The Journal of Pediatrics Editorial correspondence 8 3 3 Volume 122, Number 5, Part 1

Magnesium deficiency in primary distal tubular acidosis

To the Editor: We read with interest the excellent report on primary distal tu-

bular acidosis by Caldas et al. l We reevaluated the histories of five girls and four boys with primary distal tubular acidosis recognized at our institutions between 1970 and 1991. Distal tubular acidosis was defined by (1) persistent metabolic acidosis and plasma bicar- bonate level <17.0 mmol/L, (2) an inability to lower urinary pH to <5.50 or to increase ammonium excretion during severe acido- sis, and (3) normal glomerular filtration rate. Nephrocalcinosis or nephrolithiasis was demonstrated in six children when they were first examined but developed later in all patients. We found deaf- ness in two patients (from two families). Renal magnesium deficiency, 2 defined as (1) molar urinary magnesium/creatinine ratio >0.15 in the presence (2) of persistent hypomagnesemia (plasma magnesium level <0.75mmol/L), was recognized in four patients (from three families) with severe nephrocalcinosis (renal insufficiency developed in two of them). Metabolic acidosis may enhance urinary magnesium excretion. 1"3 In our patients with both magnesium deficiency and distal tubular acidosis, however, mag- nesium wasting persisted after correction of the metabolic acido- sis, indicating a tendency toward magnesium wasting determined by the tubulopathy itself.

Deafness and magnesium deficiency never occurred concomi- tantly in the same patient or in the same family. Furthermore, nor- mal and pathologic renal magnesium handling never occurred in two or more patients from the same family. These findings indicate the existence of at least three variants of primary distal tubular ac- idosis: (1) classic primary distal tubular acidosis, or Albright dis- ease, (2) primary distal tubular acidosis associated with deafness, and (3) primary distal tubular acidosis associated with magnesium deficiency (for this variant the eponym Michelis-Castrillo syn- drome has been suggestedh).

In primary distal tubular acidosis, nephrolithiasis and nephro- calcinosis are considered to result from prolonged hypercalciuria and hypocitraturia. However, magnesium deficiency might further aggravate the tendency. We advise alkali therapy with magnesium citrate in primary distal tubular acidosis associated with magne- sium deficiency. 2

hlario G. Bianchetti, hID Oskar H. Oetliker, MD

University Children's Hospital Inselspital

CH-3010 Berne, Switzerland

J~rg Li'~tschg, MD Children's Hospital

Bruderholzspital CH-4101 Bruderholz, Switzerland

9/35/44799

R E F E R E N C E S

1. Caldas A, Broyer M, Dechaux M, KIeinknecht C. Primary di- stal tubular acidosis in childhood: clinical study and long-term follow-up of 28 patients. J PEDIATR 1992;121:233-41.

2. Kanaka C, Pliiss CR, Oetliker OH, Bianchetti MG. Magne- sium handling in children with primary abnormalities of hydrogen ion homeostasis. J Nephrol 1991;4:257-61.

3. Rodriguez-Soriano J ,Va l lo A, Garcia-Fuentes M. Hypo- magnesemia of hereditary renal origin. Pediatr Nephrol 1987;1:465-72.

Intravenously administered immune globulin for Rh hemolytic disease

To tke Editor: Ri.ibo et al. (J PEDIATR 1992;121:93-7) found high-dose intrave-

nous immune globulin therapy to be effective in reducing the fre- quency of exchange transfusion in Rh hemolytic disease. This non- invasive treatment modality appears promising, hut the authors left certain aspects unclarified. The distribution of preterm infants among the two groups is not mentioned; certain inferences can be falsely drawn if the control group had more preterm infants. First, serum bilirubin values are higher in preterm infants, but exchange transfusions are indicated in them at bilirubin values much lower than in term infants, l Second, preterm infants have very low levels of serum IgG at birth. 2 In vitro studies have shown that native IgG does inhibit hemolysis in Rh isoimmunization ~ and that such an inhibition is possible in vivo in term infants because of their higher serum natural lgG levels. Thus some of the observed benefits of high-dose intravenous immune globulin could be due to these fac- tors, if there were more term infants in the treatment group and more preterm infants in the control group. Demonstrating a corre- lation between serum total IgG values and serum bilirubin values would have been ideal to prove the efficacy of high-dose intravenous immune globulin therapy in preventing hemolysis. Finally, because the investigators were not blinded, were they overzealous in insti- tuting exchange transfusion in the control group? The decisions apparently were based on a single bilirubin value?

Raghavendra Rao, hiD Subrata Sarkar, hID, DM

Anil Narang. hID Neonatal Unit, Department o f Pediatrics

Postgraduate Institute Medical Education and Research

Chandigarh 160 012, India 9[35[45254

REFERENCES

1. Cloherty JP. Neonatal hyperbilirubinemia. In: Cloherty JP, Stark AR, eds. Manual of neonatal care. 3rd ed. Boston: Lit- fie, Brown, 1992:298-334.

2. Ballow M, Cates KL, Rowe JC, Goetz C, Desbonnet C. De- velopment of the immune system in very low birth weight (less than 1500 g) premature infants: concentrations of plasma im- munoglobulins and patterns of infections. Pediatr Res 1986;20:899-904.

3. Urbaniak SJ. ADCC (K cell) lysis of human crythrocytes sen- sitized with Rhesus alloantihodies. II. Investigation into the mechanism of lysis. Br J Haematol 1979;42:315-28.