An understanding of immunological mechanisms in kidney diseases has advanced using mouse kidneys. However, the profiling of immune cell subsets in human kidneys remains undetermined, particularly compared with mouse kidneys. Normal human kidneys were obtained from radically nephrectomised patients with urogenital malignancy (n = 15). Subsequently, human kidney immune cell subsets were analysed using multicolor flow cytometry and compared with subsets from C57BL/6 or BALB/c mice under specific pathogen-free conditions. Twenty kidney sections from healthy kidney donors or subjects without specific renal lesions were additionally analysed by immunohistochemistry. In human kidneys, 47% ± 12% (maximum 63%) of immune cells were CD3+ T cells. Kidney CD4+ and CD8+ T cells comprised 44% and 56% of total T cells. Of these, 47% ± 15% of T cells displayed an effector memory phenotype (CCR7− CD45RA− CD69−), and 48% ± 19% were kidney-resident cells (CCR7− CD45RA− CD69+). However, the proportions of human CD14+ and CD16+ myeloid cells were approximately 10% of total immune cells. A predominance of CD3+ T cells and a low proportion of CD14+ or CD68+ myeloid cells were also identified in healthy human kidney sections. In mouse kidneys, kidney-resident macrophages (CD11blow F4/80high) were the most predominant subset (up to 50%) but the proportion of CD3+ T cells was less than 20%. These results will be of use in studies in which mouse results are translated into human cases under homeostatic conditions or with disease.

Contrast-induced nephropathy (CIN) has been increasing and seems to be associated with clinical outcomes in ischemic heart disease. This study aimed to assess the incidence, predictors, and cardiac outcomes of CIN when nonionic isosmolar contrast media (iodixanol, Visipaque(®), GE Healthcare, Cork, Ireland) was used. Between January 2005 and July 2008, 510 patients (69.2 ± 9.0 years of age, 384 men) undergoing diagnostic coronary angiography (CAG) or percutaneous coronary intervention (PCI) were divided into two groups according to the development of CIN (CIN group: n=74; non-CIN group: n=436). CIN developed in 74 patients (14.5%). They were more likely to have diabetes (55.4% vs. 42.9%, p=0.045), decreased left ventricular ejection fraction (LVEF) (50.1 ± 12.6% vs. 57.7 ± 13.9%, p<0.001), and lower baseline hematocrit level (32.4 ± 5.3% vs. 36.6 ± 5.5%, p<0.001). Multiple logistic regression analysis revealed baseline hematocrit (odds ratio 0.900, 95% confidence interval 0.851-0.952, p<0.001), decreased LVEF (odds ratio 0.967, 95% confidence interval 0.949-0.986, p=0.001), and baseline creatinine level (odds ratio 2.317, 95% confidence interval 1.252-4.286, p=0.007) as independent predictors of CIN. At 1-year follow-up, patients with CIN were found to have more adverse outcomes than without CIN in Cox proportional hazards analysis (hazard ratio 13.068, 95% confidence interval 2.425-70.434, p=0.003). CIN was mostly associated with baseline creatinine level rather than CM amount using nonionic isosmolar CM. We found that patients with CIN had worse event-free survival than patients without CIN after multifactorial adjustment.

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