- Email: [email protected]
URINARY ACIDIFICATION DEFECT IN CHRONIC INFANTILE MALNUTRITION
764 The
day after admission
to
hospital
there
appeared
on
his
nose, and in a band about 10 cm. wide round the base of his
21% lymphocytes, 3% monocytes, 1% eosinophils, and 2% Turk cells). His chest radiograph was normal.
neck and upper chest, multiple (almost confluent) lesions about 3 mm. in diameter. These were either umbilicated varioliform pustules, or tiny red shallow punched-out pits exuding serum. These more characteristic lesions enabled the diagnosis of eczema herpeticum to be made. Gamma-globulin 1-5 g. was given intramuscularly. 2 days later most of the lesions had dried, and the seropurulent crusts readily dropped off his face and neck. The facial oedema and general toxicity were diminished, though his evening temperature was 101OF, and he was still very ill. He was anxious to return with his holiday group to Germany, and next day we reluctantly allowed him to leave hospital and to travel. By then he was apyrexial, and his skin condition was improving rapidly. After discharge he made an uninterrupted recovery, and he was able to resume his studies two weeks later.
Conclusions The outstanding features of this case were the rapid onset and severe general toxicity which accompanied the eruption. The diagnosis was obscure at first because of the confluent exudative lesions and the infection. But next day the characteristic weeping varioliform lesions, associated with oedema and secondary pyogenic infection, and with regional adenitis, was in keeping with Kaposi’s (1887) classical description. Isolation of the herpessimplex virus by culture confirmed the diagnosis. It is of interest that there were no untoward effects of his premature discharge from hospital only four days later.
Investigations
patient
Swabs from the lesions grew coagulase-positive Staphyloaureus, and Lancefield group-A haemolytic streptococci; virus culture on chick embryo grew the herpes-simplex virus. The white-cell count was 9700 per c.mm. (73% polymorphs,
Brain, R. T. (1956) Brit. med. J. i, 1061. Kaposi, M. (1887) Vjschr. Derm. Syph., Wien, 14, 273. Ruchman, I., Welsh, A. L., Dodd, K. (1947) Arch. Derm. Syph, Chicago, 56,
coccus
Preliminary Communication URINARY ACIDIFICATION DEFECT IN CHRONIC INFANTILE MALNUTRITION THE ability of the kidney to lower the urinary pH after an acidifying stimulus depends on the maintenance of a hydrogen-ion (H ) gradient across the renal tubular cell, and requires intact cellular mechanisms. It is characteristic of potassium deficiency that this gradient cannot be maintained.’1 In view of the known intracellular disturbances in severe chronic malnutrition in infants,2 it was thought likely that some acidification defect might be demonstrable. In 7 malnourished children, ammonium chloride was given orally (in a dose of 0-1 g. per kg. body-weight)3 immediately on admission and again after recovery. The MINIMAL URINARY
pH
AFTER AMMONIUM CHLORIDE
WEIGHT) IN SEVEN
MALNOURISHED
(0-1G.
KG. BODY-
CHILDREN
to thank Dr. R. T. Brain, under whose care the admitted, for his advice and help in preparing this paper.
I should like was
REFERENCES
846.
adults.5 When a standard acid load is given, the lowest pH reached by the urine is a measure of the efficiency of this function, and is largely independent of factors such as glomerular filtration-rate and renal plasmaflow which are said to be altered in chronic infantile malnutrition.6 The
supply of H appears to depend on the availability of CO2 produced by the kidney 7: theoretically it could be limited either by a reduction in substrate, CO2, or by a depression of intracellular carbonic anhvdrase.
Assuming accompanying table shows that
on admission this dose did not make the urine as acid as it did later. In other malnourished children, ammonium chloride was given at various stages during recovery, and its administration was preceded by a muscle biopsy. The relation between the muscle-potassium content, expressed as Eq. K per mg. deoxynucleic acid phosphate (D.N.A.P), and the lowest urinary pH is shown graphically in 20 observations. D.N.A.P. is used as the most reliable standard of reference.4 The correlation is highly significant
(p==0-001). DISCUSSION
The
factor, it
production of H is not the limiting probable that the failure to concentrate due to potassium deficiency (see was
that the
seems
available H
figure). clear whether this renal functional disturbance plays any part in the acid-base balance in these children. In the absence of severe diarrhoea, systemic acidosis does not occur; nor would it be expected as a consequence of inability to excrete a urine of low pH, unless ammonium excretion was also impaired. It is
not
I am indebted to Dr. Oliver Wrong, who suggested this investigation when he visited the West Indies with the support of the Colonial Medical Research Committee, and to Dr. John Waterlow for his advice and encouragement.
ability to concentrate Hion is a tubular function probably as well developed in infants as in
Medical Research Council Tropical Metabolism Research Unit, University College of the West Indies, Jamaica
which is
Clarke, E., Evans, B. M., MacIntyre, I., Milne, M. D. Clin. Sci. 1955, 14, 421. 2. Frenk, S., Metcoff, J., Gomez, F., Ramos-Galvan, R., Cravioto, J., Antonowicz, I. Pediatrics, Springfield, 1957, 20, 101. 3. Davies, H. E. F., Wrong, O. Lancet, 1957, ii, 625. 4. Waterlow, J. C., Mendes, C. B. Nature, Lond. 1957, 180, 1361.
between potassium content of muscle, expressed as IlEq. Klmg. D.N.A.P., and minimal urinary pH after administration of ammonium chloride.
Relationship
1.
ROGER SMITH B.A., M.B. Cantab.
McCance, R. A., von Finck, M. A. Arch. Dis. Childh. 1947, 22, 200. Gordillo, G., Soto, R. A., Metcoff, J., Lopez, E., Antillon, L. G. Pediatrics, Springfield, 1957, 20, 303. 7. Roberts, K. E., Poppell, J. W., Randall, H. T. Fed. Proc. 1956, 15, 153. 5. 6.
day after admission
to
hospital
there
appeared
on
his
nose, and in a band about 10 cm. wide round the base of his
21% lymphocytes, 3% monocytes, 1% eosinophils, and 2% Turk cells). His chest radiograph was normal.
neck and upper chest, multiple (almost confluent) lesions about 3 mm. in diameter. These were either umbilicated varioliform pustules, or tiny red shallow punched-out pits exuding serum. These more characteristic lesions enabled the diagnosis of eczema herpeticum to be made. Gamma-globulin 1-5 g. was given intramuscularly. 2 days later most of the lesions had dried, and the seropurulent crusts readily dropped off his face and neck. The facial oedema and general toxicity were diminished, though his evening temperature was 101OF, and he was still very ill. He was anxious to return with his holiday group to Germany, and next day we reluctantly allowed him to leave hospital and to travel. By then he was apyrexial, and his skin condition was improving rapidly. After discharge he made an uninterrupted recovery, and he was able to resume his studies two weeks later.
Conclusions The outstanding features of this case were the rapid onset and severe general toxicity which accompanied the eruption. The diagnosis was obscure at first because of the confluent exudative lesions and the infection. But next day the characteristic weeping varioliform lesions, associated with oedema and secondary pyogenic infection, and with regional adenitis, was in keeping with Kaposi’s (1887) classical description. Isolation of the herpessimplex virus by culture confirmed the diagnosis. It is of interest that there were no untoward effects of his premature discharge from hospital only four days later.
Investigations
patient
Swabs from the lesions grew coagulase-positive Staphyloaureus, and Lancefield group-A haemolytic streptococci; virus culture on chick embryo grew the herpes-simplex virus. The white-cell count was 9700 per c.mm. (73% polymorphs,
Brain, R. T. (1956) Brit. med. J. i, 1061. Kaposi, M. (1887) Vjschr. Derm. Syph., Wien, 14, 273. Ruchman, I., Welsh, A. L., Dodd, K. (1947) Arch. Derm. Syph, Chicago, 56,
coccus
Preliminary Communication URINARY ACIDIFICATION DEFECT IN CHRONIC INFANTILE MALNUTRITION THE ability of the kidney to lower the urinary pH after an acidifying stimulus depends on the maintenance of a hydrogen-ion (H ) gradient across the renal tubular cell, and requires intact cellular mechanisms. It is characteristic of potassium deficiency that this gradient cannot be maintained.’1 In view of the known intracellular disturbances in severe chronic malnutrition in infants,2 it was thought likely that some acidification defect might be demonstrable. In 7 malnourished children, ammonium chloride was given orally (in a dose of 0-1 g. per kg. body-weight)3 immediately on admission and again after recovery. The MINIMAL URINARY
pH
AFTER AMMONIUM CHLORIDE
WEIGHT) IN SEVEN
MALNOURISHED
(0-1G.
KG. BODY-
CHILDREN
to thank Dr. R. T. Brain, under whose care the admitted, for his advice and help in preparing this paper.
I should like was
REFERENCES
846.
adults.5 When a standard acid load is given, the lowest pH reached by the urine is a measure of the efficiency of this function, and is largely independent of factors such as glomerular filtration-rate and renal plasmaflow which are said to be altered in chronic infantile malnutrition.6 The
supply of H appears to depend on the availability of CO2 produced by the kidney 7: theoretically it could be limited either by a reduction in substrate, CO2, or by a depression of intracellular carbonic anhvdrase.
Assuming accompanying table shows that
on admission this dose did not make the urine as acid as it did later. In other malnourished children, ammonium chloride was given at various stages during recovery, and its administration was preceded by a muscle biopsy. The relation between the muscle-potassium content, expressed as Eq. K per mg. deoxynucleic acid phosphate (D.N.A.P), and the lowest urinary pH is shown graphically in 20 observations. D.N.A.P. is used as the most reliable standard of reference.4 The correlation is highly significant
(p==0-001). DISCUSSION
The
factor, it
production of H is not the limiting probable that the failure to concentrate due to potassium deficiency (see was
that the
seems
available H
figure). clear whether this renal functional disturbance plays any part in the acid-base balance in these children. In the absence of severe diarrhoea, systemic acidosis does not occur; nor would it be expected as a consequence of inability to excrete a urine of low pH, unless ammonium excretion was also impaired. It is
not
I am indebted to Dr. Oliver Wrong, who suggested this investigation when he visited the West Indies with the support of the Colonial Medical Research Committee, and to Dr. John Waterlow for his advice and encouragement.
ability to concentrate Hion is a tubular function probably as well developed in infants as in
Medical Research Council Tropical Metabolism Research Unit, University College of the West Indies, Jamaica
which is
Clarke, E., Evans, B. M., MacIntyre, I., Milne, M. D. Clin. Sci. 1955, 14, 421. 2. Frenk, S., Metcoff, J., Gomez, F., Ramos-Galvan, R., Cravioto, J., Antonowicz, I. Pediatrics, Springfield, 1957, 20, 101. 3. Davies, H. E. F., Wrong, O. Lancet, 1957, ii, 625. 4. Waterlow, J. C., Mendes, C. B. Nature, Lond. 1957, 180, 1361.
between potassium content of muscle, expressed as IlEq. Klmg. D.N.A.P., and minimal urinary pH after administration of ammonium chloride.
Relationship
1.
ROGER SMITH B.A., M.B. Cantab.
McCance, R. A., von Finck, M. A. Arch. Dis. Childh. 1947, 22, 200. Gordillo, G., Soto, R. A., Metcoff, J., Lopez, E., Antillon, L. G. Pediatrics, Springfield, 1957, 20, 303. 7. Roberts, K. E., Poppell, J. W., Randall, H. T. Fed. Proc. 1956, 15, 153. 5. 6.