Inflammatory Cells in Nephrectomy Tissue from Patients without and with a History of Urinary Stone Disease

Abstract

Background and objectives: Urinary stone disease has been associated with inflammation, but the specific cell interactions that mediate events remain poorly defined. This study compared calcification and inflammatory cell patterns in kidney tissue from radical nephrectomy specimens of patients without and with a history of urinary stone disease. Design, setting, participants, and measurements: Non-tumor parenchyma of biobanked radical nephrectomy specimens from age- and sex-matched stone formers (n=44) and non-stone formers (n=82) were compared. Calcification was detected by Yasue staining and inflammatory cell populations by immunohistochemistry for CD68 (pro-inflammatory M1 macrophages), CD163 and CD206 (anti-inflammatory M2 macrophages), CD3 (T-lymphocytes), and tryptase (mast cells). Calcifications and inflammatory cells were quantified in cortex and medulla using Image-Pro® analysis software. Results: Calcification in the medulla of stone formers was higher than in non-stone formers (p<0.001). M1 macrophages in the cortex and medulla of stone formers were greater than in non-stone formers (p<0.001), and greater in stone former medulla than stone former cortex (p=0.02). There were no differences in age, sex, body mass index, tumor characteristics (size, stage, or thrombus), vacular disease status, or estimated glomerular filtration rate between the groups. M2 macrophages, T-lymphocytes, and mast cells did not differ by stone former status. There was a correlation between M1 macrophages and calcification in the medulla of stone formers (rho=0.48; p=0.001) and between M2 macrophages and calcification in the medulla of non-stone formers (rho=0.35; p=0.001). T-lymphocytes were correlated 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) whereas mast cells and calcification were correlated only in cortex of stone formers (rho=0.35; p=0.02). Conclusions: Higher medullary calcification stimulated accumulation of pro-inflammatory rather than anti-inflammatory macrophages in stone formers.

Antioxidant Activity of Auricularia auricula Polysaccharides with Different Molecular Weights and Cytotoxicity Difference of Polysaccharides Regulated CaOx to HK-2 Cells

“…Te formation of calcium oxalate (CaOx) kidney stones is a complex biological regulatory process [1], and it includes the nucleation, growth, crystallization, and retention of crystals in the kidney [2,3]. CaOx kidney stones have two main forms: CaOx monohydrate (COM) and CaOx dihydrate (COD).…”

Inflammation and kidney stones: cause and effect?

“…Dejban et al . [42 ▪▪ ] have taken this a step further by examining archived nephrectomy tissue samples from patients with and without a history of kidney stones. They stained the cortex and medulla to quantify areas of calcification and markers of the two main putative macrophage cell subtypes, M1 and M2: CD68 for the pro-inflammatory M1 type and CD163/206 for the anti-inflammatory M2 type.…”

“…First, Dejban et al [42 ▪▪ ] found increased calcium deposits in the kidney medulla of stone formers compared with nonstone formers (cf. Okada et al [40] cited above), although no differences in the cortex.…”

Exploring the Role of Inflammation toward the Pathogenesis of Calcium Nephrolithiasis

“…These studies led to the suggestion that immune mechanisms via inflammatory cells and, principally, macrophages could be involved in the calcification process in response to urinary crystals presentation to monocytes, activating macrophages and contributing to crystals phagocytosis in patients with idiopathic nephrolithiasis (6). In a well-designed study published in this issue of CJASN by Dejban et al (7), for the first time in a cross-sectional case-control study using nontumor nephrectomy tissue, samples levels of renal cortical and medullary calcium deposits were compared between various immune cell populations in both the kidney stone– and nonstone-forming populations. The results demonstrated that renal medullary calcification was higher in kidney stone formers than in nonstone formers.…”