Enhanced dietary Ca intake linearly increases intestinal Ca absorption in pigs, but not in broilers, suggesting potential differences in whole body Ca homeostasis. To determine the role of kidney in Ca homeostasis in these species, we varied in growing pigs in experiment (Exp) 1, the dietary Ca content 2·0 v. 9·6 g/kg and phytase 0 v. 500 FTU/kg, in broilers, in Exp 2 the dietary Ca/retainable P from 1·3 to 2·8 and phytase 0 v. 1000 FTU/kg, and in Exp 3 dietary Ca/P from 0·50 to 1·75. Increasing dietary Ca reduced renal mRNA expression of Ca-related transporters (TRPV5, TRPV6, CaBP-D28k and NCX1) and tight junctions (CLDN-12 and −16) in pigs, indicating Ca reabsorption was reduced to maintain Ca homeostasis. In broilers (Exp 2), high dietary Ca increased renal TRPV6, CaBP-D28k and CLDN-2 mRNA, indicating an increased capacity for Ca reabsorption. Moreover, the effect of dietary Ca was enhanced by inclusion of dietary phytase in pigs but reduced in broilers. Furthermore, increasing dietary Ca upregulated inorganic phosphate transporter 1 (PiT-1), while phytase downregulated xenotropic and polytropic retrovirus receptor 1 (XPR1) mRNA expression in pigs; in broilers, dietary Ca downregulated renal mRNA expression of Na-dependent phosphate transporter IIa (NaPi-IIa), PiT-1, PiT-2 and XPR1, while phytase downregulated NaPi-IIa but upregulated PiT-2 and XPR1 mRNA expression. In Exp 3, Ca/P effect on transporter mRNA expression was largely consistent with Exp 2. In conclusion of this study, together with previously measured data about Ca and P homeostasis, in pigs the kidneys play a more regulatory role in Ca homeostasis than in broilers where the intestine is more important for regulation.

Kidney failure is a major killer. Many lives could be saved through organ donation if people were less reluctant to part with their spare kidney. Should we incentive donation by paying people to do it?

Zearalenone (ZEA), a common contaminant in food and feedstuffs, threatens human and animal health. The present study aimed to investigate the protective effects of modified palygorskite (MPal), a ZEA-targeted adsorbent, on broilers (young chickens) fed a ZEA-contaminated diet. Broilers were subjected to one of three treatments for a period of 42 days: a basal diet (control group), a ZEA- contaminated diet, and a ZEA-contaminated diet supplemented with 1 g/kg of MPal. Blood was collected for serum metabolite assay, and liver and kidney were sampled to determine ZEA residue and antioxidant-related parameters, using commercial spectrophotometric kits. Compared with the basal diet, the ZEA- contaminated diet resulted in compromised growth performance (reduced daily gain and feed intake during finisher period), disordered relative liver weight (decreased at 21 days but increased at 42 days), increased ZEA residue in liver and kidney, abnormal serum metabolites (decreased total protein content but increased alanine aminotransferase activity at 21 and 42 days, reduced albumin content at 21 days, and elevated aspartate aminotransferase activity at 42 days), and disrupted antioxidant capacities of broilers (increased total superoxide dismutase (T-SOD) activity in liver at 21 and 42 days, decreased T-SOD activity in kidney at 21 and 42 days, and in serum at 42 days, greater malondialdehyde accumulation in liver and kidney at 42 days, and lower glutathione content in kidney at 21 days). The adverse consequences resulting from the ZEA-contaminated diet were relieved by the supplementation of MPal (except albumin concentration in serum and T-SOD activity in liver at 21 days), with the values of growth-performance parameters, liver weight, renal ZEA accumulation, total protein content, transaminase activity at 42 days, and antioxidant indexes being similar to those in the control group. These results suggested that MPal supplementation could promote growth performance, attenuate liver damage, and improve the antioxidant abilities of broilers fed ZEA-contaminated diet by reducing ZEA accumulation.

Methotrexate (MTX) is a cytotoxic immunosuppressant that is widely used in the treatment of tumours, rheumatoid arthritis and psoriasis. This study aims to evaluate the effects of whey proteins on MTX-induced liver and kidney damage by focusing on oxidant–antioxidant systems and eating habits. The study was conducted in four groups of thirty Sprague–Dawley rats (control, control + whey protein concentrate (WPC), MTX, MTX + WPC). A single dose of 20 mg/kg MTX was administered intraperitoneally to the MTX groups. Control and MTX groups were given 2 g/kg WPC by oral gavage every day for 10 d. At the end of day 10, blood samples were drawn and liver and kidney tissues were removed. MTX administration increased the lipid peroxidation level and decreased glutathione level, superoxide dismutase and glutathione-S-transferase activities in the liver and kidney. Administration of WPC significantly reduced the damage caused by MTX in the liver and kidney. While a decrease in serum urea level and an increase in serum creatinine level were detected in the MTX group, WPC administration reversed these results up to control group levels. Administration of WPC to the MTX group significantly reversed the histopathological damage scores of the liver and kidney. WPC administration ameliorated the MTX-induced oxidative damage in the liver and kidney tissues due to its antioxidant properties. Liver and kidney damage can be prevented by using whey proteins as a nutraceutical in MTX therapy. In conclusion, whey proteins demonstrated a protective effect against MTX-induced liver and kidney damage.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the novel global coronavirus disease 2019 (COVID-19) disease outbreak. Its pathogenesis is mostly located in the respiratory tract. However, other organs are also affected. Hence, realising how such a complex disturbance affects patients after recovery is crucial. Regarding the significance of control of COVID-19-related complications after recovery, the current study was designed to review the cellular and molecular mechanisms linking COVID-19 to significant long-term signs including renal and cardiac complications, cutaneous and neurological manifestations, as well as blood coagulation disorders. This virus can directly influence on the cells through Angiotensin converting enzyme 2 (ACE-2) to induce cytokine storm. Acute release of Interleukin-1 (IL1), IL6 and plasminogen activator inhibitor 1 (PAI-1) have been related to elevating risk of heart failure. Also, inflammatory cytokines like IL-8 and Tumour necrosis factor-α cause the secretion of von Willebrand factor (VWF) from human endothelial cells and then VWF binds to Neutrophil extracellular traps to induce thrombosis. On the other hand, the virus can damage the blood–brain barrier by increasing its permeability and subsequently enters into the central nervous system and the systemic circulation. Furthermore, SARS-induced ACE2-deficiency decreases [des-Arg9]-bradykinin (desArg9-BK) degradation in kidneys to induce inflammation, thrombotic problems, fibrosis and necrosis. Notably, the angiotensin II-angiotensin II type 1 receptor binding causes an increase in aldosterone and mineralocorticoid receptors on the surface of dendritic cells cells, leading to recalling macrophage and monocyte into inflammatory sites of skin. In conclusions, all the pathways play a key role in the pathogenesis of these disturbances. Nevertheless, more investigations are necessary to determine more pathogenetic mechanisms of the virus.

In the following interview, philosophers Leonard Fleck and Arthur Ward discuss the latter’s recent experience of being a nondirected kidney donor. The interview took place in the Center for Bioethics and Social Justice at Michigan State University.

Despite the apparent beneficial effects of probiotics/synbiotics on glucose haemostasis, lipid profile and inflammatory responses, it is not clear whether these beneficial effects also impact renal and hepatic function in diabetes. Therefore, we sought to assess the effect of probiotics/synbiotics supplementation on renal and liver biomarkers in adults with type 2 diabetes mellitus (T2DM) using a systematic review and meta-analysis of randomised controlled trials (RCT). PubMed, Scopus, Web of Science and Cochrane Library were systematically searched, up to February 2021. The pooled weighted mean difference (WMD) was estimated using a random-effects model. The methodological quality of studies, as well as certainty of evidence, was assessed using standard scales. Fifteen related trials were identified. Meta-analysis of six trials, involving 426 participants, indicated that probiotics/synbiotics supplementation reduced serum levels of creatinine (WMD = −0·10 mg/dl, 95 % CI −0·20, −0·00; P = 0·01; I 2 = 87·7 %; P-heterogeneity < 0·001), without any significant effect on blood urea nitrogen (BUN), glomerular filtration rate or microalbuminuria. No significant improvement was found on liver biomarkers following probiotics/synbiotics supplementation. The subgroup analysis showed a significant improvement in BUN when follow-up duration lasted for 12 weeks or more (WMD = −1·215 mg/dl, 95 % CI −1·933, −0·496; P = 0·001) and in creatinine levels in patients with renal dysfunction (WMD = −0·209 mg/dl, 95 % CI −0·322, −0·096; P < 0·001). Our results are insufficient to advocate the use of probiotics/synbiotics for improving renal or liver function in patients with T2DM. Indeed, due to the low certainty of evidence, these findings need to be affirmed in further high-quality RCT.

Tramadol is used worldwide and is listed in many medical guidelines to treat both acute and chronic pains. There is a growing evidence of abuse of tramadol in some African and West Asian countries. Tramadol has some side effects. The present study designed to follow up the treatment of the cellular responses which might be induced in the kidney of tramadol mice. Treated mice received daily injection of tramadol dose (125 μg/100 g b.wt) for 20 and 40 days. Other mice received tramadol for 40 days and then were divided into three groups: the first received distilled water, the second received Lagenaria siceraria, and the third received melatonin daily for 40 days. Both the daily injection of tramadol for 20 and 40 days resulted in radical, extensive, and severe alterations in the normal histological architecture of the kidney. Treatment with Lagenaria siceraria or melatonin after tramadol administration for a long-term, markedly changed the collagen content and other chemical components, that may reach nearly normal levels. Such findings propose that although tramadol has many cytological and histopathological side effects on the kidneys of male mice, the treatments via Lagenaria siceraria and melatonin have effective therapeutic impacts on the tramadol side effects.

Intrauterine growth restriction (IUGR) due to uteroplacental insufficiency results in a placenta that is unable to provide adequate nutrients and oxygen to the fetus. These growth-restricted babies have an increased risk of hypertension and chronic kidney disease later in life. In rats, both male and female growth-restricted offspring have nephron deficits but only males develop kidney dysfunction and high blood pressure. In addition, there is transgenerational transmission of nephron deficits and hypertension risk. Therefore, epigenetic mechanisms may explain the sex-specific programming and multigenerational transmission of IUGR-related phenotypes. Expression of DNA methyltransferases (Dnmt1and Dnmt3a) and imprinted genes (Peg3, Snrpn, Kcnq1, and Cdkn1c) were investigated in kidney tissues of sham and IUGR rats in F1 (embryonic day 20 (E20) and postnatal day 1 (PN1)) and F2 (6 and 12 months of age, paternal and maternal lines) generations (n = 6–13/group). In comparison to sham offspring, F1 IUGR rats had a 19% decrease in Dnmt3a expression at E20 (P < 0.05), with decreased Cdkn1c (19%, P < 0.05) and increased Kcnq1 (1.6-fold, P < 0.01) at PN1. There was a sex-specific difference in Cdkn1c and Snrpn expression at E20, with 29% and 34% higher expression in IUGR males compared to females, respectively (P < 0.05). Peg3 sex-specific expression was lost in the F2 IUGR offspring, only in the maternal line. These findings suggest that epigenetic mechanisms may be altered in renal embryonic and/or fetal development in growth-restricted offspring, which could alter kidney function, predisposing these offspring to kidney disease later in life.

Concurrent three-dimensional imaging of the renal vascular and tubular systems on the whole-kidney scale with capillary level resolution is labor-intensive and technically difficult. Approaches based on vascular corrosion casting and X-ray micro computed tomography (μCT), for example, suffer from vascular filling artifacts and necessitate imaging with an additional modality to acquire tubules. In this work, we report on a new sample preparation, image acquisition, and quantification protocol for simultaneous vascular and tubular μCT imaging of whole, uncorroded mouse kidneys. The protocol consists of vascular perfusion with the water-soluble, aldehyde-fixable, polymeric X-ray contrast agent XlinCA, followed by laboratory-source μCT imaging and structural analysis using the freely available Fiji/ImageJ software. We achieved consistent filling of the entire capillary bed and staining of the tubules in the cortex and outer medulla. After imaging at isotropic voxel sizes of 3.3 and 4.4 μm, we segmented vascular and tubular systems and quantified luminal volumes, surface areas, diffusion distances, and vessel path lengths. This protocol permits the analysis of vascular and tubular parameters with higher reliability than vascular corrosion casting, less labor than serial sectioning and leaves tissue intact for subsequent histological examination with light and electron microscopy.

Disasters occur regularly, and frequently large numbers of patients treated with maintenance dialysis or with the recent onset of acute kidney injury are put at risk owing to the lack of access to dialysis care precipitating also a kidney failure disaster. The absence of necessary dialysis treatments can result in excessive emergency department visits, hospitalizations, morbidity, or an early death. Those with kidney failure are often evaluated in disaster medical locations or hospitals without nephrologists in attendance. Here we offer guidance for medical personnel evaluating such patients so that dialysis-dependent individuals can be properly assessed and managed with the need for urgent dialysis recognized. A disaster dialysis triage system is proposed. (Disaster Med Public Health Preparedness. 2019;13:782–790)