Binswanger, U.

Probst, W.

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706 LettersA 58-year-old Caucasian man was admitted for evaluation ofa nephrotic syndrome. He had a past history of mild hyperten-sion which had been treated with a combination of hydrochlor-othiazide and amiloride. Blood pressure was 130/70 mmHg;there was no oedema. Serum electrolytes were normal, creati-nine 112umol/l, albumin 29 g/l, gammaglobulin 5.3 g/1, totalcholesterol 10.2 mmol/1; 24-h urinary protein ranged from 3 to5 g; urinary sediment was normal, and urine culture sterile. GFRwas 86 ml/min per 1.73 m2, as assesssed by I23I Iothalamateclearance. Light microscopy and immunofluorescence studies ofthe specimens obtained by percutaneous renal biopsy revealed atypical pattern of stage 2 membranous nephropathy.Further evaluation showed normal blood cell count, serumcomplement, alphafetoprotein, and carcinoembryonic antigen;there was absence of anti-DNA antibodies, hepatitis B virusmarkers, antithyroglobulin and antimicrosomal antibodies,cryoglobulinaemia, and mercury in urine. VDRL and FTA testswere negative. There was no evidence of neoplasia, sarcoidosis,or multisystemic or infectious diseases.Drug inquiry revealed that the patient had been taking feno-profen 600-1500 mg daily for the preceding 12 months, becauseof loin pain following a vertebral trauma. Fenoprofen was with-drawn while antihypcrtensive treatment was maintained, andcomplete remission of proteinuria occurred within 6 months,without steroid or immunosuppressive therapy, and waspersisting 2 years later.Nephrotic syndrome induced by NSAID has been related tominimal-change glomerulopathy and has been most oftenassociated with acute renal failure and severe intersitial nephritis[1]. NSAID-associated membranous glomerulonephritis is ex-tremely unusual. We are aware of only four reported cases, threewith diclofenac [2-4] and one with ketoprofen, a propionic-acidderivative like fenoprofen [5]. All patients presented with thenephrotic syndrome, and complete remission occurred in allwithin 12 months of stopping the presumed causative drug.Thus, a search for a prior NSAID treatment should beincluded in the drug inquiry conducted in every patient withmembranous glomerulonephritis.Division of NephrologyLyon-South University Medical Centre69310 Pierre-BeniteFranceR. CahenP. TrollietB. FranccoisC. Chazot1. Clive DM, SlofTJS. Renal syndromes associated with nonsteroidalanti-inflammatory drugs N Engl J Med 1984: 310: 563-5722. Ducret F, Pointet P, Pichot C. Membranous glomerulonephritisduring rheumatoid arthritis. Probable toxicity of diclofenac.Nephrologie 1980; I: 143-1443. Hurault de Ligny B. Faure G. Bene MC, Kessler M, Huriet C.Extra-membranous glomerulonephritis during the treatment ofrheumatoid polyarthritis with diclofenac. Nephrologie 1984; 5:135-1364. Schillinger F, Montagnac R. Milcent T. Membranous glomerulo-nephritis after diclofenac treatment. Kidney Int 1987; 32: 428-429,(Abstract)5. Sennesaeal J. Van Den Houtte K. Verbcelen D. Reversible membra-nous glomerulonephritis associated with ketoprofen. dm Nephrol1986:26:213-215Systemic and Disseminated Candidiasis ComplicatingRenal FailureSir,—We read with great interest the paper 'Systemic and dissemi-nated candidiasis complicating acute renal failure' by Stevensand co-workers [1].It was rather disconcerting to note that none of their patientswere on prophylactic oral antifungal treatment. In a controlledtrial Ledingham and co-workers [2] using a Selective Parenteraland Enteral Antisepsis Regimen (SPEAR) which included sys-temic cefotaxime, oral polymyxin E, tobramycin and ampho-tericin B were able to demonstrate a substantial reduction in theincidence of acquired infection (10% vs 24%). The isolation ofyeasts from stomach, throat and trachea declined appreciablyduring days 2-4 in the test group, but changed little with time inthe control group.It has been our time-honoured practice to give nystatin100 000 units 6-hourly to all patients admitted to our RegionalRenal Unit, irrespective of the type of renal failure, therebyobtaining gratifying results. However, we were recently involvedin the management of a patient with acute myeloid leukaemiawho had not received oral nystatin and had developed hepaticcandidial abscesses and septicaemia; despite treatment withamphotericin B and flucytosine, the patient died with renalfailure.One of us (P.McC) recently investigated 27 patients whorequired ventilation and dialysis for a period of more than 5days. Cultures (1641) were taken from trachea! aspirate, urine,wound and blood. Of 1011 cultures in 15 patients using SPEARtherapy, 103 were positive for yeasts (10.4%). Of the 630 cul-tures taken in the remaining 12 control patients, 137 werepositive for yeasts (21.7%). Our study is in agreement with thefindings reported by Ledingham and co-workers [2]. We cannotbut emphasise the importance of oral antifungal therapy, whichis not only a simple, but also a cheap method of preventingcandidiasis.Regional Renal UnitRoyal Liverpool HospitalPrescott StreetLiverpool, UKM. YaqoobP. McClellandR. Ahmad1. Stevens PE. Rainford DJ, Green AD, Masterton RG. Systemic anddisseminated candidiasis complicating acute renal failure. NephrolDial Transplant 1988; 3:84-862. Ledingham 1A, Eastaway AT, McKay IC, Alcock SR, McDonaldJC, Ramsay G. Triple regimen of selective decontamination of diges-tive tract, systemic cefotaxime, and microbiological surveillance forprevention of acquired infection in intensive care. Lancet 1988; 1:785-790More on an Easily Obtained Accurate Dialysis IndexSir,—The search for quantification of dialysis treatment as stimulatedby the NCDS study resulted in different approaches to collectingdata in order to calculate K xt/V (K = clearance; t = treatmenttime; V = distribution volume). K was most often taken from invitro data provided by the manufacturers of filters, whereas thedistribution volume was either set at 0.58 x bodyweight, or wascalculated from urea extraction divided by change of blood ureaconcentration before and after treatment.We measured urea extraction by collecting dialysate, andobtained measurements for blood urea before and after treat-ment. Results for K. x t/V obtained from these 'true data' werecompared with those obtained from both calculated and invitro data. Furthermore, a formula is derived which permitsthe estimation of the 'true' dialysis index from blood ureameasurements before and after treatment.Letters 707123Calculation modeK: in vitro dataV:0.58xBWK:in vivo dataV: 0.58 x BWK:) in vivo dialysateV: J and blood ureaK225.36 ±25.15173.00 +23.69*173.00 +23.96*V34.34 ±4.5634.34 +4.5639.12 +10.95Kxt /V1.05 +0.150.80 +0.09*0.74 +0.17*M ± S D ; n = 14;'Significance: 1 vs2, 1 vs3:/><0.001Results (Table) indicate that the 'true' dialysis index accord-ing to formula F3 is 25% lower than the calculated value using invitro clearance data and 0.58 x BW distribution volume (Fl).Replacing the estimated clearance data by measured values(F2) adapts the index value partially to the true finding. Thecalculation of the 'true' dialysis index from extracted urea indialysate and concentration pre- and post-treatment includedclearance (K) = urea extracted/treatment time(cone, pre + cone. post)/2urea extractedurea distribution volume (V) =cone, pre —cone, postCombining these formulae for calculation ofKx t1 = - results in1 = cone, pre —cone, post(cone, pre + cone. post)/2In conclusion, the 'true' dialysis index, taking into accountin vivo filter clearance and individually calculated distributionvolume, is easily obtained from routine pre- and post-dialysisblood urea measurements.Note added in proof. This formula was recently described byBarth and Berlyne in abstract form {Kidney International 1988;33,216)Section of Nephrology W.ProbstDepartment of Internal Medicine U. BinswangerUniversity Hospital Zurich, SwitzerlandTreatment of Pseudomonas aeruginosa Peritonitis in aCAPD Patient with CiprofloxacinSir,—CAPD-associated peritonitis caused by Pseudomonas aeruginosais a very serious complication of CAPD treatment, oftenresulting in catheter removal. Ciprofloxacin, one of the newquinolones, seems to have promising properties for thetreatment of serious Pseudomonas aeruginosa infections [1,2].A 58-year-old woman treated by CAPD for 10 monthssuffered five episodes of Staphylococcus aureus peritonitis. Shedeveloped a further episode of peritonitis and Pseudomonasaeruginosa was cultured from the effluent fluid. She was treatedwith intraperitoneal gentamicin and ticarcillin for 8 days andafter 4 days of treatment the cultures became negative. Therapywas continued, but after another 4 days Pseudomonas aeruginosawas again cultured.Ciprofloxacin was started with an initial intravenous dose of400 mg, followed by intraperitoneal administration of 50 mgq.d.s. Serum levels were between 0.2 and 0.6 mg/1 and peritonealdialysate levels varied between 1.4 and 2.2 mg/1. The mini-mum inhibitory concentration (MIC) of ciprofloxacin for thePseudomonas aeruginosa strain was 0.05 mg/1. After 2 days,dialysate cultures became negative. Because of persistent highleucocyte counts in the peritoneal fluid, gentamicin was added tothe regimen after 8 days of ciprofloxacin therapy. The culturesremained negative and leucocyte counts returned to normalafter another 3 days. No side-effects were observed.Ciprofloxacin has a bactericidal action against Gram-negative bacteria including Pseudomonas aeruginosa [3). Thequinolones have a low incidence of side-effects [4]. Ciprofloxacinwas very well tolerated by our patient. Intraperitoneal doses of50 mg q.d.s. resulted in adequate ciprofloxacin levels in theperitoneal dialysate, which were 30 to 40 times the MIC value ofthe infecting organism. Ciprofloxacin seems to be a very promis-ing drug in the treatment of CAPD-associated peritonitis causedby Pseudomonas aeruginosa.Departments of Medicine and W. GraveMedical Microbiology A. W. SturmSt Laurentius HospitalPost Box 920, 6040 AX RoermondThe Netherlands1. Bayer AS, Blomquist IK, Kwang Sik Kim. Ciprofloxacin in exper-imental aortic valve endocarditis due to Pseudomonas aeruginosa. J.Antimicrob Chemother 1986; 17: 641-6492. Isaacs D, Slack MPE, Wilkinson AR, Westwood AW. Successfultreatment of pseudomonas ventnculitis with ciprofloxacin. JAntimicrob Chemother 1986; 17: 535-5383. Jones BM, Geary I, Lee ME, Duerden BI. Activity of pefloxacin andthirteen other antimicrobial agents in-vitro against isolates from hos-pital and genitourinary infections. J Antimicrob Chemother 1986; 17:739-7464. Scully BE, Neu HC, Parry MF, Mandell W. Oral ciprofloxacintherapy of infections due to Pseudomonas aeruginosa. Lancet 1986; 1:819-822A Modification to the 'Shaldon Technique' when InguinalFibrosis is PresentSir,—Shaldon's introduction of the Seldinger technique to catheterisethe femoral vein [1] was a milestone in the management of theuraemic patient. Since then thousands of patients with acuterenal failure and chronic renal insufficiency have benefited fromthis procedure. However, its repeated use has occasionallyresulted in a zone of fibrous tissue in the inguinal region due toeither consecutive localised haematomas and/or the effect of thelocal anaesthesia. In these cases its use is then not viable, as evenif the vessel can be localised and the guidewire inserted, thecatheter cannot be advanced because of the underlying fibrosis.Although the development of different vascular access tech-niques [2], the use of unipuncture systems for undertakinghaemodialysis sessions [3], or the permanence of catheters in thefemoral vein for long periods of time [4] have decreased theincidence of this problem, it is still necessary on occasionsto resort to the use of the classic Shaldon technique for theintroduction of a vascular catheter.We suggest a modification in the technique described byShaldon to introduce a femoral venous catheter through aninguinal region when fibrosis makes its use impracticable. Thefemoral vein is localised in the traditional way, using a needle ofCournand through which a guidewire is passed. The needle is

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