Aims: To determine in a case-control study possible associations between the development of acute renal failure in preterm newborns and therapeutic interventions, particularly drug treatments. Methods: The study population was 172 preterm infants of ,38 weeks gestation; 71 had acute renal failure and 101 were controls closely matched for gestational age and birth weight. Maternal and neonatal information was collected for both groups through questionnaires and interviews. Routine data on renal variables were also collected. Univariate and multivariate logistic regression analyses were performed. Results: Very low birthweight infants were at high risk of acute renal failure (79% of cases were ,1500 g). However, the acute renal failure was transient. Mothers of infants with acute renal failure received more drugs during pregnancy and delivery (mainly antibiotics and non-steroidal anti-inflammatory drugs). Of the possible therapeutic interventions, intubation, catheterisation, and phototherapy were mainly applied to case subjects. A low Apgar score and patent ductus arteriosus were diagnosed in a greater percentage of neonates with acute renal failure. Moreover, in the first few days of life and before diagnosis of acute renal failure, case subjects received more drugs (antibiotics, non-steroidal anti-inflammatory drugs, and diuretics) and for a longer time. In the multivariate logistic analysis, medullary hyperechogenicity (odds ratio (OR) 4.491; 95% confidence interval (CI) 1.879 to 10.731) and ceftazidime administration (OR 5.082; 95% CI 1.493 to 17.297) were associated with a greater risk of acute renal failure. Conclusions: The results suggest the need for careful monitoring of very low birthweight infants and attention to drug treatments, as it is difficult to differentiate between normality and renal failure in the first few days of life.

These recommendations are endorsed by the Italian Society of Pediatric Nephrology. They can also be a tool of comparison with other existing guidelines in issues in which much controversy still exists.

Amphotericin B is the gold standard for antifungal treatment for the most severe mycoses. However, adverse effects are common, with nephrotoxicity being the most serious, occurring early in the course of treatment, and usually being reversible in most patients. Tubular damage is a well known problem associated with amphotericin B therapy but acute renal failure is the most serious complication. Recent studies have examined ways to ameliorate the well-known toxicities of amphotericin B. A new approach has been to complex the drug with lipids or entrap it in liposomes. This review will concern amphotericin B-induced nephrotoxicity, whose mechanisms are not completely clear. Nephrotoxicity seems related to direct amphotericin B action on the renal tubules as well as to drug-induced renal vasoconstriction. The main mechanisms of nephrotoxicity suggested in the literature are presented. The clinical picture at different ages (adults, children, newborns), interactions of clinical significance, strategies for prevention of amphotericin B-induced nephrotoxicity are summarized. To provide optimal patient care, it is imperative that the clinician understand the etiology of and the signs and symptoms associated with nephrotoxicity, as well as interventions to prevent nephrotoxicity in patients receiving amphotericin B.

Since few data are available about factors affecting renal maturation especially in the lower gestational ages (G.A.), the aim of this work was to study postnatal renal function in a representative population sample of preterm newborns (G.A.

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Human cystatin C, a basic low molecular mass protein with 120 amino acid residues, is freely filtered by the glomerulus and almost completely reabsorbed and catabolized by the proximal tubular cells. Cystatin C has been recently proposed as a new sensitive endogenous serum marker for the early assessment of changes in the glomerular filtration rate. To define a reference basis for future clinical investigations in the perinatal period, we investigated the relationship between maternal and neonatal serum cystatin C in comparison with that of creatinine. We also defined reference values in healthy women at full-term pregnancy and in full-term newborns over the first 5 days of life. Seventy-eight women with uncomplicated pregnancy, aged between 19 and 40 years, and their infant newborns (43 males, 35 females) were enrolled in the study. The gestational age ranged from 37 to 43 weeks, and the birth weight from 2.50 to 4.15 kg. Blood samples were taken from all the women immediately before delivery and from their newborns at birth, 72 and 96 h after birth. Maternal and neonatal renal function was evaluated by standards parameters and by calculating creatinine clearance. In all serum samples, we measured cystatin C, creatinine, and urea. At term gestation, serum cystatin C ranged from 0.64 to 2.30 mg/L. At birth, serum cystatin C values ranged from 1.17 to 3.06 mg/L, significantly decreasing after 3 and 5 days of life. No correlation was found between maternal and neonatal serum cystatin C values (r = 0.09). As cystatin C serum levels in newborns are not significantly correlated with the respective maternal levels, neonatal serum cystatin C may originate almost exclusively in the neonate.

The renal excretion of a drug can essentially be divided schematically into three functional processes: glomerular filtration, tubular reabsorption and tubular secretion. When assessing nephrotoxicity, the tubular secretion system, which allows transport of the drug from the blood to the urine via the tubular cells, is particularly important. Historically, two distinct tubular secretion mechanisms have been described for drugs: one via organic cations and the other via organic anions. More recently, a third tubular secretion mechanism has been identified, mediated by P-glycoprotein. In the present review, a number of examples will be given relating to antibiotic-induced kidney damage determined via the tubular reabsorption mechanism (aminoglycosides, amphotericin B) and via the tubular secretion mechanism (cephalosporins, vancomycin), respectively. Drug transport within the tubular cells is the first fundamental stage in the onset of the nephrotoxic process. Knowledge of these concepts is important for the prevention of iatrogenic kidney damage, particularly in patients with underlying disease receiving concomitant treatment with several potentially nephrotoxic molecules.

Ultrasound has been effective for early detection of renal and urinary tract anomalies. In addition, this screening has proved to be very useful for the early identification and management of both renal and extra-renal precancerous as well as cancerous lesions. However, most patients requiring surgery in this study (0.24%) would probably have been symptomatic and come to medical attention without routine screening. On the basis of our results screening is not justified.