely to have zinc deficiency than HD patients due to reduced appetite, lower serum albumin, and peritoneal protein losses. As there are limited small studies with differing results investigating zinc deficiency in PD patients, we audited plasma zinc levels in a stable PD population. PATIENTS & METHODS Plasma zinc levels were measured in 152 chronic stable PD outpatients, mean age 58 years (23-89), 51.3% male, 28.9% diabetic, and median dialysis vintage 11 months (1-157). Plasma samples were collected in specially prepared tubes designed to minimize external trace element contamination, and zinc, copper, and selenium were measured by atomic absorption spectroscopy. Serum biochemistry and hematology samples were analyzed with standard multi-channel analyzers. Body composition analysis was performed with multi-frequency bioelectrical impedance analysis (InBody 720 Body Composition Analysis,

BackgroundCancer antigen 125 (CA125) is made by peritoneal mesothelial cells and can be measured in spent dialysate effluent from peritoneal dialysis (PD) patients. It has been suggested that CA125 is a marker of peritoneal mesothelial cell mass and turnover. As PD CA125 increases during peritoneal inflammation, we wished to determine whether measuring PD CA125 during peritonitis provided additional information in determining outcome of peritonitis.MethodsWe prospectively measured peritoneal CA125 in 127 adult PD patients presenting with 187 acute episodes of PD peritonitis, measuring peritoneal CA125 from a sample of dialysate effluent obtained from a 4 hour 2 litre 13.6 g/l dextrose peritoneal dwell.ResultsMean patient age 60.8 ± 17.1 years, 62.6% male, 33.7% diabetic and the median PD vintage was 22 (11-48) months. 127 patients (66.8%) presented with their first episode of peritonitis, 20% their second episode, 13.2% third or greater. Gram positive bacteria accounted for 64.7% of all peritonitis episodes and Gram negative bacteria 21.1%. Treatment was successful for 151 episodes of PD peritonitis (81.1%). The median PD effluent total WBC was 1240 (430-3660) /ml and serum CRP 67 (20-144) mg/l, with a PD CA125 of 38 (20.3-72.3) IU/l on presentation. There were positive correlations between PD effluent CA125 concentrations and total WBC on presentation (r = 0.41, p = <0.001) and dialysis vintage (r = -0.43, p < 0.001) but not with patient age, diabetic status, or serum CRP.There was no difference in PD effluent CA125 concentrations between Gram positive, and Gram negative peritonitis or between those episodes which responded to treatment, median 38 IU/ml (21-69) vs those with treatment failures 38 IU/ml (15-94).ConclusionWe did not find any additional diagnostic or prognostic benefit for measuring effluent CA125 in PD patients presenting with acute peritonitis compared to standard investigations, including peritoneal WBC and serum CRP. As such our study would not support the routine measurement of peritoneal CA125 during episodes of peritonitis.