PubMed Health⌕ Search

PubMed · 12434682

[Radioconstrast nephropathy].

Abstract

INTRODUCTION: Hospital-acquired acute renal failure increased in the last years from about 5 to 6.4%, while mortality remained high and according to newest investigations it is about 60% on average. Radiocontrast-induced nephropathy is the third cause of death in hospital-acquired acute renal failure. RISK FACTORS FOR RADIOCONTRAST-INDUCED NEPHROPATHY: Risk factors for radiocontrast-induced nephropathy include: the existing kidney disease, diabetes, dehydratation, multiple myeloma, older age and earlier kidney damage by contrast substances. COURSE OF RADIOCONTRAST-INDUCED NEPHROPATHY: The clinical course of radiocontrast-induced nephropathy may manifest from asymptomatic picture to development of oliguric form of acute renal failure. PREVENTION AND TREATMENT MODALITIES OF RADIOCONTRAST-INDUCED NEPHROPATHY: Modalities of prevention and treatment of radiocontrast-induced nephropathy are as follows: adequate hydration of patients, appropriate application of diuretics, calcium channel blockers nonionizing radiocontrast and preventive haemodialysis. EXPERIMENTAL STUDIES IN PREVENTION AND TREATMENT OF RADIOCONTRAST-INDUCED NEPHROPATHY: Experimental studies indicate application of atrial natriuretic peptide, endothelin, prostaglandin. CASE REVIEW: Two patients treated at the Clinic for Nephrology and Clinical Immunology in Novi Sad, presented with radiocontrast-induced nephropathy. In one patient it appeared after panaortography and in the second after computerized tomography of the abdomen. In both cases aggravation occurred due to already existing renal failure caused by radiocontrast substances. CONCLUSION: The problem is particularly important because there is a large number of patients in whom there is a risk of radiocontrast-induced nephropathy and it is necessary to carry out adequate prophylaxis and accurate assessment of kidney function before application of radiocontrast substances.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tatjana Durdević-Mirković, Slobodan Curić, Slavenka Vodopivec, Igor Mitić, Dusan Bozić, Lada Petrović, Tatjana Ilić. [Radioconstrast nephropathy].. https://doi.org/10.2298/mpns0208333d

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

The identification of novel potential injury mechanisms and candidate biomarkers in renal allograft rejection by quantitative proteomics.

Early transplant dysfunction and failure because of immunological and nonimmunological factors still presents a significant clinical problem for transplant recipients. A critical unmet need is the noninvasive detection and prediction of immune injury such that acute injury can be reversed by proactive immunosuppression titration. In this study, we used iTRAQ -based proteomic discovery and targeted ELISA validation to discover and validate candidate urine protein biomarkers from 262 renal allograft recipients with biopsy-confirmed allograft injury. Urine samples were randomly split into a training set of 108 patients and an independent validation set of 154 patients, which comprised the clinical biopsy-confirmed phenotypes of acute rejection (AR) (n = 74), stable graft (STA) (n = 74), chronic allograft injury (CAI) (n = 58), BK virus nephritis (BKVN) (n = 38), nephrotic syndrome (NS) (n = 8), and healthy, normal control (HC) (n = 10). A total of 389 proteins were measured that displayed differential abundances across urine specimens of the injury types (p < 0.05) with a significant finding that SUMO2 (small ubiquitin-related modifier 2) was identified as a "hub" protein for graft injury irrespective of causation. Sixty-nine urine proteins had differences in abundance (p < 0.01) in AR compared with stable graft, of which 12 proteins were up-regulated in AR with a mean fold increase of 2.8. Nine urine proteins were highly specific for AR because of their significant differences (p < 0.01; fold increase >1.5) from all other transplant categories (HLA class II protein HLA-DRB1, KRT14, HIST1H4B, FGG, ACTB, FGB, FGA, KRT7, DPP4). Increased levels of three of these proteins, fibrinogen beta (FGB; p = 0.04), fibrinogen gamma (FGG; p = 0.03), and HLA DRB1 (p = 0.003) were validated by ELISA in AR using an independent sample set. The fibrinogen proteins further segregated AR from BK virus nephritis (FGB p = 0.03, FGG p = 0.02), a finding that supports the utility of monitoring these urinary proteins for the specific and sensitive noninvasive diagnosis of acute renal allograft rejection.

Acute Kidney Injury↗

Protective effect of SnCl2 on K2Cr2O7-induced nephrotoxicity in rats: the indispensability of HO-1 preinduction and lack of association with some antioxidant enzymes.

We have shown that the ameliorative effect of stannous chloride (SnCl2) pretreatment on potassium dichromate (K2Cr2O7)-induced renal damage 24 h after K2Cr2O7 injection was associated with the induction of heme oxygenase-1 (HO-1). In this work we evaluated: (a) if the protective effect of SnCl2 (given 12 h before K2Cr2O7) is associated with changes in the renal activity of HO-1, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) 24 and 48 h after K2Cr2O7 injection, and (b) if HO-1 induction is indispensable before K2Cr2O7 injection. It was found that the protective effect of SnCl2 on renal function was observed both at 24 and 48 h reaching its maximum at 24 h when HO-1 expression was higher. Cu,Zn-SOD, Mn-SOD, and GR activities remained unchanged whereas GPx and CAT activities decreased at 48 h in K2Cr2O7-treated rats. The activity of Cu,Zn-SOD, Mn-SOD, GPx, CAT, and GR was unchanged in the SnCl2-treated rats. To fulfill the objective (b) groups of rats treated with K2Cr2O7 and SnCl2 (given at the same time or 12 h after K2Cr2O7) were studied 24 h after K2Cr2O7-injection. The simultaneous injections of SnCl2 and K2Cr2O7 had no protective effect whereas the injection of SnCl2 12 h after K2Cr2O7 exacerbated renal damage. In conclusion, the protective effect of SnCl2 on K2Cr2O7-induced nephrotoxicity is associated with HO-1 induction and not with other antioxidant enzymes (Cu,Zn-SOD, Mn-SOD, GPx, GR, and CAT) and SnCl2 has a preventive and not a therapeutic effect on renal damage induced by K2Cr2O7.

Acute Kidney Injury↗

Reversible acute renal failure after unilateral extracorporeal shock-wave lithotripsy.

Extracorporeal shock-wave lithotripsy (ESWL) is the treatment of choice for the majority of patients with renal or proximal ureteral stones. We describe an unusual case of anuric renal failure following ESWL, in absence of obstruction or myoglobinuria, in the presence of unilateral nephrolithiasis and two normally functioning kidneys. A mechanism for this patient's acute renal failure (ARF) is postulated. Although the frequency of ARF after ESWL is extremely rare and the mechanism responsible for ARF is not understood, the appearance of ARF, when ureteral obstruction or hematoma are absent, should be included among complications following EWSL. Attention should be paid to older patients.

Acute Kidney Injury↗