In the classic form of hemolytic uremic syndrome associated with toxins of gram-negative enterobacteria, mortality in the acute stage has been lower than 5% since 1978 (data from the Nephrology Committee, Argentine Society of Pediatrics). Children usually die because of severe involvement of the central nervous system, intestine, or myocardium and its complications, or because of intercurrent infection. Treatment in this phase is supportive, and efforts should be put into prevention of infection by Shiga-like toxin-producing enterohemorrhagic Escherichia coli. Of the 95% who survive, approximately one third is at risk for having chronic sequelae. Motor, sensory, or intellectual deficits, intestinal strictures, myocardial infarctions, or diabetes are infrequent. The more-frequent chronic renal lesion is characterized by the hyperfunction of nephrons remaining after the acute necrotizing lesion, which leads to progressive scarring, and not by persistence or recurrence of the microangiopathic process. Three courses of progression to end-stage renal failure have been described. Children with most severe forms do not recover from acute renal failure and enter directly into a dialysis and transplantation program. A second group recovers renal function partially, with persistent proteinuria and frequently hypertension; progression to end-stage renal failure occurs in 2 to 5 years. The third group may recover normal serum creatinine and creatinine clearance, with persistent proteinuria. They are at risk of progressing to chronic renal failure and end-stage renal disease after more than 5 years, and sometimes as late as 20 years, after the acute disease. Treatment should aim at preventing the mechanisms associated with progressive renal scarring. Transplantation is indicated in this form of hemolytic uremic syndrome, because there is little, if any, risk of recurrence, and the prognosis is similar to that of transplantation for other diseases.

No abstract

In a previous work we pointed out the hlgh correlation among the presence of antithyroid antibodies (AB), thyrold function alteration and clinical symptans in children with insulin dependent diabetes mellitus (DMID). In the actual study, the chronic lymphocitic thyrolditis (CLT), antithyroid AC and alteration function in patients wlth DMID was evaluated. From a total of 228 pts,in 78 (age 11.6 + 4.31, basal TSH and/or post TRH, T4, T3 by RIE and microscmal antifraction (MiAE) antithyroid AC and antlthyrcqlobulin (A'lg) haemoglutlnation was done. CLT presence (Fisher's criteria) was determined in 20 pts (25%): 16 girls, 4 boys; 11,6 years + 3. 43, 90% (18/20) of which presented thyroid functlon alteration with high basal TSH -X 7.39 + 3.49 u W (p-x 0.001) and or frank hyper response to TRH (>of 25 uLknl). 85% of the patients presented cllnical symptans; goiter was detected in 65%. CLT prevalence was significatively greater in the first four years of the diabetes evolution. The frequency of MiAF positive titles was 15.4% of the diabetlc and 50% of CLT patients. m e to the high prevalence, 258, we conclude that thyroid function study, AC dosage and clinical exam must be lncluded In all the children with DMID, specially in the flrst four years after the onset of the dlsease. In all patlents during the first year of life(range:O-10 months,X:3 nonths).Seven died before one year of age,and two when they were 3 years old(range:O-36 months,X:1,7 years).source of infection was: blood transfusion in 3(2 nothers and 1 child),tatm in both parents in 1,drug adlctlon in parents in 4,durg adiction and prctrusculty in 1.Autopsles were performed and processed routinely.5/9 had hepathomegaly;3/9 splenomegaly;2/9 cardimqa1y;and 1 child had lntraventrlcular bleedlnq.Lwphoid depletion in nodes was observed In 5/9 while heperplasia in lj9~Thymic involution was observed In 1/9 while 4/9 had lymphold depletion in their thymuses. In 1/9 the thymus was normal. Hepatic steatosis was observed in 7/9 and non speclflc hepatitis ln 6/9.Dlffuse alveolar damage was recorded in 4/9,PHL/LIP In 2/9 and lung angimtosis in 2/9.Acute myocarditls was found in 2/9 and myocardial lnfarctlon in 1/9. Sepsis by CMV was found in 3/9, and South Pmerican trypanosmiasis, histoplasmosis,congenital syphllls and pneumxystis carinii,one case each.We did not see neoplastic diseases,proMly becuase of the early age of death of our cases. Abut 80-90% of post-transfusional hepatitis and 50% of sporadlc hepatltis,so called non A non B Hepatitis, are produced by HVC. The prevalence of Anti-HVC is about 0.4-2.28 in blccd donors.AEter an acuteHVC infection,50-60%of patlentswill progress to a chronic state,and 20% of then wlll have an hepatic cirrhosis.The objetive of this study was to evaluate the anti HVC prevalence in different high risk groups.subjects and Methcds:131 patients considered as high risk groups were selected:a)69 wlth hepatic disease (fD,34 boys,r:lm -18y);b)23 wlth hemato-oncolqic disease (H-0,13 boys,r:2.5-16y);c) 39 with chronic renal failure (CRF,19 b...

Keywords Procalcitonin · C-reactive protein · Cut-off point · Acute pyelonephritis Sirs,We read with interest the article "Procalcitonin as a marker of acute pyelonephritis in children" [1]. However, we could not find the description of the methodology utilized to select the cut-off points [procalcitonin (PCT) 0.5 µg/l, C-reactive protein (CRP) 20 mg/l] used for the calculation of sensitivity, specificity, and predictive value. We then reviewed the two papers cited [2, 3] that used the same research design, and found that the cut-off points for CRP and PCT were different from those in this article. The study by Benador et al.[2] (PCT 0.6 µg/l,