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Despite preventive guidelines, iatrogenic contrast-induced nephropathy (CIN) ranks third as a cause of hospital-acquired AKI, impacts significantly on morbidity and mortality, and is associated with longer stays in hospitals, with higher medical costs. [1][2][3][4] The rates of CIN vary, depending on the study definitions employed and underlying risk factors, and range from 0.6% to 30% or higher among risk groups. [5][6][7][8] CIN is also associated with increased duration of hospitalisation and early and late mortality. In-hospital mortality due to CIN ranges from 7% to 22%. [9] McCullough et al. [9] reported early mortality of 1.1% in controls, 7.1% in CIN patients, and 35% in CIN patients that required dialysis. Owing to increased comorbidities, hospitalised patients have increased risk for developing CIN compared with ambulatory patients .[10]Inflammation and endothelial dysfunction, together with reactive oxygen species (ROS), are implicated in the pathogenesis of CIN. [8] Iodinated contrast media directly injures the renal tubular epithelium by producing ROS radicals that cause intra-renal vasoconstriction leading to ischaemia and death of tubular cells. [8,10,11] Serum albumin is an important antioxidant that reduces the formation of oxygen free radicals and is important in expanding intravascular volume. [12,13] However, the role of serum albumin in reducing the incidence of CIN remains unexplored.Sub-Saharan Africa has a dearth of data on rates of CIN. This study investigated the rates of CIN together with the influence of serum albumin, albuminuria, age, haemoglobin, and glomerular filtration rate (GFR) levels on CIN and patient outcomes. Methods Study design, setting and populationThis study was a prospective observational study conducted at Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa, from 1 July 2014 to 30 July 2015. Ethical approval was obtained from the human research ethics committee (HREC) of the University of the Witwatersrand and informed written consent was obtained from all patients. We consecutively recruited hospitalised patients undergoing computed tomography (CT) and angiography from the Divisions of Radiology and Cardiology, respectively. The following exclusion criteria were used: <18 years of age; evidence of pre-existing AKI (clinical or laboratory); end-stage renal disease (ESRD); renal replacement therapy (RRT); prior contrast media administration in the preceding 7 days; pregnancy; or incomplete data. Study proceduresThe study physician reviewed participants' medical records and examined the participants in order to determine pre-existing risk factors for CIN. The medical records were reviewed to determine patient duration of hospitalisation, dialysis requirements and mortality. Study phlebotomists collected blood samples prior to and post contrast media administration. Pre contrast, urine was collected and analysed for microalbuminuria using the Chemistrip Micral 30 immune assay test (Roche 11544039172). Serum creatinine was analysed using the Jaff...

Glomerular injury, occurring either as primary glomerular disease or as part of a systemic disease process, is usually a result of immune-mediated mechanisms. The morphologic reaction pattern has a diverse spectrum of appearance, ranging from normal by light microscopy in minimal change disease to crescentic forms of glomerulonephritis, with conspicuous disruption of the normal glomerular morphology. The mechanisms of glomerular immune deposit formation include trapping of circulating antigen-antibody complexes and the in situ formation of immune complexes within the glomerulus. While the majority of postinfectious immune-complex-mediated glomerulonephritides are believed to result from the deposition of circulating antigen-antibody complexes, preformed outside of the kidney and secondarily deposited in the kidney, the notion of forming in situ antigen-antibody complexes to either planted antigens or to integral structural components of the glomerulus, through "cross-reacting" autoimmune reactions, is gaining popularity in a variety of forms of glomerulonephritides. Patients with HIV infection may develop a spectrum of renal pathology, the glomerular manifestations of which include both antigen-antibody complex and nonimmune-complex-mediated pathogenetic mechanisms. Similarly, patients with Streptococcal infections, Hepatitis B virus, or Hepatitis C virus infection may develop a spectrum of glomerulonephritides, which are predominantly immune-complex-mediated. Therapy for glomerular diseases due to HIV, hepatitis B, or C virus infections remains a challenge.