- Email: [email protected]
KIDNEY TRANSPLANT REGRAFT RESULTS IMPROVED BY PEROPERATIVE BLOOD TRANSFUSIONS
634
practitioner, community nurse, and social worker supervision. To provide respite to families or hostels and in the best interests of the patients they are readmitted to hospital when necessary. In hospital they behave remarkably well, to the surprise of the community mental handicap team, the family, and even hospital staff. Patients (and their relatives) often beg to be allowed to stay in hospital. Their hospital stay is not the unhappy recurrence predicted by some organisations. The Department of Health should pause and study the situation before embarking upon a project that would involve great expenditure from public funds and would be detrimental to the long-term interests of mentally handicapped patients. Unit of Mental Handicap,
Brockhall Hospital,
U.
Blackburn BB6 8AZ
J. DEY
THIAZIDE-INDUCED DILUTIONAL HYPONATRAEMIA MASQUERADING AS SUBARACHNOID HAEMORRHAGE
SIR,-Dr Benfield and colleagues (Aug 9,
p 341) report a induced by ’Moducren’ (hydrochlorthiazide 25 mg, amiloride 2-5 mg, timolol 10 mg) masquerading as subarachnoid haemorrhage. We report a similar case in which ’Moduretic’ (amiloride 5 mg, hydrochlorthiazide 50 mg) and later bendrofluazide sequentially induced severe dilutional hyponatraemia mimicking a subarachnoid haemorrhage. We conclude that thiazide diuretics were the agents responsible. An otherwise fit 83-year-old woman was prescribed one moduretic tablet a day for mild congestive cardiac failure. (The following morning her serum sodium was 130 mmol/1.) Over the next 4 days she experienced episodic confusion, but on the fifth day she rapidly deteriorated with headache and vomiting. She was confused and unable to stand. On admission to hospital she was afebrile and drowsy, with generalised muscle weakness, hypertonia, brisk reflexes, and extensor plantar responses; marked neck stiffness and photophobia were elicited. A retinal haemorrhage was present close to the right optic disc. Her blood pressure was 170/110 mm Hg and the pulse was 64/min in sinus rhythm. A subarachnoid haemorrhage was suspected. Her chest X-ray showed slight cardiomegaly and upper lobe venous prominence. Her white cell count was 8-1 x 109/1. She was severely hyponatraemic (112 mmol/1) and her serum potassium was 4-2 mmol/l, urea 7-7 mmol/l, creatinine 95 lunol/1, and sugar 7 mmot/1. Serum osmolality was reduced to 228 mosmol/kg with a urine osmolality of 780 mosmol/kg. A cranial computerised tomographic scan revealed no abnormality. CSF obtained (after a traumatic lumbar puncture) at a low opening pressure contained 12 000 red cells1, no white cells, and no xanthochromia. She was treated by slow infusions of hypertonic saline and fluid restriction to 1 litre per day, and the moduretic was stopped. A rapid clinical and biochemical improvement occurred over the next 72 h and she returned to complete wellbeing. 10 days after her hospital admission her ankles became oedematous and diuretics were reintroduced, bendrofluazide 5 mg daily being prescribed. Within three days her serum sodium had fallen from 134 to 115 mmol/1. She became confused, with a headache and vomiting. The signs of meningism recurred and again there was generalised muscle weakness, hypertonia, brisk reflexes, and extensor plantar responses. Hypertonic saline infusions and fluid restriction were initiated and bendrofluazide was stopped. 72 h later the biochemical picture and her clinical condition were normal. She was discharged on no medication. 2 months later she is well, with normal serum electrolytes, on no treatment. Our case confirms Benfield and colleagues’ view that a dilutional hyponatraemia may masquerade as a subarachnoid haemorrhage. A thiazide diuretic is the common component in these two cases implicating these agents (hydrochlorthiazide and bendrofluazide) as being responsible for the syndromes. case
of dilutional
hyponatraemia
Department of Medicine, Southmead General Hospital, Bristol BS10 5NB
P. G. BAIN W. EGNER P. R. WALKER
MONOCLONAL ANTIBODY TO DETECT PNEUMOCYSTIS CARINII
SiR,—Dr Kovacs and co-workers (July 5, p 1) report the successful use of a monoclonal antibody to detect Pneumocystis carinii in bronchoalveolar lavage (BAL) fluid and. impression smears of infected lung tissue. Since the autumn of 1985 we have investigated 130 lung derived samples by immunofluorescence using monoclonal antibodies to detect this parasite. Most of the impression smears, BAL fluids, and induced sputum samples studied were from suspected AIDS patients at the department of infectious disease, Karolinska Institute. 1/9 biopsy samples, 13/72 BAL fluids, and 3/49 sputum samples were positive. The method is specific, sensitive, and simple. We have identified the target antigen recognised by the monoclonal antibodies as a 82 000 molecular weight parasite component that resists denaturing. The antibodies can be used to detect parasites in variously fixed material, including samples to which 50% ethanol has been added to inactivate human immunodeficiency virus. Brief trypsination of such samples (immersion of the fixed sample for 15 min in 1% trypsin) was included for improved penetration but also for the removal of in vivo bound immunoglobulins. The antibodies also reacted with P carinii in paraffin sections of lung tissue. We have tried to answer some of the questions raised by Kovacs et al. P carinii parasites were easily detectable in induced sputum samples after ’Sputolysin’ (Behring Diagnostics) treatment. Direct labelling of antibodies with fluorescein isothiocyanate gave a useful reagent, but the yield of isolated mouse immunoglobulin from ascites fluid for the production of labelled antibodies needs to be improved. Antigenic variation between P carinii organisms from different individuals does not seem to be a problem. The specific antibodies 2E3 and 3F6 were used in a retrospective study to detect the parasite in paraffin sections of 30 lung biopsy specimens from immunosuppressed children with leukaemia treated at the children’s clinic, University Central Hospital, Helsinki. This study showed agreement between immunofluorescence and conventional histological staining with modified methenamine-silver technique. Our results support the optimism expressed in the study by Kovacs and coworkers about the future use of the immunofluorescence method. Department of Parasitology, National Bacteriological Laboratory, 5-105 21 Stockholm, Sweden
EWERT LINDER KERSTIN ELVIN ANDERS BjORKMAN
Department of Infectious Disease, Karolinska Institute, Roslagstull Hospital,
SUSANNE BERGDAHL LINDA MORFELDT-MANSSON LARS MOBERG ANDERS SONNERBORG
Stockholm
KIDNEY TRANSPLANT REGRAFT RESULTS IMPROVED BY PEROPERATIVE BLOOD TRANSFUSIONS
SiR,-Although cadaver kidney transplant success rates have improved by 12-20% at one year with the introduction of cyclosporin,1,2 second transplants are not so significantly affected.3 We find that transfusions given at the time of transplantation (peroperative) improve retransplant success rates with or without cyclosporin. Such peroperative transfusion did not improve success rates of first grafts, regardless of whether cyclosporin was used or not, as shown in the figure. An 11 % improvement was noted for first grafts at one year with the use of cyclosporin. Peroperative transfusion improved survival by only 1% in non-cyclosporintreated patients and reduced it by 2% in cyclosporin-treated patients. In regrafted patients cyclosporin improved the results by 4% at one year. Peroperative transfusions had a 5% effect in cyclosporin patients and 4% effect in non-cyclosporin patients. Patients who received peroperative transfusions and cyclosporin had significantly higher (p < 0-05) survival rates than those who had no peroperative transfusion and no cyclosporin. Other comparisons
635 RED-CELL SURFACE CHARGE IN GLOMERULAR DISEASE
Effect of peroperative transfusions
on
cadaver donor transplant.
significant. A 6% improvement in survival rate of retransplants with peroperative transfusions was also seen among patients who had received transfusions before transplantation (p<0-05) (figure), as well as those without preoperative transfusions. As in the cyclosporin/non-cyclosporin comparison, though peroperative transfusions had an effect on regrafts they had no effect on primary transplants. Although it was thought that peroperative transfusions may be of benefit to patients receiving primary grafts’-6 or to patients who had never received preoperative transfusions it now seems that transfusions given on the day of transplantation are not of much benefit.8 However, for regrafts, a significant improvement is obtained by peroperative transfusions. It is unlikely that the mechanism of this effect is the same as that of cyclosporin, thus, when used in combination, an additive effect might be obtained. Peroperative transfusions may neutralise antibodies formed by the rejection of the first graft. The effect of peroperative transfusions is mostly within the first few months after transplantation (see figure). Indeed, even first day function is improved from 71-6% (268 patients) to 75-2% (262 patients) by peroperative transfusion. Among sensitised patients receiving first grafts, one-year survival of 68% was noted without peroperative transfusions (744 patients) and 66% with peroperative transfusions (550 patients). Since sensitised first-graft patients do not demonstrate the effect of peroperative transfusions, it is likely that antibodies generated by transfusions differ from those generated by a graft rejection. We conclude that peroperative transfusions are a simple and effective adjunctive treatment for retransplants. Since such regrafts have poor survival rates, even with cyclosporin, treatment with peroperative transfusions may be worth considering. were not
UCLA Tissue Typing Laboratory, University of California Los Angeles, Los Angeles, California, USA
KAZUO TOKUNAGA PAUL I. TERASAKI
SIR,-Electrical charge is a crucial determinant of functional integrity at the glomerular basement membrane; loss of negative charge at this site results in proteinuria in clinical and experimental glomerular disease. Levin and his colleagues1 reported reduced binding of the cationic dye, alcian blue, to red cells of children with minimal change nephrotic syndrome and focal glomerulosclerosis during episodes of heavy proteinuria. Dr Boulton-Jones and colleagues (July 26, p 186) used the same technique to study red-cell charge of patients whose glomerular disease is quiescent in order to investigate disease susceptibility. To confirm a relation between red-cell surface charge and proteinuria we have measured alcian blue (AB) binding to red cells1 in 14 healthy controls, in 16 patients with end-stage renal failure without heavy proteinuria, and in 16 patients with nephrotic syndrome (urine protein > 3 g/24 h, serum creatinine < 300 pmol/1). The causes of the nephrotic syndrome were: membranous nephropathy (6), diabetic nephropathy (3), mesangiocapillary glomerulonephritis (2), lupus nephritis (2), and 1 each with focal glomerulosclerosis, amyloidosis, and minimal change nephrotic syndrome. AB binding did not fall outside the control range in any patient with nephrotic syndrome but was modestly diminished in patients with uraemia:
*p < 0 05 (unpaired t test) when compared with controls. No correlation was found between AB binding and age, serum albumin, urine protein excretion, or glycosylated haemoglobin concentration. Our 6 patients with membranous nephropathy did not have a lower mean AB binding, as was reported by BoultonJones and colleagues for patients with the same disease in remission. We studied sequentially AB binding in 1 child with minimal change nephrotic syndrome-AB binding was normal when the patient was in relapse (before treatment) and remained the same a week later, when proteinuria had resolved in response to corticosteroids. Our preliminary findings suggest that red-cell charge may be somewhat reduced in severe uraemia, so renal function ought to be defined in any study of red-cell charge in nephrotic syndrome. More importantly, our study does not confirm any relation between red-cell charge and proteinuria in patients with nephrotic syndrome due to a spectrum of glomerular diseases. In the nephrotic child investigated sequentially we could not confirm the reported red-cell charge abnormality in relapse! or any alteration in red-cell charge when proteinuria was abolished by corticosteroids. Thus, we have found no evidence that red-cell charge measurements reliably mirror the glomerular capillary wall charge; another more specific method is required.
Departments of Medicine and Nephrology, Leicester General Hospital, Leicester LE5 4PW
J. FEEHALLY A. SAMANTA H. KINGHORN A. C. BURDEN J. WALLS
M, Smith C, Walters MDS, Gascoine P, Barratt TM. Steroid-responsive nephrotic syndrome: a generalised disorder of membrane negative charge. Lancet 1985; ii: 239-42.
1. Levin
1. Calne RY, Wood AJ. Cyclosporin in cadaveric renal transplantation: 3-year follow-up of a European multicentre trial. Lancet 1985; ii: 549. 2. Opelz G. Correlation of HLA matching with kidney graft survival in patients with or without cyclosporine treatment. Transplantation 1985; 40: 240-43. 3. Terasaki PI, et al. Patients’ graft and functional survival rates: an overview. In: Terasaki PI, ed. Clinical kidney transplant 1985. UCLA Tissue Typing
Laboratory, Los Angeles, 1985: 1-26. CR, Sinclair NR, Sheppard RR, et al. Beneficial effect of operation-day blood-transfusions on human renal-allograft survival. Lancet 1978; i: 169-70. 5. Hunsicker LG, Oei LS, Freeman RM, et al. Transfusion and renal allograft survival. ArchSurg 1980; 115: 737-41. 6. Feduska NJ, Amend WJ, Vincenti F, et al. Blood transfusions before and on the day of transplantation: Effects on cadaver graft survival. Transplant Proc 1982; 14: 4. Stiller
302-04. 7. Williams KA, Ting A, French ME, Oliver D. Peroperative blood-transfusion improves cadaveric renal allograft survival in non-transfused recipients. Lancet 8
1980; i: 1104-06. Opelz G, Terasaki PI. Importance of preoperative (not peroperative) transfusions for cadaver kidney transplants. Transplantation 1981; 31: 106-08.
SiR,—While attempting to repeat Levin’s experiments on red-cell charge measurements in minimal change nephropathyl we observed some methodological problems that cast doubt on the validity of using alcian blue (AB) for this purpose; these difficulties are equally relevant to the experiments of Dr Boulton-Jones and
colleagues (July 26, p 186). We have tested 9 batches of alcian blue supplied variously by BDH, Sigma, ICI, Royal Manchester Children’s Hospital, and Levin’s group. When dissolved at 02 mg/ml in phosphate buffered saline at pH 74 with 25 mmol/I MgCl2 and 2 g/1 glucose (PBS), as done by Levin et al, some of them, including the sample sent by
practitioner, community nurse, and social worker supervision. To provide respite to families or hostels and in the best interests of the patients they are readmitted to hospital when necessary. In hospital they behave remarkably well, to the surprise of the community mental handicap team, the family, and even hospital staff. Patients (and their relatives) often beg to be allowed to stay in hospital. Their hospital stay is not the unhappy recurrence predicted by some organisations. The Department of Health should pause and study the situation before embarking upon a project that would involve great expenditure from public funds and would be detrimental to the long-term interests of mentally handicapped patients. Unit of Mental Handicap,
Brockhall Hospital,
U.
Blackburn BB6 8AZ
J. DEY
THIAZIDE-INDUCED DILUTIONAL HYPONATRAEMIA MASQUERADING AS SUBARACHNOID HAEMORRHAGE
SIR,-Dr Benfield and colleagues (Aug 9,
p 341) report a induced by ’Moducren’ (hydrochlorthiazide 25 mg, amiloride 2-5 mg, timolol 10 mg) masquerading as subarachnoid haemorrhage. We report a similar case in which ’Moduretic’ (amiloride 5 mg, hydrochlorthiazide 50 mg) and later bendrofluazide sequentially induced severe dilutional hyponatraemia mimicking a subarachnoid haemorrhage. We conclude that thiazide diuretics were the agents responsible. An otherwise fit 83-year-old woman was prescribed one moduretic tablet a day for mild congestive cardiac failure. (The following morning her serum sodium was 130 mmol/1.) Over the next 4 days she experienced episodic confusion, but on the fifth day she rapidly deteriorated with headache and vomiting. She was confused and unable to stand. On admission to hospital she was afebrile and drowsy, with generalised muscle weakness, hypertonia, brisk reflexes, and extensor plantar responses; marked neck stiffness and photophobia were elicited. A retinal haemorrhage was present close to the right optic disc. Her blood pressure was 170/110 mm Hg and the pulse was 64/min in sinus rhythm. A subarachnoid haemorrhage was suspected. Her chest X-ray showed slight cardiomegaly and upper lobe venous prominence. Her white cell count was 8-1 x 109/1. She was severely hyponatraemic (112 mmol/1) and her serum potassium was 4-2 mmol/l, urea 7-7 mmol/l, creatinine 95 lunol/1, and sugar 7 mmot/1. Serum osmolality was reduced to 228 mosmol/kg with a urine osmolality of 780 mosmol/kg. A cranial computerised tomographic scan revealed no abnormality. CSF obtained (after a traumatic lumbar puncture) at a low opening pressure contained 12 000 red cells1, no white cells, and no xanthochromia. She was treated by slow infusions of hypertonic saline and fluid restriction to 1 litre per day, and the moduretic was stopped. A rapid clinical and biochemical improvement occurred over the next 72 h and she returned to complete wellbeing. 10 days after her hospital admission her ankles became oedematous and diuretics were reintroduced, bendrofluazide 5 mg daily being prescribed. Within three days her serum sodium had fallen from 134 to 115 mmol/1. She became confused, with a headache and vomiting. The signs of meningism recurred and again there was generalised muscle weakness, hypertonia, brisk reflexes, and extensor plantar responses. Hypertonic saline infusions and fluid restriction were initiated and bendrofluazide was stopped. 72 h later the biochemical picture and her clinical condition were normal. She was discharged on no medication. 2 months later she is well, with normal serum electrolytes, on no treatment. Our case confirms Benfield and colleagues’ view that a dilutional hyponatraemia may masquerade as a subarachnoid haemorrhage. A thiazide diuretic is the common component in these two cases implicating these agents (hydrochlorthiazide and bendrofluazide) as being responsible for the syndromes. case
of dilutional
hyponatraemia
Department of Medicine, Southmead General Hospital, Bristol BS10 5NB
P. G. BAIN W. EGNER P. R. WALKER
MONOCLONAL ANTIBODY TO DETECT PNEUMOCYSTIS CARINII
SiR,—Dr Kovacs and co-workers (July 5, p 1) report the successful use of a monoclonal antibody to detect Pneumocystis carinii in bronchoalveolar lavage (BAL) fluid and. impression smears of infected lung tissue. Since the autumn of 1985 we have investigated 130 lung derived samples by immunofluorescence using monoclonal antibodies to detect this parasite. Most of the impression smears, BAL fluids, and induced sputum samples studied were from suspected AIDS patients at the department of infectious disease, Karolinska Institute. 1/9 biopsy samples, 13/72 BAL fluids, and 3/49 sputum samples were positive. The method is specific, sensitive, and simple. We have identified the target antigen recognised by the monoclonal antibodies as a 82 000 molecular weight parasite component that resists denaturing. The antibodies can be used to detect parasites in variously fixed material, including samples to which 50% ethanol has been added to inactivate human immunodeficiency virus. Brief trypsination of such samples (immersion of the fixed sample for 15 min in 1% trypsin) was included for improved penetration but also for the removal of in vivo bound immunoglobulins. The antibodies also reacted with P carinii in paraffin sections of lung tissue. We have tried to answer some of the questions raised by Kovacs et al. P carinii parasites were easily detectable in induced sputum samples after ’Sputolysin’ (Behring Diagnostics) treatment. Direct labelling of antibodies with fluorescein isothiocyanate gave a useful reagent, but the yield of isolated mouse immunoglobulin from ascites fluid for the production of labelled antibodies needs to be improved. Antigenic variation between P carinii organisms from different individuals does not seem to be a problem. The specific antibodies 2E3 and 3F6 were used in a retrospective study to detect the parasite in paraffin sections of 30 lung biopsy specimens from immunosuppressed children with leukaemia treated at the children’s clinic, University Central Hospital, Helsinki. This study showed agreement between immunofluorescence and conventional histological staining with modified methenamine-silver technique. Our results support the optimism expressed in the study by Kovacs and coworkers about the future use of the immunofluorescence method. Department of Parasitology, National Bacteriological Laboratory, 5-105 21 Stockholm, Sweden
EWERT LINDER KERSTIN ELVIN ANDERS BjORKMAN
Department of Infectious Disease, Karolinska Institute, Roslagstull Hospital,
SUSANNE BERGDAHL LINDA MORFELDT-MANSSON LARS MOBERG ANDERS SONNERBORG
Stockholm
KIDNEY TRANSPLANT REGRAFT RESULTS IMPROVED BY PEROPERATIVE BLOOD TRANSFUSIONS
SiR,-Although cadaver kidney transplant success rates have improved by 12-20% at one year with the introduction of cyclosporin,1,2 second transplants are not so significantly affected.3 We find that transfusions given at the time of transplantation (peroperative) improve retransplant success rates with or without cyclosporin. Such peroperative transfusion did not improve success rates of first grafts, regardless of whether cyclosporin was used or not, as shown in the figure. An 11 % improvement was noted for first grafts at one year with the use of cyclosporin. Peroperative transfusion improved survival by only 1% in non-cyclosporintreated patients and reduced it by 2% in cyclosporin-treated patients. In regrafted patients cyclosporin improved the results by 4% at one year. Peroperative transfusions had a 5% effect in cyclosporin patients and 4% effect in non-cyclosporin patients. Patients who received peroperative transfusions and cyclosporin had significantly higher (p < 0-05) survival rates than those who had no peroperative transfusion and no cyclosporin. Other comparisons
635 RED-CELL SURFACE CHARGE IN GLOMERULAR DISEASE
Effect of peroperative transfusions
on
cadaver donor transplant.
significant. A 6% improvement in survival rate of retransplants with peroperative transfusions was also seen among patients who had received transfusions before transplantation (p<0-05) (figure), as well as those without preoperative transfusions. As in the cyclosporin/non-cyclosporin comparison, though peroperative transfusions had an effect on regrafts they had no effect on primary transplants. Although it was thought that peroperative transfusions may be of benefit to patients receiving primary grafts’-6 or to patients who had never received preoperative transfusions it now seems that transfusions given on the day of transplantation are not of much benefit.8 However, for regrafts, a significant improvement is obtained by peroperative transfusions. It is unlikely that the mechanism of this effect is the same as that of cyclosporin, thus, when used in combination, an additive effect might be obtained. Peroperative transfusions may neutralise antibodies formed by the rejection of the first graft. The effect of peroperative transfusions is mostly within the first few months after transplantation (see figure). Indeed, even first day function is improved from 71-6% (268 patients) to 75-2% (262 patients) by peroperative transfusion. Among sensitised patients receiving first grafts, one-year survival of 68% was noted without peroperative transfusions (744 patients) and 66% with peroperative transfusions (550 patients). Since sensitised first-graft patients do not demonstrate the effect of peroperative transfusions, it is likely that antibodies generated by transfusions differ from those generated by a graft rejection. We conclude that peroperative transfusions are a simple and effective adjunctive treatment for retransplants. Since such regrafts have poor survival rates, even with cyclosporin, treatment with peroperative transfusions may be worth considering. were not
UCLA Tissue Typing Laboratory, University of California Los Angeles, Los Angeles, California, USA
KAZUO TOKUNAGA PAUL I. TERASAKI
SIR,-Electrical charge is a crucial determinant of functional integrity at the glomerular basement membrane; loss of negative charge at this site results in proteinuria in clinical and experimental glomerular disease. Levin and his colleagues1 reported reduced binding of the cationic dye, alcian blue, to red cells of children with minimal change nephrotic syndrome and focal glomerulosclerosis during episodes of heavy proteinuria. Dr Boulton-Jones and colleagues (July 26, p 186) used the same technique to study red-cell charge of patients whose glomerular disease is quiescent in order to investigate disease susceptibility. To confirm a relation between red-cell surface charge and proteinuria we have measured alcian blue (AB) binding to red cells1 in 14 healthy controls, in 16 patients with end-stage renal failure without heavy proteinuria, and in 16 patients with nephrotic syndrome (urine protein > 3 g/24 h, serum creatinine < 300 pmol/1). The causes of the nephrotic syndrome were: membranous nephropathy (6), diabetic nephropathy (3), mesangiocapillary glomerulonephritis (2), lupus nephritis (2), and 1 each with focal glomerulosclerosis, amyloidosis, and minimal change nephrotic syndrome. AB binding did not fall outside the control range in any patient with nephrotic syndrome but was modestly diminished in patients with uraemia:
*p < 0 05 (unpaired t test) when compared with controls. No correlation was found between AB binding and age, serum albumin, urine protein excretion, or glycosylated haemoglobin concentration. Our 6 patients with membranous nephropathy did not have a lower mean AB binding, as was reported by BoultonJones and colleagues for patients with the same disease in remission. We studied sequentially AB binding in 1 child with minimal change nephrotic syndrome-AB binding was normal when the patient was in relapse (before treatment) and remained the same a week later, when proteinuria had resolved in response to corticosteroids. Our preliminary findings suggest that red-cell charge may be somewhat reduced in severe uraemia, so renal function ought to be defined in any study of red-cell charge in nephrotic syndrome. More importantly, our study does not confirm any relation between red-cell charge and proteinuria in patients with nephrotic syndrome due to a spectrum of glomerular diseases. In the nephrotic child investigated sequentially we could not confirm the reported red-cell charge abnormality in relapse! or any alteration in red-cell charge when proteinuria was abolished by corticosteroids. Thus, we have found no evidence that red-cell charge measurements reliably mirror the glomerular capillary wall charge; another more specific method is required.
Departments of Medicine and Nephrology, Leicester General Hospital, Leicester LE5 4PW
J. FEEHALLY A. SAMANTA H. KINGHORN A. C. BURDEN J. WALLS
M, Smith C, Walters MDS, Gascoine P, Barratt TM. Steroid-responsive nephrotic syndrome: a generalised disorder of membrane negative charge. Lancet 1985; ii: 239-42.
1. Levin
1. Calne RY, Wood AJ. Cyclosporin in cadaveric renal transplantation: 3-year follow-up of a European multicentre trial. Lancet 1985; ii: 549. 2. Opelz G. Correlation of HLA matching with kidney graft survival in patients with or without cyclosporine treatment. Transplantation 1985; 40: 240-43. 3. Terasaki PI, et al. Patients’ graft and functional survival rates: an overview. In: Terasaki PI, ed. Clinical kidney transplant 1985. UCLA Tissue Typing
Laboratory, Los Angeles, 1985: 1-26. CR, Sinclair NR, Sheppard RR, et al. Beneficial effect of operation-day blood-transfusions on human renal-allograft survival. Lancet 1978; i: 169-70. 5. Hunsicker LG, Oei LS, Freeman RM, et al. Transfusion and renal allograft survival. ArchSurg 1980; 115: 737-41. 6. Feduska NJ, Amend WJ, Vincenti F, et al. Blood transfusions before and on the day of transplantation: Effects on cadaver graft survival. Transplant Proc 1982; 14: 4. Stiller
302-04. 7. Williams KA, Ting A, French ME, Oliver D. Peroperative blood-transfusion improves cadaveric renal allograft survival in non-transfused recipients. Lancet 8
1980; i: 1104-06. Opelz G, Terasaki PI. Importance of preoperative (not peroperative) transfusions for cadaver kidney transplants. Transplantation 1981; 31: 106-08.
SiR,—While attempting to repeat Levin’s experiments on red-cell charge measurements in minimal change nephropathyl we observed some methodological problems that cast doubt on the validity of using alcian blue (AB) for this purpose; these difficulties are equally relevant to the experiments of Dr Boulton-Jones and
colleagues (July 26, p 186). We have tested 9 batches of alcian blue supplied variously by BDH, Sigma, ICI, Royal Manchester Children’s Hospital, and Levin’s group. When dissolved at 02 mg/ml in phosphate buffered saline at pH 74 with 25 mmol/I MgCl2 and 2 g/1 glucose (PBS), as done by Levin et al, some of them, including the sample sent by