Acute kidney injury (AKI) is a common and serious condition in both the inpatient and outpatient settings, and its diagnosis depends on serum creatinine measurements. Unfortunately, creatinine is a delayed and unreliable indicator of AKI. The lack of early biomarkers has limited our ability to translate promising experimental therapies to human AKI. Fortunately, understanding the early stress response of the kidney to acute injuries has realized a number of potential biomarkers. For example, neutrophil gelatinase-associated lipocalin is emerging as an excellent stand alone troponin-like biomarker in the plasma and urine for predicting and monitoring clinical trials and in the prognosis of AKI. In recent years, a number of new biomarkers of AKI with more favorable test characteristics than creatinine have been identified and studied in a variety of experimental and clinical settings. This review will consider the most well-established biomarkers of AKI.

Background: Adiponectin (ADPN) levels are consistently elevated among patients with advanced chronic kidney disease, but its relationship with cardiovascular outcomes in this population remains controversial. The aim of our study was to measure the plasma levels of ADPN in patients with end-stage renal disease on maintenance hemodialysis (HD) and we studied its correlates to cardiovascular outcomes and mortality. Methods: Our study included 133 HD patients (79 male and 54 female patients) with a mean age of 54.6 ± 17.3 years who had been receiving regular HD for at least 6 months in the nephrology units of Theodor Bilharz Research Institute, Cairo, Egypt. The clinical and biochemical correlates of plasma ADPN levels were investigated and the predictive power of ADPN levels with respect to cardiovascular events and mortality was prospectively tested in HD patients, who were monitored for 24 ± 9 months. Plasma ADPN levels were measured by using a sensitive enzyme-linked immunosorbent assay. Results: Plasma ADPN levels were 3 times higher (p < 0.0001) among HD patients (18.1 ± 6.8 µg/ml) than among healthy subjects (6.2 ± 1.8 µg/ml). Plasma ADPN levels were lower (p < 0.007) among patients who experienced new cardiovascular events (13.9 ± 6.4 µg/ml) than among event-free patients (18.6 ± 8.4 µg/ml). The relative risk of cardiovascular events was 1.96 times (95% confidence interval 1.290–2.977, p = 0.0016) higher among patients in group 1 (ADPN <15.1 µg/ml), compared with those in group 2 (ADPN ≥15.1 µg/ml). Plasma ADPN levels were inversely related to BMI, insulin levels, homeostatic model assessment index values, triglyceride and LDL-C, CRP and left ventricular mass index. Furthermore, plasma ADPN levels were directly related to HDL-C. Conclusion: Plasma ADPN is an independent (inverse) predictor of cardiovascular events and mortality among HD patients. The directions of the relationships between ADPN and several metabolic risk factors indicate that ADPN has a protective role in prevention of CVD.

Several observations suggest that the evolution of schistosomal glomerulopathy into clinically overt and progressive disease may involve pathogenetic mechanisms other than simple glomerular deposition of parasitic antigens. In a previous study, IgA was suggested to be a mediator of late glomerular lesions in this disease. This issue is further addressed in this work. The study includes 32 patients with hepatosplenic schistosomiasis, of whom 16 had overt glomerular involvement, along with four control groups: (a) 15 healthy volunteers; (b) 15 patients with simple intestinal mansoniasis; (c) 17 patients with non-schistosomal chronic liver disease; and (d) 21 subjects with primary nephrotic syndrome not associated with schistosomiasis. Routine assessment was done for all subjects including confirmatory tests for schistosomal infection, liver and renal function tests, hepatitis viral markers and abdominal ultrasonography. The total serum concentrations of IgG, IgM, IgA were measured, as well as their respective circulating immune complexes, rheumatoid factors, anti-gliadin- and anti-DNA-antibodies. Liver and renal biopsies were obtained from the relevant groups and studied by light microscopy. Renal biopsies were also examined by immunofluorescence. Patients with simple intestinal schistosomiasis had a significant increase in IgM antigliadin antibodies. Those complicated with hepatosplenic involvement also had a significant increase in the mean IgG anti-gliadin antibodies, IgG rheumatoid factor and IgM anti-DNA activity. Cases further complicated by overt glomerular disease showed a distinct IgA predominance, mainly expressed in the serum anti-gliadin antibody pool and anti-DNA activity. This profile was essentially similar to that observed in control cirrhotics. There was a significant increase in the frequency of IgA glomerular deposits in renal biopsies obtained from patients with overt schistosomal glomerulopathy, in contrast to control nephrotics. The deposits were mainly mesangial, but were also encountered in subendothelial, subepithelial and peritubular locations. Their frequency was significantly higher with more advanced lesions as seen by light microscopy. The relevance of these data is discussed, leading to the following conclusions: (a) serum IgA-anti-gliadin and -anti-DNA antibodies, and glomerular IgA deposits are markers of significant renal involvement in patients with hepatosplenic schistosomiasis. (b) IgA may be involved in the pathogenesis of advanced glomerular pathology when superimposed on parasite-induced lesions. (c) There is a significant increase in serum auto-reactivity in hepatosplenic schistosomiasis, which may also have pathogentic implications. (d) Increased production by the inflammatory bowel lesions, impaired clearance by the fibrotic livers and probable switching of immunoglobulin synthesis are suggested to explain the observed IgA predominance in those who develop renal complications.

This study demonstrates for the first time that the immunomodulatory effects of chitotriosidase enzyme could be implicated in the development of nephropathy in type 2 diabetes.