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Many pathogenetic factors may enhance coagulation process and induce thrombosis. The Authors report a case of hemolytic-uremic syndrome, with marked evidence of macroscopic kidney thrombotic involvement, in which an important dyslipidemia (hypertriglyceridemia and hypercholesterolemia) was detected during the phase of clinical improvement. These findings, and the contemporary marked reduction of fibrinolytic activity, seem to be relevant pathogenetic factors in this case. The treatment with polyunsaturated fatty acids Omega 3 may have been helpful in modifying these serum abnormalities and maybe could have brought to the clinical improvement.

Feto-neonatal hypoxia can cause a functional kidney impairment, which is often temporary and not clinically overt, but sometimes leading to acute renal failure. Hypoxic stress may result in a tubulo-interstitial damage, and kidney tubular enzymes determination has proved to be an easy, early, and non invasive method to define a tubular interstitial lesion. A major target of nephrotoxicity is the proximal tubular cell: alterations in brush-border membrane and cytoplasm result in increased turnover processes in the kidney cortex, following by a corresponding increased excretion of alanine-aminopeptidase (AAP) and N-acetyl-glucosaminidase (NAG) from the proximal tubular cells, long before glomerular or tubular functions are impaired. AAP and NAG excretion is directly correlated with the strength and the duration of toxic alteration of the proximal tubule. NAG and AAP have been already studied in the adults and the children; they have been chosen for this investigation with a double aim: 1) to define the amount of their urinary excretion in relation with gestational age at birth; 2) to evaluate if in the newborn, independently of the gestational age, their urinary concentration may be increased by ischaemic conditions caused by hypoxia. We studied 52 healthy newborns (7 preterm of 33-36 weeks and 45 full-term) and 16 newborns with feto-neonatal hypoxia (8 preterm of 26-36 weeks and full-term) at the forth day of life. Urinary NAG and AAP were assayed by colorimetric methods and the results expressed as mU/mg. creatininuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Neutropenia is the most common hematologic abnormality detected as consequence of Trimethoprim Sulfamethoxazole (TMP-SMX) therapy. Its incidence is evaluated in 27 children affected by urinary tract anomalies and treated with low doses of TMP SMX (2 + 10 mg/kg/die) for more than one month. A slight neutropenia was detected in 8 children (6 of these were in their first two years of life). In all the 27 cases a supplementation of folinic acid was started: a significant increase of PMN count was noted in all cases. Neutropenia can also appear after low (prophylactic) dosage of TMP-SMX, and can be prevented by concomitant administration of folinic acid.