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Biomedical subjects

L Cataldi

Publications and source records attributed to L Cataldi.

58 records · Page 4Linked to original sources

[Aminoglycosides, risk factors and neonatal kidney].

Antibiotics are the leading cause of drug-induced kidney disease, and among them the aminoglycosides (AMG) are the main nephrotoxic agents, bringing about kidney damage via a direct dose-dependent mechanism. The combination of an aminoglycoside and a penicillin derivative is still the most commonly recommended and used first-line treatment modality in the empirical therapy of neonatal sepsis, despite the low therapeutic index of AMG. The immaturity of neonatal kidney function, particularly in preterm neonates, makes newborn infants particularly susceptible to AMG-induced kidney damage. Numerous factors intervene in bringing about AMG-induced kidney damage, such as factors related to the antibiotic itself (intrinsic toxicity, administration route, type of monitoring of blood concentrations), those related to the subject treated (neonatal age, constitutional sensitivity), and others related to associated pathology (neonatal anoxia, renal hypoperfusion, respiratory distress/mechanical ventilation, hyperbilirubinaemia/phototherapy, electrolyte disorders, and even the acute sepsis calling for antibiotic therapy), as well as pharmacological factors (concomitant therapies such as diuretics, indomethacin and other antibiotics, particularly glycopeptides and cephalosporins).

Aminoglycosides↗

[Infections of the urinary tract in the newborn and infants].

Urinary tract infections (UTIs) are not an uncommon event in the neonatal population. The reported incidence of UTIs in the newborns ranges from 0.1% to 5.5%, depending on the characteristics of the population studied and the diagnostic criteria used. A review of epidemiology, clinic, laboratory findings, imaging and therapy of neonatal UTIs is presented. Particular emphasis is given to the experience of the Italian Neonatal Nephrology Study Group.

Antibiotic Prophylaxis↗

[Determination of blood cystatin C in pregnant women during labor and in their newborns].

INTRODUCTION: Human cystatin C is a basic low molecular mass protein (M(r) = 13,359) freely filtered by the glomerulus and almost completely reabsorbed and catabolized by the proximal tubular cells. In this study, we determined maternal and neonatal serum cystatin C levels both in a group of healthy pregnant women and in their newborns over the first five days of life. PATIENTS AND METHODS: Fifty healthy pregnant women, aged from 19 to 40 years, were selected. Newborns (31 males, 19 females) demonstrated the 1-min Apgar score ranging between 8 and 10, and the 5-min between 9 and 10. Their gestational age (GA) ranged between 37 and 43 weeks. Cystatin C was determined by using the cystatin C PET kit (Dako, Milano, Italy). We also determined serum creatinine and urea in all patients by using the Ektachem enzymatic assay (Ortho Diagnostic Division, Milano, Italy). RESULTS: In pregnant women, serum cystatin C was 1.52 +/- 0.39 mg/L, ranging from 0.69 to 2.30 mg/L. Serum creatinine was 58.9 +/- 11.5 mumol/L, and serum urea was 3.117 +/- 0.729 mmol/L. In newborns, serum cystatin C was at birth 2.29 +/- 0.52 mg/L, ranging from 1.17 to 4.84 mg/L. Subsequently, cystatin C significantly decreased over the first five days of life. Serum creatinine was at birth 80.08 +/- 14.26 mumol/L. By using analysis of variance (ANOVA) we found a statistically significant difference between maternal and neonatal cystatin C (p < 0.001) as well as between maternal and neonatal creatinine (p +/- 0.001). However, no correlation has been demonstrated by simple linear regression between maternal and neonatal cystatin C (r = 0.05), while maternal and neonatal creatinine significantly correlated (r = 0.45). CONCLUSIONS: Our preliminary findings suggest that cystatin C does not cross the placental barrier. Thus, in the neonate cystatin C serum levels may solely derived from himself.

Adult↗

[Microscopic hematuria in children].

Hematuria is a common finding on a urinalysis, with a prevalence rate between 1% and 2%. The execution of screening of hematuria in children is controversial. Once hematuria has been identified, it is useful to identify sources of bleeding, as either glomerular or non-glomerular. If microscopic hematuria is confirmed, investigations would include: hypercalciuria screen, blood examinations (full blood count, renal function tests, complement and autoantibody screen), renal tract ultrasound, urinalysis of family members, audiogram, if family history of deafness is present, or family members present a positive dipstick. If all these tests are negative and microscopic hematuria persists, then a renal biopsy is advocated.

Child↗