Inflammation has been linked to urinary stone illness, although the particular cell contacts that mediate events were unknown. For a study, researchers evaluated the calcification and inflammatory cell patterns in kidney tissue from radical nephrectomy specimens from patients with and without a history of urinary stone illness. Nontumor parenchyma was studied in biobanked radical nephrectomy tissues from age- and sex-matched stone formers (n=44) and non-stone formers (n=82). Yasue staining was used to identify calcification, and immunohistochemistry was used to detect inflammatory cell groups such as CD68 (proinflammatory M1 macrophages), CD163, and CD206 (anti-inflammatory M2 macrophages), CD3 (T lymphocytes), and tryptase (mast cells). Image-Pro analysis software was used to quantify calcifications and inflammatory cells in the brain and medulla.
Calcification was greater in the medulla of stone formers than in non-stone formers (P<0.001). M1 macrophages were higher in stone formers’ cortex and medulla than in non-stone formers (P<0.001), and higher in stone former medulla than the stone former cortex (P=0.02). There were no differences between the groups in terms of age, gender, BMI, tumor features (size, stage, or thrombus), vascular disease status, or eGFR. Stone former status had no effect on M2 macrophages, T lymphocytes, or mast cells. M1 macrophages were associated with calcification in the medulla of stone formers (rho=0.48; P=0.001), while M2 macrophages were associated with calcification in the medulla of non-stone formers (rho=0.35; P=0.001). T lymphocytes were found to be connected with calcification in the cortex of both non-stone formers (rho=0.27; P=0.01) and stone formers (rho=0.42; P=0.004), but mast cells were found to be correlated with calcification only in the cortex of stone formers (rho=0.35; P=0.02). In stone formers, increased medullary calcification enhanced the growth of pro-inflammatory rather than anti-inflammatory macrophages.