Search PubMedSearch

PubMed · 3968822

Renal dysfunction after arteriography.

Abstract

Acute renal failure has been observed in patients undergoing angiography in which a hypertonic triiodinated contrast medium is used. To ascertain the incidence of renal dysfunction and the clinical risk factors, we did a prospective study in which creatinine clearance was measured before and immediately after 120 arteriographic procedures. Thirty-seven patients (31%) sustained a significant reduction in creatine clearance after arteriography. No specific risk factor could be determined. Our findings, however, indicate that patients with preexisting renal insufficiency or diabetes mellitus are not at a higher risk for sustaining a fall in creatinine clearance after angiography.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R A Mason, L A Arbeit, F Giron. 1985-02-15. Renal dysfunction after arteriography.. https://pubmed.ncbi.nlm.nih.gov/3968822/

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

Protein metabolism in acute renal failure.

The hallmark of metabolic alterations in acute renal failure (ARF) is accelerated protein breakdown which, unfortunately, cannot be suppressed effectively by provision of exogenous nutritional substrates. Causes of excessive protein catabolism are manifold and present a combination of unspecific mechanisms induced by the acute disease process and underlying illness or associated complications, effects induced by the acute loss of renal function and, finally, the type and intensity of renal replacement therapy. Specific uremic toxic effects, insulin resistance, hormonal derangements, metabolic acidosis, circulating proteases, inflammatory mediators, and dialysis-related losses of nutritional substrates all contribute to the activation of protein degradation. Metabolism in ARF is also affected by an impairment of the multiple metabolic and endocrine functions of the kidney. Various amino acids are synthesized or interconverted by the kidneys and may become conditionally indispensable. The kidney is also an important organ in the degradation of peptides, such as peptide hormones. As a consequence of these metabolic aberrations, imbalances in amino acid pools in plasma and in the intracellular compartment occur in ARF and elimination and utilization of infused amino acids is altered. Protein or amino acids requirements are influenced more by the nature of the illness causing ARF, by the extent of hypercatabolism, by associated complications, and by the type and frequency of renal replacement therapy than by renal dysfunction per se. In noncatabolic patients, an intake of 1 g/kg body weight per day may be sufficient, while in critically ill hypercatabolic patients undergoing continuous renal replacement therapy, 1.5 g amino acids/kg body weight per day should be provided to minimize nitrogen losses. For the future, we need to identify safe methods to control the accelerated catabolism in order to improve the efficiency of nutritional interventions in patients with ARF.

Acute Kidney Injury

Upregulation of osteopontin in ischemia-induced renal failure in rats: a role for ET-1?

In this study, the involvement of osteopontin in a rat model of ischemia-induced acute renal failure (ARF) was evaluated. In unilaterally nephrectomized Sprague Dawley rats where the left artery was occluded for 30 min., plasma creatinine levels increased significantly within two hours following reperfusion indicating the onset of renal failure. Northern analysis of kidney cortical RNA from these rats showed a time-dependent increase in osteopontin mRNA expression that was significantly higher than sham-operated rats. Since endothelin-1 (ET-1) is implicated as a mediator of acute renal failure, we evaluated its effects on osteopontin expression in a rat mesangial cell-line. Data from in vitro studies indicated that endothelin-1 (ET-1) caused a modest but reproducible increase in osteopontin mRNA in these cells. While the signal for osteopontin upregulation in the rat model is not known, ET-1, which is known to be increased during ischemia, may contribute at least in part to this process.

Acute Kidney Injury