Increase in Extracellular Hydration Status After Initiating Peritoneal Dialysis Electively.

Renal replacement therapy is designed to treat uremic symptoms and correct hypervolemia. We hypothesized that starting peritoneal dialysis (PD) should reduce overhydration, and we measured body composition and hydration status using bioimpedance in PD patients prior to training and then at the first assessment of peritoneal membrane function. We studied 100 consecutive patients with a planned start to PD, without peritoneal infections or mechanical catheter problems, mean age 54.7 ± 17.1 years, 57% male and 25% diabetic. Extracellular water (ECW) overhydration increased from -0.06 (-1.21 to 0.97) L to 0.96 (0.50 to 3.01) L, p < 0.001. Fat mass increased from 22.7 ± 11.1 to 23.7 ± 11.3 kg, p = 0.007). The change in ECW/total body water (TBW) was associated with age (ß 0.065, p < 0.001), increasing comorbidity (ß 1.107, p = 0.005), faster peritoneal protein transport (ß 1.84, p < 0.04), and negatively with serum albumin (ß -0.208, p < 0.001), and residual renal function (ß -0.725, p = 0.026). Patients who had an increase in ECW/TBW had higher C-reactive protein (CRP) both before starting (16.8 ± 24.1 vs 7.7 ± 18.9 mg/L), and when established on PD (15.0 ± 31.8 vs 4.6 ± 5.1 mg/L), p < 0.05. Rather than a reduction in ECW hydration status, overhydration increased after starting PD. This was greater for older more comorbid patients and those with an inflammatory milieu and lower residual renal function. These factors should be considered when deciding upon initial PD prescriptions to limit ECW overhydration before information on peritoneal membrane function becomes available.

Measurement of Muscle Strength in Haemodialysis Patients by Pinch and Hand Grip Strength and Comparison to Lean Body Mass Measured by Multifrequency Bio-Electrical Impedance.

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 (ß 0.37, p < 0.001) and PS with appendicular muscle mass (ß 0.06, p < 0.001). Both HGS and PS were independently associated with the ratio of extracellular water (ECW) to total body water (TBW); ß -139.5, p = 0.024, ß -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.

Strategies for preserving residual renal function in peritoneal dialysis patients.

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.

Does the presence of an arteriovenous fistula alter changes in body water following hemodialysis as determined by multifrequency bioelectrical impedance assessment?

Multifrequency bioelectrical impedance assessments (MFBIAs) aid clinical assessment of hydration status for hemodialysis (HD) patients. Many MFBIA devices are restricted to whole body measurements and as many patients dialyze using arteriovenous fistulas (AVFs), we wished to determine whether AVFs affected body water measurements. We reviewed pre- and post-HD segmental MFBIA measurements in 229 patients attending for midweek HD sessions. Up to 144 were dialyzed with a left arm AVF (L-AVF), 42 with a right arm AVF (R-AVF), and 43 by central venous access catheter (CVC). Water content and lean tissue were greater in the left compared to right arm in those patients with L-AVFs both pre and post dialysis (pre 2.1 ± 0.7 vs. 2.0 ± 0.7 L, and post 1.9 ± 0.6 vs. 1.8 ± 0.6 L and pre 2.65 ± 0.9 vs. 2.56 ± 0.8 kg, and post 2.34 ± 0.8 vs. 2.48 ± 0.8 vs. 2.34 ± 0.8 kg, respectively) and were also greater in the right compared to left arm for those patients dialyzing with R-AVFs (pre-HD 1.92 ± 0.5 vs. 1.86 ± 0.6 L and post-HD 1.79 ± 0.5 vs. 1.7 ± 0.5 L, and pre-HD 2.47 ± 0.6 vs. 2.38 ± 0.7 kg and post-HD 2.3 ± 0.74 vs. 1.28 ± 0.7 kg, respectively), all Ps < 0.05. There were no significant differences in arm volumes or composition pre or post dialysis in those dialyzing with CVCs. Segmental MFBIA detects differences in arm water and lean mass in patients with AVFs. The presence on an AVF increases the water content in the ipsilateral arm both pre and post HD. This increased water content of the fistula arm will not be detected by whole body bioimpedance devices.

Predialysis NTproBNP predicts magnitude of extracellular volume overload in haemodialysis patients.

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 (ß 0.007, p = 0.000), weight (ß -0.008, p = 0.001), valvular heart disease (ß 0.342, p = 0.015, ECW/TBW (ß 1.3, p = 0.019) and log CRP (ß 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.

Diagnostic and prognostic role of peritoneal CA 125 in peritoneal dialysis patients presenting with acute peritonitis.

BACKGROUND: Cancer 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. METHODS: We 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. RESULTS: Mean 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). CONCLUSION: We 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.

Brain-kidney crosstalk.

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.