- Email: [email protected]
DIABETES WITH KIDNEY FAILURE
1285
compared with 0-008 in a conventionally treated group.’ This rate in patients is similar to rates reported in other studies in comparison was made with conventional treatmentnamely 0’15,8 024,9 and 0-1210 episodes per patient per year. In subsequent years the rate of ketoacidosis in our CSII-treated patients fell, once the potential problem had been recognised and patients had been warned about ketoacidosis and re-educated in self-management at times of deteriorating blood glucose control.6 This reduction of ketoacidosis with increased experience of CSII is similar to that reported by Bending et al:l during the first years of experience of CSII the rate was 6 episodes per patient per year, falling to zero in 1984. Any "reassurance" drawn from studies showing that ketoacidosis rates in patients on CSII and in those on conventional treatment do the CSII which no
differ should be viewed with caution because these studies were done at centres with considerable experience of CSII and the lower rates of ketoacidosis emerged as physicians and patients gained experience of the treatment. In the report by Teutsch et all’ of deaths during CSII treatment 4 of 7 deaths attributed to ketoacidosis were in patients with less than 6 months’ experience of CSII. Physicians contemplating the use of CSII need to realise that the increased risk of ketoacidosis is greater during CSII than with conventional injection treatment, and they should pay special attention to patient selection and patient education.
difference between the groups for rates of ketoacidosis at 12 months. The high rate of ketoacidosis reported by the Kroc study was confined to two centres. Plasma hypertonicity influences transcellular potassium fluxes in both diabetics and non-diabetics.5 Plasma hypertonicity causes cellular dehydration, increased intracellular potassium concentrations, and increased outward passive potassium diffusion but there is no evidence that intracellular protein breakdown, insulin deficiency, or metabolic acidosis are important prerequisites.ED. L. no
1. Launtzen
2.
not
G. KNIGHT J. D. WARD
Royal Hallamshire Hospital, Sheffield S10 2JF
1. Bending JJ, Pickup JC, Keen H. Frequency of diabetic ketoacidosis and hypoglycemic coma during treatment with continuous subcutaneous insulin infusion. Am J Med 1985; 79: 685-91. 2. Sonnenberg GE, Muhlhauser I, Chantelau E, Berger M. Incidence of ketoacidosis and severe hypoglycemia in conventionally and CSII treated type I diabetic patients. Diabetes 1985; 34 (suppl 1): 117A. 3. Kroc Collaborative Study Group. Blood glucose control and the evolution of diabetic 1984; 311: 365-72. retinopathy and albuminuria. N Engl Med J 4. Pickup JC, Sherwin RS, Tamborlane WV, Rizza RA, Service F for the Kroc Collaborative Study Group. The pump life: Patient responses and clinical and technological problems. Diabetes 1985; 34 (suppl 3): 37-40. 5. Kashiwagi S, Wiefels K, Schleppinghof B, Gries FA, and DFI Group. Risk-benefit analysis of strict metabolic control in diabetics—the Dusseldorf prospective study. Diabetes Res Clin Pract 1985; 1 (suppl 1)· 5289. 6. Knight G, Boulton AJM, Drury J, et al. A feasibility study of the use of continuous subcutaneous insulin infusion m a diabetic clinic: patients’ choice of treatment. Diabetic Med 1984; 1: 267-72.
Knight G, Jennings AM, Boulton AJM, Tomlinson S, Ward JD. Severe hyperkalaemia and ketoacidosis during routine treatment with an insulin pump. Br Med J 1985; 291: 371-72. 8. Mecklenburg RS, Benson EA, Benson JW, et al. Acute complications associated with insulin infusion pump therapy. JAMA 1984; 252: 3265-69. 9. Peden NR, Braaten JT, McKendry JBR. Diabetic ketoacidosis during long term 7.
treatment
with continuous subcutaneous insulin infusion. Diabetes Care 1984; 7:
1-5. 10.
Irsigler K, Kritz H, Najemnik C, Fleissner M, Hagmueller G. Long-term treatment with external and implanted insulin infusion devices. Diabetes 1984; 33 (suppl 1):
73A. 11. Teutsch
SM, Herman WH, Dwyer DM, Lane JM. Mortality among diabetic patients using continuous subcutaneous insulin-infusion pumps. N Engl J Med 1984; 310: 361-68.
SIR,-Your editorial (Oct 11,
p
854)
seems
to
contain
a
fundamental misconception-namely, the view that potassium can be abstracted from cells by osmotic forces. That can only happen if the cell
proteins
are
being catabolised, which,
of course, is the
situation in insulin deficiency. Most of the potassium and sodium ions within a cell are bound to proteins, or are otherwise sequestered in the cytosol.1 E. N. WARDLE
Ling GN, Ochsenfeld MM. Sodium and potassium levels in living cells: do they depend on the outward transport of potassium? Physiol Chem Phys 1976; 8: 389-96.
* In
the
prospective study cited by Dr Knight
and Dr
Ward,
patients were not randomly allocated to CSIII or CIT. At least three other
investigationsi-3 with
4.
5.
DIABETES WITH KIDNEY FAILURE
SIR,-Professor Cameron and Dr Challah (Oct 25, p 962) review experience in treating uraemic diabetics in the UK in 1975-84 and note that in 1983-84 76% of newly accepted patients were type I. Continuous ambulatory peritoneal dialysis was the most popular long-term treatment (48 % of 446 under treatment at Dec 31,1984). The number of type I patients will be overestimated because the UK registry during the-years surveyed did not distinguish between a true insulin dependent diabetic (type I) and a type II patient treated with insulin by physician choice. We have studied this in our patients under treatment in fourteen dialysis centres, where 87 of 139 (62-6%) patients who are clearly type II diabetics have been or with insulin.1 From across the Atlantic, it seems that grave problems still exist in the British approach to uraemia therapy for the diabetic. Most diabetics with kidney failure in the United States are older type IIs-in Brooklyn, where type I patients constitute only 16-5% of diabetics undergoing maintenance haemodialysis, the mean age of 232 diabetics on dialysis on March 10, 1986, was 59-6years. The type II major patient subset appears to be excluded in the UK, a conclusion inferred from the lower mean age of 45years in treated patients reported by Cameron and Challah. In terms of survival and rehabilitation peritoneal dialysis and haemodialysis-the prevalent therapies in the UK- are inferior to transplantation.2 Although a rising proportion of uraemic patients accepted for treatment in the UK is diabetic (11’% in 1984, contrasting with 26 % in the USA) it is a sad reality that in the UK more than 50% of diabetics with kidney failure die without treatment. are on treatment
Renal Diseases Division, Department of Medicine, SUNY Health Science Center, Brooklyn, NY 11203, USA 1. Lowder
GM, Pern NA, Thiruvengadam tation and diabetes type in diabetics
ELI A. FRIEDMAN T,
Friedman EA
on maintenance
Employment, rehabilihemodialysis American
Society of Nephrology (abstr) (in press). EA, Peterson CM, eds. Diabetic nephropathy. Boston: Nijhoff,
2 Friedman
1986
TRIMETHOPRIM RESISTANCE
King Saud College of Medicine, Abha, Saudi Arabia 1.
3.
T, Frost-Larson K, Larson H-W, et al. Effect of 1 year of near-normal blood glucose levels on retinopathy in insulin-dependent diabetics. Lancet 1983; i: 200-04. Dahl-Jørgensen K, Brinchmann-Hansen O, Hansen KF, et al. Effect of nearnormoglycaemia for two years on progression of early diabetic retinopathy, nephropathy and neuropathy: the Oslo study Br Med J 1986; 293: 1195-99 Coustan DR, Reece A, Sherwin RS, et al. A randomised trial of the insulin pump vs intensive conventional therapy in diabetic pregnancies. JAMA 1986; 255: 631-36 DCCT Research Group. Results of feasibility phase of the Diabetes Control and Complications Trial (DCCT): glycemic control, follow-up and complications of therapy. Diabetes 1986; 35 (suppl 1): 3A. Moreno M, Murphy C, Goldsmith C. Increase in serum potassium resulting from the administration of hypertonic mannitol and other solutions. J Lab Clin Med 1969; 73: 291-98.
random
allocation
revealed
no
difference or a lower frequency of ketoacidisis on CSII versus CIT. In the feasibility phase of the Diabetes Control and Complications
Trial,4 in which 278 diabetics were randomly assigned to standard therapy or an intensified regimen which included CSII, there was
SIR,-Your Oct 4 editorial states that "the overall level of trimethoprim usage will have the greatest influence in the future on the incidence of trimethoprim resistance". The use of antibiotics does indeed cause resistance! but you do not answer the questionHow widely should trimethoprim be used? Trimethoprim resistance has been spread whether trimethoprim is used alone or in combination.2-4 If use of trimethoprim, alone or in combination, is concentrated in hospitals, especially geriatric hospitals, the spread of resistance is more than probable.4 We have seen this clearly in a geriatric hospital with annual consumption of trimethoprim of 5-10 g per bed. However, in outpatients the
compared with 0-008 in a conventionally treated group.’ This rate in patients is similar to rates reported in other studies in comparison was made with conventional treatmentnamely 0’15,8 024,9 and 0-1210 episodes per patient per year. In subsequent years the rate of ketoacidosis in our CSII-treated patients fell, once the potential problem had been recognised and patients had been warned about ketoacidosis and re-educated in self-management at times of deteriorating blood glucose control.6 This reduction of ketoacidosis with increased experience of CSII is similar to that reported by Bending et al:l during the first years of experience of CSII the rate was 6 episodes per patient per year, falling to zero in 1984. Any "reassurance" drawn from studies showing that ketoacidosis rates in patients on CSII and in those on conventional treatment do the CSII which no
differ should be viewed with caution because these studies were done at centres with considerable experience of CSII and the lower rates of ketoacidosis emerged as physicians and patients gained experience of the treatment. In the report by Teutsch et all’ of deaths during CSII treatment 4 of 7 deaths attributed to ketoacidosis were in patients with less than 6 months’ experience of CSII. Physicians contemplating the use of CSII need to realise that the increased risk of ketoacidosis is greater during CSII than with conventional injection treatment, and they should pay special attention to patient selection and patient education.
difference between the groups for rates of ketoacidosis at 12 months. The high rate of ketoacidosis reported by the Kroc study was confined to two centres. Plasma hypertonicity influences transcellular potassium fluxes in both diabetics and non-diabetics.5 Plasma hypertonicity causes cellular dehydration, increased intracellular potassium concentrations, and increased outward passive potassium diffusion but there is no evidence that intracellular protein breakdown, insulin deficiency, or metabolic acidosis are important prerequisites.ED. L. no
1. Launtzen
2.
not
G. KNIGHT J. D. WARD
Royal Hallamshire Hospital, Sheffield S10 2JF
1. Bending JJ, Pickup JC, Keen H. Frequency of diabetic ketoacidosis and hypoglycemic coma during treatment with continuous subcutaneous insulin infusion. Am J Med 1985; 79: 685-91. 2. Sonnenberg GE, Muhlhauser I, Chantelau E, Berger M. Incidence of ketoacidosis and severe hypoglycemia in conventionally and CSII treated type I diabetic patients. Diabetes 1985; 34 (suppl 1): 117A. 3. Kroc Collaborative Study Group. Blood glucose control and the evolution of diabetic 1984; 311: 365-72. retinopathy and albuminuria. N Engl Med J 4. Pickup JC, Sherwin RS, Tamborlane WV, Rizza RA, Service F for the Kroc Collaborative Study Group. The pump life: Patient responses and clinical and technological problems. Diabetes 1985; 34 (suppl 3): 37-40. 5. Kashiwagi S, Wiefels K, Schleppinghof B, Gries FA, and DFI Group. Risk-benefit analysis of strict metabolic control in diabetics—the Dusseldorf prospective study. Diabetes Res Clin Pract 1985; 1 (suppl 1)· 5289. 6. Knight G, Boulton AJM, Drury J, et al. A feasibility study of the use of continuous subcutaneous insulin infusion m a diabetic clinic: patients’ choice of treatment. Diabetic Med 1984; 1: 267-72.
Knight G, Jennings AM, Boulton AJM, Tomlinson S, Ward JD. Severe hyperkalaemia and ketoacidosis during routine treatment with an insulin pump. Br Med J 1985; 291: 371-72. 8. Mecklenburg RS, Benson EA, Benson JW, et al. Acute complications associated with insulin infusion pump therapy. JAMA 1984; 252: 3265-69. 9. Peden NR, Braaten JT, McKendry JBR. Diabetic ketoacidosis during long term 7.
treatment
with continuous subcutaneous insulin infusion. Diabetes Care 1984; 7:
1-5. 10.
Irsigler K, Kritz H, Najemnik C, Fleissner M, Hagmueller G. Long-term treatment with external and implanted insulin infusion devices. Diabetes 1984; 33 (suppl 1):
73A. 11. Teutsch
SM, Herman WH, Dwyer DM, Lane JM. Mortality among diabetic patients using continuous subcutaneous insulin-infusion pumps. N Engl J Med 1984; 310: 361-68.
SIR,-Your editorial (Oct 11,
p
854)
seems
to
contain
a
fundamental misconception-namely, the view that potassium can be abstracted from cells by osmotic forces. That can only happen if the cell
proteins
are
being catabolised, which,
of course, is the
situation in insulin deficiency. Most of the potassium and sodium ions within a cell are bound to proteins, or are otherwise sequestered in the cytosol.1 E. N. WARDLE
Ling GN, Ochsenfeld MM. Sodium and potassium levels in living cells: do they depend on the outward transport of potassium? Physiol Chem Phys 1976; 8: 389-96.
* In
the
prospective study cited by Dr Knight
and Dr
Ward,
patients were not randomly allocated to CSIII or CIT. At least three other
investigationsi-3 with
4.
5.
DIABETES WITH KIDNEY FAILURE
SIR,-Professor Cameron and Dr Challah (Oct 25, p 962) review experience in treating uraemic diabetics in the UK in 1975-84 and note that in 1983-84 76% of newly accepted patients were type I. Continuous ambulatory peritoneal dialysis was the most popular long-term treatment (48 % of 446 under treatment at Dec 31,1984). The number of type I patients will be overestimated because the UK registry during the-years surveyed did not distinguish between a true insulin dependent diabetic (type I) and a type II patient treated with insulin by physician choice. We have studied this in our patients under treatment in fourteen dialysis centres, where 87 of 139 (62-6%) patients who are clearly type II diabetics have been or with insulin.1 From across the Atlantic, it seems that grave problems still exist in the British approach to uraemia therapy for the diabetic. Most diabetics with kidney failure in the United States are older type IIs-in Brooklyn, where type I patients constitute only 16-5% of diabetics undergoing maintenance haemodialysis, the mean age of 232 diabetics on dialysis on March 10, 1986, was 59-6years. The type II major patient subset appears to be excluded in the UK, a conclusion inferred from the lower mean age of 45years in treated patients reported by Cameron and Challah. In terms of survival and rehabilitation peritoneal dialysis and haemodialysis-the prevalent therapies in the UK- are inferior to transplantation.2 Although a rising proportion of uraemic patients accepted for treatment in the UK is diabetic (11’% in 1984, contrasting with 26 % in the USA) it is a sad reality that in the UK more than 50% of diabetics with kidney failure die without treatment. are on treatment
Renal Diseases Division, Department of Medicine, SUNY Health Science Center, Brooklyn, NY 11203, USA 1. Lowder
GM, Pern NA, Thiruvengadam tation and diabetes type in diabetics
ELI A. FRIEDMAN T,
Friedman EA
on maintenance
Employment, rehabilihemodialysis American
Society of Nephrology (abstr) (in press). EA, Peterson CM, eds. Diabetic nephropathy. Boston: Nijhoff,
2 Friedman
1986
TRIMETHOPRIM RESISTANCE
King Saud College of Medicine, Abha, Saudi Arabia 1.
3.
T, Frost-Larson K, Larson H-W, et al. Effect of 1 year of near-normal blood glucose levels on retinopathy in insulin-dependent diabetics. Lancet 1983; i: 200-04. Dahl-Jørgensen K, Brinchmann-Hansen O, Hansen KF, et al. Effect of nearnormoglycaemia for two years on progression of early diabetic retinopathy, nephropathy and neuropathy: the Oslo study Br Med J 1986; 293: 1195-99 Coustan DR, Reece A, Sherwin RS, et al. A randomised trial of the insulin pump vs intensive conventional therapy in diabetic pregnancies. JAMA 1986; 255: 631-36 DCCT Research Group. Results of feasibility phase of the Diabetes Control and Complications Trial (DCCT): glycemic control, follow-up and complications of therapy. Diabetes 1986; 35 (suppl 1): 3A. Moreno M, Murphy C, Goldsmith C. Increase in serum potassium resulting from the administration of hypertonic mannitol and other solutions. J Lab Clin Med 1969; 73: 291-98.
random
allocation
revealed
no
difference or a lower frequency of ketoacidisis on CSII versus CIT. In the feasibility phase of the Diabetes Control and Complications
Trial,4 in which 278 diabetics were randomly assigned to standard therapy or an intensified regimen which included CSII, there was
SIR,-Your Oct 4 editorial states that "the overall level of trimethoprim usage will have the greatest influence in the future on the incidence of trimethoprim resistance". The use of antibiotics does indeed cause resistance! but you do not answer the questionHow widely should trimethoprim be used? Trimethoprim resistance has been spread whether trimethoprim is used alone or in combination.2-4 If use of trimethoprim, alone or in combination, is concentrated in hospitals, especially geriatric hospitals, the spread of resistance is more than probable.4 We have seen this clearly in a geriatric hospital with annual consumption of trimethoprim of 5-10 g per bed. However, in outpatients the