Hyperuricemia is particularly common in patients with arterial hypertension, metabolic syndrome, or kidney disease. Its role, however, as a risk factor for both renal and cardiovascular outcomes and in the context of the well-established interrelationship between cardiovascular disease and chronic kidney disease (CKD) is debated. For decades high serum uric acid levels were mainly considered the result of renal dysfunction and not a true mediator of renal disease development and progression. However, recent epidemiological studies suggest an independent association between asymptomatic hyperuricemia and increased risk of arterial hypertension, CKD, cardiovascular events, and mortality. Furthermore, data from experimental models of hyperuricemia have provided robust evidence in this direction. Hyperuricemia causes increased arterial pressure, proteinuria, renal dysfunction, and progressive renal and vascular disease in rats. The main pathophysiological mechanisms of these deleterious effects caused by uric acid are endothelial dysfunction, activation of local renin–angiotensin system, increased oxidative stress, and proinflammatory and proliferative actions. A small number of short-term, single-center clinical studies support the beneficial influence of pharmaceutical reduction of serum uric acid on total cardiovascular risk, as well as on renal disease development and progression. Hyperuricemia is probably related to the incidence of primary hypertension in children and adolescents, as serum uric acid lowering by allopurinol has an antihypertensive action in this group of patients. Finally, it is clear that adequately powered randomized controlled trials are urgently required to elucidate the role of uric acid in cardiovascular events and outcomes, as well as in the development and progression of CKD.

Renal transplantation with expanded criteria donors: Which is the optimal immunosuppression?

A case of immunoglobulin A nephropathy (IgAN) complicating a 10-year history of biopsy-proven Crohn's disease in a 31-year-old man is described. The patient presented with mild proteinuria and impaired renal function in the setting of an exacerbation of Crohn's disease. Renal biopsy showed IgAN. The patient responded to steroid treatment with clinical remission of the bowel disease and improvement of renal function, while proteinuria remained unchanged. IgA glomerulonephritis is rarely associated with Crohn's disease with only a few previously described cases. We briefly review these cases together with an overview of potential pathophysiological connections between these two diseases.

Background: Use of uncuffed catheters (UCs) in hemodialysis patients is common practice. An antibiotic lock has been recommended to prevent catheter-related bacteremia (CRB), although insufficient data are available about the appropriate antimicrobial agent and dose with prolonged use of UCs. Methods: This open-label randomized study was conducted to compare gentamicin/heparin (group A) and taurolidine/citrate (group B), as catheter-lock solutions, in 119 chronic hemodialysis patients in whom a total of 150 UCs were placed. A well-matched historical control group (heparin) included 67 UCs in 58 patients (group C). Results: CRB episodes developed in 6 and 8 patients in groups A and B, respectively, significantly fewer than in group C (20 patients). Cumulative CRB-free catheter survival at 90 days was 82% for A and 78% for B, which is significantly higher than the 26% for C. Similar Gram-positive infection rates were found in all groups. The Gram-negative infection rate was significantly lower in B compared to C. No significant differences in thrombosis rates were observed between the groups. Conclusions: Gentamicin/heparin and taurolidine/citrate, used for locking UC, were similarly effective at preventing CRB and catheter thrombosis for up to 3 months, until a functional permanent vascular access became available. Both antimicrobial lock solutions were superior to heparin in CRB prevention with similar thrombosis rates.

Contrast-induced nephropathy (CIN) is a common cause of hospital-acquired acute kidney injury (AKI) and a source of significantly increased short- and long-term mortality. Studies of large cohorts have revealed that more than half of these cases are in subjects undergoing cardiac catheterization and intra-arterial coronary angiography, and nearly a third follow computed tomography (CT) scans. Neutrophil gelatinase-associated lipocalin (NGAL) represents an early predictive troponin-like biomarker for AKI. Its role in the timely diagnosis of CIN has already been examined in adults and children undergoing coronary angiography and a meta-analysis revealed a very good performance of plasma or urine NGAL in the prediction of CIN. Much of these data have been extrapolated to patients receiving intravenous (IV) contrast agent for CT scans, although major differences in patient populations, contrast volume administered and intra-procedural complications between the two settings exist. In this context, a recent prospective study by our group evaluated plasma NGAL, measured using standardized Τriage® NGAL test (Biosite Incorporated, San Diego, CA) at baseline and 6-h post-procedure, for early detection of CIN among hospitalized patients undergoing elective contrast-enhanced CT. CIN, defined as an increase in serum creatinine (SCr) of >25% or >0.5 mg/dL from baseline within 48-h post-procedure, was found in 8.51% of subjects. In contrast, significant elevation of plasma NGAL was found at 6-h post-procedure with excellent performance characteristics. This review presents the current status of NGAL in the prediction of CIN after IV contrast administration among hospitalized patients undergoing elective contrast-enhanced CT.

Contrast-induced nephropathy (CIN) is a common cause of hospital-acquired acute kidney injury (AKI). Neutrophil gelatinase-associated lipocalin (NGAL) represents a promising biomarker for AKI. Its role in the early diagnosis of CIN has already been examined in adults and children undergoing coronary angiography. This study was designed to prospectively evaluate plasma NGAL compared with serum creatinine (SCr) for early CIN detection among hospitalized patients undergoing contrast-enhanced computed tomography (CT). We prospectively enrolled consecutive hospitalized patients undergoing elective CT with intravenous (IV), low-osmolar contrast administration. Patients with pre-procedure SCr >150 μmol/L (1.7 mg/dL), congestive heart failure, haemodynamic instability, sepsis, or urinary tract infection were excluded. Plasma NGAL was measured using the standardized Triage^® NGAL test (Biosite Incorporated, San Diego, CA, USA) at baseline and 6 h post-procedure. SCr, blood urea nitrogen (BUN), albumin and sodium (Na) were measured and eGFR MDRD₄ was calculated at the same intervals, as well as at 24 and 48 h post-procedure. CIN was defined as an increase in SCr of >25% or >44 μmol/L (0.5 mg/dL) from baseline within 48 h post-procedure, in the absence of other obvious causes. Forty-seven patients, male/female 27/20, median age 68 (31–88) years, 16/47 diabetics, with baseline SCr 91.94 ± 20.33 μmol/L (1.04 ± 0.23 mg/dL) and eGFR MDRD₄ 68.40 ± 18.22 mL/min/1.73 m² were enrolled. A contrast volume of 120 mL (range 100–150 mL) was administered. CIN was found in four subjects (8.51%), but detection by SCr was only possible 24 h in 1 and 48 h post-procedure in three. In contrast, significant elevation of plasma NGAL was found at 6 h post-procedure in those with versus those without CIN (779.25 ± 361.49 versus 82.30 ± 40.64 ng/mL, P < 0.001). Using a cutoff value of 200 ng/mL, sensitivity, specificity and area under the receiver-operating characteristic (ROC) curve of 6-h plasma NGAL for CIN prediction were excellent (100, 100 and 1.00%, respectively). Subjects with CIN did not differ in baseline demographics, renal function and diabetes status compared with those without CIN. No differences in any variable were noted between diabetics and non-diabetics. Plasma NGAL at 6 h (R² = 0.24, P < 0.001) was found to be an independent predictor of CIN. Plasma NGAL 6 h after contrast administration measured by the rapid, point-of-care Triage^® NGAL test appears to be a useful biomarker in the early prediction of CIN among hospitalized patients undergoing elective contrast-enhanced CT. However, the small sample size and the very small number of CIN events are important limitations. In any case, according to our evaluation, CIN incidence in this well-controlled population underlines the importance of early detection by an adequate and simple procedure such as the 6-h plasma NGAL test.