The relative roles of hepatic lipase and lipoprotein lipase in the pathogenesis of uremic lipid abnormalities were studied in 92 hemodialysis patients. Fasting serum cholesterol, triglyceride, and HDL-cholesterol concentrations were measured. Plasma lipoprotein electrophoretic patterns were determined in all patients. Hepatic lipase and lipoprotein lipase activities were selectively measured in post-heparin plasma in 59 patients. Hemodialysis patients had higher serum triglyceride and lower HDL-cholesterol concentrations than did their age and sex-matched control subjects. Both hepatic and lipoprotein lipase activities were reduced in hemodialysis patients. An inverse relation between lipoprotein lipase activities and serum triglyceride concentrations emerged. Lipoprotein lipase activities correlated with in vivo post-heparin fractional clearance rates of Intralipid. A positive correlation between lipoprotein lipase activities and HDL-cholesterol concentrations probably reflected impaired catabolism of triglyceride-rich lipoproteins being responsible for the low HDL-cholesterol concentrations. Hemodialysis patients (41.3%) had an abnormal lipoprotein (the 'mid-band'). While hepatic lipase activities did not correlate with any parameters of lipid metabolism, patients with 'low' hepatic lipase activities had a significantly higher prevalence of 'mid-bands' than did those with 'normal' activities. No evidence was developed to prove that the 'mid-band' lipoproteins were remnant particles.

Measurements of dialysate sodium are used to estimate peritoneal dialysis sodium losses and sodium sieving, a measure of hydraulic permeability of the peritoneum. Peritoneal dialysates differ from serum samples in terms of pH, osmolality, protein and glucose concentration. We wished to determine whether these factors affected sodium measurement. Dialysate samples were taken from 52 consecutive peritoneal dialysis patients attending for a standard peritoneal dialysis equilibrium test (PET), 20 with standard lactate dialysate and 32 with neutral pH dialysate and sodium was measured by both flame photometry and indirect ion selective electrode (ISE). Sodium measured by ISE consistently overestimated that measured by flame photometer, mean bias 1.5 mmol/L (95% confidence limits 1.2 to 1.8), P < 0.001. Sodium was lower in fresh neutral pH dialysates by both methods - flame 125.3 ± 1.17 vs. 131.6 ± 0.39 mmol/L, than standard lactate dialysates ISE 127.4 ± 1.05 vs 132.7 ± 0.27 mmol/L, P < 0.001. Glucose was higher in fresh neutral pH dialysates 122.7 ± 1.1 vs. standard lactate dialysates 116.7 ± 0.4 mmol/L, P < 0.001. On multiple regression analysis, only glucose was found to be an independent factor for sodium measurement, F = 14.78, β = -0.0851, SEM 0.022, 95% confidence limits -1.28 to -0.042. In this study there was a small but consistent difference between sodium measurements by ISE and flame photometry during the PET. Sodium measurements by either method appeared to be affected by hypertonic dialysates, but there were differences with pH. This may potentially lead to errors in both overestimating peritoneal sodium losses and the proportion of patients with ultrafiltration failure due to loss of sodium sieving.

Background: The Department of Health launched a cardiovascular disease risk assessment initiative with particular reference to reducing health inequalities in ethnic minorities. Collaboration between HEART UK, Royal Free Hampstead NHS Trust and Hindu Temples resulted in vascular screening in North London. Methods: Subjects of South Asian origin were screened. A full lipid profile and glucose were measured using a point of care testing (POCT) Cholestech LDX analyser (LDX). Venous samples were analysed in our hospital laboratory. Results:The results (215 men; 191 women) were divided into tertiles and Bland-Altman plots were used to assess agreement. At high-density lipoprotein cholesterol (HDL-C) concentrations ,1.0 mmol/L the LDX underestimated values by 20.2 mmol/L (P,0.0001). At HDL-C concentrations .1.3 mmol/L this bias disappeared. For total cholesterol the concentration-dependent negative bias was evident at concentrations of ,4.1 mmol/L (P , 0.0001). This bias was less evident at higher concentrations. A similar pattern was seen for low-density lipoprotein cholesterol. There were also small variations in glucose and triglyceride values. However, there was excellent agreement in calculated cardiovascular disease risk using kappa analysis for JBS2, QRISK2, ETHRISK and Framingham (k ¼ 0.86, 0.92, 0.94 and 0.88, respectively). This was a high-risk population since 9.7 -19.4% had a !20% 10-y probability of a vascular event depending on the risk engine and assay method used. The corresponding values for intermediate risk (11 -19%) were 18.6-25.7%. Conclusions: There was a minimum mismatch irrespective of the type of risk calculator used. POCT measurements are adequate for the

Lipoprotein(a) (Lp(a)) has recently been recognized to be a risk factor for coronary heart disease. Lp(a) median values in the absence of renal disease are around 10 mg/dl. Higher levels (greater than or equal to 30 mg/dl) correlate with the occurrence of coronary heart disease, particularly in the presence of elevated cholesterol. We have studied Lp(a) in 76 adults with proteinuria. Fifty had glomerular diseases and 26 non-glomerular diseases, with renal function varying from normal to advanced chronic renal failure. Lp(a) values were shifted to the right, with a median of 21.0 mg/dl, and 25% of patients had values of 30 mg/dl or more. Lp(a) did not correlate with cholesterol, age, lipoprotein subclasses, apoproteins A-I or B-100, albumin, creatinine, or creatinine clearance. Median Lp(a) values did not differ significantly comparing men versus women, or glomerular versus non-glomerular disease. Lp(a) may inhibit fibrinolysis, and is deposited in atherosclerotic lesions. Although the cause of these elevated Lp(a) levels is uncertain, we propose that they contribute to the increased risk of coronary heart disease in the nephrotic syndrome, and may play a role in progressive renal disease.

Background A 'one stop shop' model for multifactorial risk factor management in a culturally sensitive environment may improve cardiovascular disease and diabetes prevention. A full biochemical profile for cardiovascular disease risk assessment includes a lipid profile, glucose, glycated haemoglobin and urine albumin creatinine ratio measurements. This may require the use of more than one point of care testing instrument. Methods Individuals who attended a community cardiovascular disease risk screening or an audit programme of the diabetic care pathway in the community were sampled. Bland-Altman and Deming regression plots were used to assess agreement between methods for total cholesterol, high-density lipoprotein cholesterol, triglycerides, glycated haemoglobin and urine albumin creatinine ratio. Results There was good agreement between the Afinion AS100 analyser, Cholestech LDX and the laboratory methods for total cholesterol, high-density lipoprotein cholesterol and triglycerides ( n = 232). The Afinion AS100 agreed well with the laboratory method for glycated haemoglobin ( n = 255) and urine albumin creatinine ratio ( n = 176). There was statistically significant bias ( p = 0.03 to <0.0001) for several measurements. However, these were judged not to be clinically relevant. Specifically for the total cholesterol and high-density lipoprotein cholesterol values, we obtained good agreement (weighted kappa: 0.91 and 0.94 for the Afinion AS100 vs. Cholestech LDX and Afinion AS100 vs. laboratory method, respectively) for cardiovascular disease risk calculation using QRISK2. Conclusions Point of care testing can support a 'one stop shop' approach by providing rapid, reliable results. The Afinion AS100 analyser provides a multi-analyte platform and compares well with laboratory-based methods and another well-established point of care testing analyser.