N-acethyl-cysteine reduces the occurrence of contrast-induced acute kidney injury in patients with renal dysfunction: a single-center randomized controlled trial.

BACKGROUND: The occurrence of contrast-induced acute kidney injury (CIAKI) has paralleled the increased number of diagnostic interventions requiring radiographic contrast media (CM). Several strategies aimed at preventing renal injury following iodine have been carried out over the last several years. The aim of this study was to evaluate the impact of three different strategies aimed at preventing CIAKI in patients with renal dysfunction (serum creatinine >1.25 mg/dl or estimated creatinine clearance <45 ml/min) receiving low osmolar CM for diagnostic-therapeutic procedures. METHODS: Candidates received 154 mmol NaHCO3 solution (B0) at a rate of 3 ml/kg/h from at least 2 h before the procedure and at 1 ml/kg/h during and for the next 6-12 h; the same schedule plus N-acethyl-cysteine (NAC) 600 mg twice daily the day before and the day of the procedure (BN) or NAC as above plus 154 mmol NaCl solution at a rate of 3 ml/kg/h from at least 2 h before the procedure and at 1 ml/kg/h during and for the next 6-12 h (SN). Serum creatinine (SCr) was measured at baseline and on days 2 or occasionally 3 after CM. The main outcome measure was the occurrence of CIAKI, defined as a ≥25% increase in SCr within 2-3 days of CM. RESULTS: The three groups were similar with regard to age, gender distribution, weight, baseline serum levels of creatinine, sodium, potassium, urate and estimated creatinine clearance. A larger proportion of individuals received ACEIs/ARAs in the BN group (p < 0.05), but in the SN group, more patients declared a past history of acute myocardial infarction or had high blood pressure, and few displayed mild-moderate left ventricular dysfunction (p < 0.05). CIAKI occurred in 24/123 (19.5%) assessable patients (15/42 in the B0 group, 3/43 in the BN group and 6/38 in the SN group; p < 0.01). Thus, 15/42 patients who did not receive NAC developed CIAKI in contrast to 9/81 who did (p < 0.01). Multivariate logistic regression models showed that the use of NAC was the unique factor associated with a statistically significant influence for the occurrence of CIAKI (OR: 0.18; 95% CI: 0.04-0.72; p = 0.016). CONCLUSIONS: The results from this study show that: (1) the occurrence of CIAKI after low-osmolar CM administration is similar to that reported worldwide. (2) NAC-based renoprotective measures are superior for the prevention of CIAKI in patients with previous renal dysfunction. (3) They also demonstrate that bicarbonate expansion alone has limited value in preventing CIAKI. For those individuals at risk, combination prophylaxis including volume expansion plus NAC should be recommended to reduce the chance of overt kidney injury following CM administration.

Nefropatía por Ig A: Un caso que ilustra sus controversias / Ig A Nephropathy: A case that illustrates its controversies

La nefropatía por IgA (N IgA)es una glomerulonefritis que se caracteriza por evidenciar depósitos mesangiales difusos de IgA. Fue por primera vez descripta en 1968 por el patólogo francés Jean Berger, coincidiendo su aparición con la introducción de técnicas de inmunofluorescencia (IF) en las biopsias renales. De ahí el hecho de que esta patología sea conocida también como Enfermedad de Berger.La nefropatía por IgA es la única glomerulopatía que se define por la presencia de un tipo de depósito en la IF, más allá del patrón morfológico descripto en la biopsia. Los hallazgos en la microscopía óptica son tan variables que no permiten la elaboración de un score universal y a la vez determinar la correlación de la histopatología con la clínica.Durante muchos años la N IgA fue considerada una patología benigna. Hoy se sabe sin embargo que muchos casos evolucionan hacia la insuficiencia renal (hasta un 50%)... (AU)

IgA nephropaty (IgAN) is a mesangial proliferative glomerulonephritis characterized by diffuse mesangial deposition of IgA. IgAN is unique among glomerular diseases in being defined by the presence of an inmune reactant rather than by another morphologic feature found in renal biopsy. Light microscopic changes are so variable that there is no universal score and it is not possible to correlate pathology with clinical manifestations... (AU)

Nefropatía por Ig A: Un caso que ilustra sus controversias / Ig A Nephropathy: A case that illustrates its controversies

La nefropatía por IgA (N IgA)es una glomerulonefritis que se caracteriza por evidenciar depósitos mesangiales difusos de IgA. Fue por primera vez descripta en 1968 por el patólogo francés Jean Berger, coincidiendo su aparición con la introducción de técnicas de inmunofluorescencia (IF) en las biopsias renales. De ahí el hecho de que esta patología sea conocida también como Enfermedad de Berger.La nefropatía por IgA es la única glomerulopatía que se define por la presencia de un tipo de depósito en la IF, más allá del patrón morfológico descripto en la biopsia. Los hallazgos en la microscopía óptica son tan variables que no permiten la elaboración de un score universal y a la vez determinar la correlación de la histopatología con la clínica.Durante muchos años la N IgA fue considerada una patología benigna. Hoy se sabe sin embargo que muchos casos evolucionan hacia la insuficiencia renal (hasta un 50%)...

IgA nephropaty (IgAN) is a mesangial proliferative glomerulonephritis characterized by diffuse mesangial deposition of IgA. IgAN is unique among glomerular diseases in being defined by the presence of an inmune reactant rather than by another morphologic feature found in renal biopsy. Light microscopic changes are so variable that there is no universal score and it is not possible to correlate pathology with clinical manifestations...