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El sindrome Urémico Hemolítico D+ (SUH) es la segunda causa de insuficiencia renal crónica terminal (IRCT) en edad pediátrica. La proteinuria es el principal modulador de la evolución a la cronicidad. En un grupo de pacientes tratados con dieta controlada en proteínas e inhibidores de la enzima de conversión de la Angiotensina II se demostró un enlentecimiento significativo en la progresión de la nefropatía a la IRCT. El objetivo de este trabajo fue evaluar, en una primera etapa, el impacto de la dieta normoproteica y normosódica sobre la proteinuria en pacientes con nefropatía secuelar por SUH y función renal normal (CI Cr >80ml/min/1.73m2). Métodos: como parte de un estudio de fase III longitudinal, multicéntrico, aleatorizado, doble ciego, de grupos paralelos (placebo y activo controlado con enalpril y losartan), se evaluó la diferencia entre la proteinuria antes y después de una dieta normósódica y mormoprotica, indicada según RDA. La ingesta proteica fue estimada mediante recordtorio de 72 horas y el cálculo de excreción de urea en orina de 24 horas. La proteinuria se dosó en orina de 24 hs. al comienzo del estudio, a los 30 y 60 días. Resultados: se incluyeron 102 pacientes cuyo rango de proteinuria fue entre 5.3 y 40.0 mg/kg/día de los cuales negativizaron 65 (63.7 por ciento) y no respondieron 37 (36,3 por ciento ). La mediana de edad del comienzo de la enfermedad fue de 16,5 meses (rango: 7.0-85.0 meses). El tiempo de evolución post SUG fue de 4.0 a 155.0 meses (mediana 48.0 meses) El valor de la proteinuria inicial en los 65 niños que respondieron fue de x 9.83 mg/kg/día (ES 0 o,34) y post dieta de de x =2,44 (ES 0 0,12) P < 0.0001. La media de las diferencias entre la natriuresis pre y post dieta no fue estadísticamente diferente de 0; t = 0,97 (x /ES). Conclusión: la dieta normoproteica es capaz de normalizar la proteinuria en el 63.7 por ciento de los pacientes con proteinuria significativa secundaria a SUH y función renal normal.

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Esta publicación que hoy presentamos constituye una suerte de testimonio que aquel emprendimiento académico cuyo acto formal de cierre tuvo lugar en diciembre de 2004.

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BACKGROUND: Cationic streptococcal proteinase (erythrotoxin B) and its precursor, zymogen, are putative nephritogenic antigens. The present study was designed to test whether serum titers to these antigens were good markers of streptococcal infection associated with glomerulonephritis. METHODS: We studied 153 patients (male/female = 104/49, age range, 2 to 23 years old) with acute poststreptococcal glomerulonephritis (APSGN) from three countries (Venezuela, Chile and Argentina). The site of the initial infection was the skin in 84 patients, the throat in 55 patients and was unknown in 14 patients. In addition, we studied 23 patients (1 to 24 years old) with streptococcal infection not associated with glomerulonephritis (14 patients with impetigo and 9 patients with pharyngitis). As control group, 93 healthy individuals (54 males, 2 to 19 years old) were studied. Anti-zymogen and anti-proteinase titers were determined in a single laboratory by ELISA, and the intra- and interassay coefficients of variation were 5.3% and 8.5%, respectively. ASO titers and anti-DNAse B titers were also done. RESULTS: Anti-zymogen titers of 1:800 to 1:3200 had likelihood ratios (sensitivity/1-specificity) for detection of streptococcal infection in APSGN patients ranging from 2.00 to 44.2 in Argentina, Chile and Venezuela. Anti-zymogen titers decreased one to two months after APSGN and they were 1 to 3 log2 dilutions higher that anti-proteinase titers. Receiver operating characteristic (ROC) curves showed that anti-zymogen titers were consistently superior to anti-streptolysin O and anti-DNAse B titers as markers for streptococcal infection in APSGN. CONCLUSIONS: These results suggest that increased anti-zymogen antibody titers are the best available marker for streptococcal infection associated with acute glomerulonephritis.

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Serum erythropoietin (EPO) levels were measured in ten previously non-transfused children with hemolytic uremic syndrome (HUS). Complete blood cell count, serum EPO, and renal function tests were carried out upon admission and weekly thereafter. Blood samples were obtained: (1) prior to the first transfusion; (2) after the first transfusion but before recovery from renal failure; (3) during the recovery stage. All patients required transfusions (mean 1.8+/-0.8 per child). Absolute values of EPO correlated positively with the hematocrit during the three stages (r = 0.53, 0.36, and 0.12, respectively) which is opposite to expected results. The observed EPO logarithm/predicted EPO logarithm upon admission was low (0.70+/-0.08), falling further during stage 2 (0.57+/-0.03), but increasing thereafter (0.78+/-0.07) without reaching normal values. The reticulocyte production rate followed a parallel course (0.74+/-0.14, 0.54+/-0.11, and 0.60+/-0.10, respectively). On comparing the observed serum EPO levels with those expected, 9 of 11 pre-transfusion samples showed low values; in stage 2, all samples were below normal; in the recovery phase most (77.8%) were still low. Our results show an inadequate EPO synthesis in children with HUS, which could play an important pathogenic role, since it aggravates the severity of the existing hemolytic anemia; the secondary inhibitory effect of repeated transfusions exacerbates this inadequate synthesis.

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Since resistance to several oral antimicrobials useful for the treatment of pediatric urinary tract infections (UTI) is overwhelming in Argentina, an in vitro investigation was performed testing 400 isolates obtained from urines of children suffering UTI's, 200 collected in 1990 and 200 in 1991. Their susceptibility against oral antimicrobials marketed in Argentina and appropriate for the treatment of UTI was determined by the agar dilution methods. An increase of the resistance to aminopenicillin combined with beta-lactamase inhibitors and to fluoroquinolones was observed comparing the two periods. Cefpodoxime (CPD), cefixime and fluoroquinolones except norfloxacin were the sole oral antimicrobials showing in vitro activity at the 90 per cent level. Unfortunately fluoroquinolones are not yet approved for pediatric use. Consequently we realized an in vitro and in vivo pharmacokinetic study in order to determine CPD activity against E. coli isolated in UTI cases. Five children (6-10 y) showing E. coli UTI infections received 10 mg/kg/d CPD in a single oral daily dose and were treated up to 10 days, 3 had lower UTI and 2 upper UTI. All patients were clinical and bacteriologically cured. Cultures obtained up to 4 weeks after treatment were negative. CPD serum levels at 2 hours after the first dose of treatment showed a median of 2.7 mg/l (2.3-3.4 range). Bactericidal serum titers at the same time against the patients own strain and an E. coli TEM-1 hyperproducer strain (MIC 4,096 mg/l for ampicillin and 0.5 mg/l for CPD) showed a median value of 1/8 against patients strains and 1/2 against the THP strain.(ABSTRACT TRUNCATED AT 250 WORDS)

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Metabolic acidosis occurs frequently in newborns. Net acid excretion (NAE) in 34 preterm and 12 term infants was measured during the first week of life. Twenty preterm infants received breast milk or formula; the remaining infants received total parenteral nutrition (TPN) -- synthetic amino acids or casein hydrolysate solution. NAE for breast milk vs formula fed infants was 5.4 +/- 0.4 and 7.8 +/- 0.6 muEq/min/m2 (mean +/- SEM). The corresponding values for the two TPN solutions in preterm infants were significantly higher at 12.5 +/- 1.4 and 19.4 +/- 3.5 muEq/min/m2. Term infants produced even greater amount of net acid, 20.6 +/- 2.9 and 35 +/- 3.7 muEq/min/m2 respectively for the two TPN solutions. Milk fed infants are less prone to acidosis because of base generated from milk consumption. Due to its inherent acidogenic effect, TPN solutions induce acidosis more readily. Infants receiving TPN are therefore required to generate a higher NAE rate to maintain acid-base homeostasis compared to milk fed infants.

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The nephrotic syndrome is rarely associated with renal tubular defects, and the combination has been reported only in association with advanced renal insufficiency. We report here five children with nephrotic syndrome and multiple tubular defects which evolved when glomular filtration rate ranged between 56 and 90 ml/minute/1.73 m2. The tubular defects were first noted at 3, 4, 4, 7, and 22 months after the onset of the nephrotic syndrome, and renal glycosuria was the first sign in all five children. Glycosuria was intermittent in three patients, constant in two, and ceased with loss of kidney function. Four patients had hyperaminoaciduria and renal tubular acidosis (two of four tested had distal renal tubular acidosis). Three patients had decreased tubular reabsorption of phosphorus and defective maximum concentrating capacity. All five had focal segmental glomerulosclerosis proven by renal biopsy. Over a follow-up period of seven years, all of the children have developed advanced renal insufficiency, four of the five have required dialysis or transplantation within 21 to 72 months after onset, and one has stabilized renal function at 35 ml/minute/1.73 m2. The one patient receiving a kidney transplant has had recurrence of focal segmental glomerulosclerosis in the transplanted kidney and became nephrotic with three subsequent transplants. Our experience suggests that the nephrotic syndrome associated with tubular defects in children forms a subgroup of focal segmental glomerulosclerosis, with rapid progression to renal insufficiency and the potential for recurrence of the lesion in the transplanted kidney.

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Juvenile rats fed a diet containing 1% lead acetate for 7 weeks, in addition to an impaired growth rate and renal function derangements, suffered malabsorption of glucose and certain amino acids, as assessed by an in vivo perfusion technique. The reduction in glucose absorption ranged between 10% and 31% when the carbohydrate was pumped in concentrations of 2-80 mM. This alteration was compatible with a noncompetitive type of transport inhibition. The intestinal absorption of glycine, lysine, and phenylalanine were, respectively, decreased 22, 18, and 15% when these amino acids were present at 1 mM levels. Sodium transport was severely reduced (57.6 +/- 17.9 (SEM) vs. 124.2 +/- 17.4 muEq/min-cm) and intestinal mucosa (Na+-K+)-ATPase was concomitantly lower in the lead-intoxicated rats (186.4 +/- 19.0 vs 268.4 +/- 29.8 nmol P/min-mg protein). However, this enzyme was not altered in liver and kidney. Furthermore, intestinal mucosa fructose-1,6-diphosphatase, succinic dehydrogenase, pyruvate kinase, and tryptophan hydroxylase were not different in experimental and control animals. These studies substantiate the presence of functional and biochemical abnormalities in the intestinal mucosa of young rats when fed substantial amounts of a soluble lead salt. It is, therefore, reasonable to accept the possibility that physiologic damage occurs in tissues directly subjected to high and persistent levels of a toxic agents, as it occurs in other organs, underscoring the parallelism between transport mechanisms at the renal and intestinal levels.

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The administration of 1.5 or 9.0 mmoles/kg ip of maleate to rats induced, in addition to renal alterations similar to those occurring in the Fanconi syndrome, a decline in the intestinal mucosa (Na+-K+)-ATPase with a simultaneous decrease in sodium intestinal transport and an increase in potassium absorption. Further differences in the behavior of the two electrolytes were observed when the concentration of sodium in the perfusates was altered. No changes occurred in amino acid or glucose transport in experimental animals.

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