Conflicting evidence exists regarding the effect of platelet to lymphocyte ratio (PLR) and lymphocyte to monocyte ratio (LMR) on the prognosis of renal cell carcinoma (RCC) patients. Here we quantify the prognostic impact of these biomarkers and assess their consistency in RCC. Eligible studies were retrieved from the PubMed, Embase and Web of Science databases. Pooled hazard ratios (HRs), odds ratios (ORs), and 95% confidence intervals (CIs) were calculated. Sixteen studies containing 6,223 patients met criteria for inclusion. Overall, elevated PLR was associated with poorer overall survival (OS, HR 1.76, 95% CI 1.41–2.19, P < 0.001), progression-free survival (PFS, HR 2.81, 95% CI 1.40-5.63, P = 0.004) and recurrence-free survival (RFS, HR 2.64, 95% CI 1.35–5.14, P = 0.004). Conversely, high LMR was correlated with more favorable OS (HR 0.62, 95% CI 0.51–0.77, P < 0.001) and RFS (HR 0.53, 95% CI 0.42–0.67, P < 0.001). Moreover, low LMR was significantly associated with some clinicopathological characteristics that are indicative of poor prognosis and disease aggressiveness. By these results, elevated PLR was associated with poor outcomes, while high LMR correlated with more favorable survival in RCC patients. Pretreatment PLR and LMR can serve as prognostic factors in RCC patients.

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Background: To examine the potential prognostic significance of pretreatment De Ritis ratio (aspartate transaminase/alanine transaminase ratio) in urological cancers, including upper tract urothelial cancer (UTUC), renal cell carcinoma (RCC), prostate cancer (PCa), bladder cancer (BCa). Methods: Potential literatures were searched with PubMed, Embase, Cochrane Library, and Web of Science in December 2019. Merged hazard ratios (HRs) and 95% confidence intervals (CIs) were used to evaluate the associations. Results: Totally, 15 studies with 8,565 patients were included. Merged results showed that an elevated pretreatment De Ritis ratio was correlated with poorer OS (HR 1.80, 95% CI 1.61-2.01), CSS (HR 2.15, 95% CI 1.80-2.56), PFS (HR 1.57, 95% CI 1.34-1.85), BRFS (HR 1.67, 95% CI 1.11-2.53) for urological cancers. Subgroup analyses by cancer type for OS found that De Ritis ratio can be a predictor in UTUC (

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The expression of calcium epithelium TRPV5, alcium binding protein Calbindin-D28k and Na(+)/Ca(2+) exchanger NCX1 was detected in renal distal convoluted tubule, and their effects on urine calcium reabsorption and the possible pathogenic mechanism in idiopathic hypercalciuria (IH) were investigated. Genetic hypercalciuric stone-forming (GHS) rats were chosen as animal models to study urine calcium reabsorption and IH. The cognate female and male rats that had maximal urine calcium were matched to breed next generation. Twelve GHS rats and 12 normal control (NC) SD rats were selected. Western blot and real time quantitative PCR were used to detect the protein and gene expression of TRPV5, Calbindin-D28k and NCX1 respectively. The expression levels of TRPV5 protein and mRNA in GHS rats were significantly lower than in NC rats (P<0.05). Western blot revealed that the expression levels of Calbindin-D28k in GHS rats and NC rats were 0.49+/-0.02 and 0.20+/-0.01 respectively, with the difference being significant between them (P<0.05). By using real time quantitative PCR, it was found that there was no significant difference in Calbindin-28k mRNA expression levels between GHS rats and NC rats (P>0.05). There was no significant difference in the NCX1 expression between GHS rats and NC rats (P>0.05). It was suggested that TRPV5 and Calbindin-D28k might play an important role in urine calcium reabsorption and IH, but they differently contributed to the pathogenesis: The down-regulation of TRPV5 decreases urine calcium reabsorption, directly leading to loss of the urine calcium and resulting in hypercalciuria, and the increased Calbindin-D28k expression could relieve, neutralize and decrease intracellular Ca(2+) concentration to maintain calcium balance. NCX1 is not the key protein in urine calcium reabsorption.

What’s known on the subject? and What does the study add? Experimental data have shown that VDR overexpression in the duodenum and kidney cortex is a biological characteristic of genetic hypercalciuric stone‐forming rats (GHS rat), and a link between idiopathic calcium stone formation and the microstatellite marker D12S339 (near the VDR locus) has been proven in humans. Our study shows that VDR can positively regulate the mRNA and protein expression of TRPV5, calbindin‐D28k and PMCA1b in NRK cell lines. VDR knockdown results in a decrease in intracellular Ca2+ concentration in NRK cell lines. The effect of the elevated VDR level in the kidney on hypercalciuria and the underlying mechanisms need to be further addressed. OBJECTIVE • To determine the effects of vitamin D receptor (VDR) on hypercalciuria and the mechanisms underlying such effects. MATERIALS AND METHODS • The adenovirus vector‐delivered microRNA targeting rat VDR was constructed. We infected the normal rat kidney epithelial cell line NRK (Cellbank, China) with the adenovirus and then collected the cells at 0, 48, 72, 96, 120 h after infection. The mRNA and protein levels of VDR and VDR‐dependent epithelial Ca2+ transport proteins were detected using real‐time polymerase chain reaction and Western blot assays, respectively. • Fluorescent Ca2+ indicator Fluo‐4 NW (Fluo‐4 NW calcium assay kit, Molecular Probes, Invitrogen, USA) and laser scanning confocal microscope (Olympus, FV500‐IX71, Japan) were used to detect the cytosolic free Ca2+ concentration at different time points after infection. RESULTS • The mRNA and protein level of VDR, transient receptor potential vanilloid receptor subtype 5 (TRPV5), calbindin‐D28k and plasma membrane Ca2+‐ATPase (PMCA1b) in infected NRK cells was significantly lower at 72 and 96 h after infection than that in control cells. • There was no significant difference between the two groups in the mRNA and protein level of TRPV6 and the Na+/Ca2+‐exchanger (NCX1). • Furthermore, VDR knockdown results in a decrease in intracellular Ca2+ concentration ([Ca2+]i) in NRK cell lines. CONCLUSIONS • Our study shows that VDR can positively regulate the mRNA and protein expression of TRPV5, calbindin‐D28k and PMCA1b, but not of TRPV6 or NCX1, in NRK cell lines. VDR knockdown results in a decrease in [Ca2+]i in NRK cell lines. • The effect of the elevated VDR level in the kidney on hypercalciuria and the mechanisms underlying need to be further addressed.

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