Biocompatible dialysis membranes do not reduce plasma leptin levels

Nephrol Dial Transplant (2000) 15: 925

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ARAS is probably two sudden jumps at the times of renal artery occlusion. The first jump is often not clinically evident with serum creatinine remaining normal or only slightly raised. The ideal patient for renal revascularization will have a useless kidney beyond an occluded artery and a wellpreserved kidney beyond a tight stenosis. Unless such a patient is coincidentally prescribed an ACE inhibitor or angiotensin II receptor antagonist, they will have a nearnormal serum creatinine and there may be no clinical clues that they are at high risk of ESRF due to bilateral renal artery occlusion. When the rationale for intervention is prevention of occlusion, monitoring of clinical outcome becomes difficult—one cannot expect any improvement in renal function. A clinically successful intervention is one which delays renal artery occlusion—something which simply cannot be assessed in individuals. There is no doubt that renal revascularization by whatever means has a role—in patients with hypertension and fibromuscular dysplasia, bilateral tight ARAS and pulmonary oedema, tight ARAS to a solitary functioning kidney to either prevent occlusion or allow ACE inhibitor use, and recently occluded arteries to viable kidneys. Probably all these categories combined are outnumbered by patients with hypertension, generalised vascular disease, chronic renal failure and coincidental ARAS. Farmer et al. have given us the explanation why intervention is doomed to failure in most of these patients, in whom we need to concentrate on blood pressure control, smoking cessation and lipid lowering. Renal Unit South Cleveland Hospital Middlesbrough UK

J. Main

1. Farmer CKT, Cook GJR, Blake GM, Reidy J, Scoble JE. Individual kidney function in atherosclerotic nephropathy is not related to the presence of renal artery stenosis. Nephrol Dial Transplant 1999; 14: 2880–2884 2. Scoble JE, Maher ER, Hamilton G, Dick R, Sweny P, Moorhead JF. Atherosclerotic renovascular disease causing renal impairment—a case for treatment. Clin Nephrol 1989; 31: 119–122 3. Mailloux LU, Napolitano B, Belluci AG, Vernace M, Wilkes BM, Mossey RT. Renal vascular disease causing end-stage renal disease, incidence, clinical correlates and outcomes: a 20-year clinical experience. Am J Kidney Dis 1994; 24: 622–629

Biocompatible dialysis membranes do not reduce plasma leptin levels Sir, There is evidence that biocompatible dialysis membranes (BCM ) lead to a lesser degree of malnutrition than bioincompatible membranes (BICM ) [1]. Lindsay et al. suggested [2] that this may be attributable to a beneficial effect on nutrient intake of BCM dialysis, although it was not clear whether this was related to the flux properties or biocompatibility of the membrane. Leptin suppresses appetite and increases basal metabolic rate in rodent models. It is present in supra-normal concentrations in dialysis patients and may suppress nutrient intake [3]. Leptin synthesis increases in the presence of high concentrations of cytokines, particularly TNF-a and IL-1 [4]. This led us to hypothesize that dialysis with a BICM may stimulate leptin synthesis and suppress appetite. We tested this hypothesis using a low-flux polyethylene glycol grafted cellulose

(PEGC ) membrane [5] and standard Cuprophan in this prospective randomized cross-over study. Thirty-two patients were studied (22 male, 10 female; median age 63, range 28–83; median BMI 23.9 kg/m2, range 17.2–32.7 kg/m2). All patients had been stable on regular bicarbonate haemodialysis with a Cuprophan membrane for at least 3 months. They were randomized to either continue with Cuprophan (Gambro ‘Alwall’, Gambro Dialysatoren, Hechingen, Germany) or change to a PEGC membrane (Asahi AM-Bio-Wet, Asahi Medical Co., Ltd, Tokyo, Japan) with equivalent clearance. They dialysed for 2 months, after which at 07:30 a pre-dialysis blood specimen was taken. Each patient then converted to the other membrane and the blood sample was repeated after two more months. Plasma leptin and CRP were compared on paired samples. In a second study (23 patients; 15 male, 8 female; median age 65; range 28–83) leptin, CRP and albumin levels were measured immediately before and after a morning dialysis session. Leptin and CRP results were not normally distributed so median values and interquartile ranges are quoted and nonparametric analyses used. The other results were normally distributed and compared by paired t-tests. Contrary to our hypothesis, plasma leptin levels (BCM 11.9 (5.7–40.1) ng/ml vs BICM 10.3 (4.5–36.1) ng/ml, P