Renal Tubular Lumen Research Articles

Evaluation of in-vitro anti-urolithiatic activity of ethanolic extract of sterculia urens

All individuals have traditionally considered medicinal plants as a healthy source of life, and its therapeutic characteristics have proven to be quite effective in treating a wide range of illnesses. Another benefit of using medicinal plants is that they are completely natural. Since ancient times, people have utilized traditionally to treat common infectious disorders, and the belief that some plants possessed therapeutic properties was widely recognized even before mankind discovered there were microorganisms. Due to their antibacterial qualities, several plants have been utilised in traditional medicine for a long time. The therapeutic benefit of these plants is specifically found in a few chemical compounds that have a clear physiological effect on the human or animal body. Alkaloids, flavonoids, tannins, and phenolic compounds are among these bioactive ingredients, which are primarily secondary metabolites, that are most significant. Cells of microorganisms are poisoned by these phytochemicals. Individuals with Nephrolithiasis or kidney stone disease, is a condition that accumulate calculi (stones) within the renal pelvis and tubular lumens. Stones are formed when crystals precipitate (separate) from urine. When the urine concentration of compounds that help prevent stone formation (citrate) is low or when that of substances that help create crystals (calcium, oxalate, and uric acid) is high, stones may form. Current research aims for assessment of the invitro anti urolithiatic activity of Sterculia urens by employing the method such as nucleation assay Our study indicates that, sterculia urens can be a great source of antiurolithiatic agents, which are most likely mediated by the suppression of CaOx crystallization.

Effect of Oral Administration of 3-Methylmorphine (Codeine) Induced Renal Toxicity in Adult Wistar Albino

Codeine (3-Methylmorphine) is the most common opiate consumed worldwide, it is widely used for its analgesic, antitussive and antidiarrheal activities. The study aims to determine the effect of oral administration of codeine induced renal toxicity in adult Wistar Albino Rats. Twenty albino rats weighing between 150-200g were used. Animals were divided into 4 groups (A, B, C and D). Group A served as the control group. Group B received 30mg/kg, group C received 60mg/kg and group D received 90mg/kg codeine orally for 28 days. Data obtained were calculated for one-way analysis of variance (ANOVA), followed by a Post Hoc test. Results were expressed as mean ± standard error of the mean. Statement of differences was based on significance level at p<0.05. The results showed a slight decrease in the mean values of Na+ , Cl- , and HCO3 – levels which are not significant, while K+ level showed an increase in group B and C followed by a decrease in group D which were not statistically significant (p<0.05). Creatinine level did not show any variation when compared with the control group but there was an increase in urea level which was also not statistically significant at p<0.05. Photomicrographs of rat’s kidneys in the treatment group showed; degeneration of the glomerulus, hydrophobic changes in the renal tubular lumen, fatty tissue, multi-focal interstitial haemorrhages, infiltration of inflammatory lymphoid cells, mild mononuclear cells infiltration in the renal cortex and mass aggregation of lymphoid cells in the cellular medullar when compared to control.

Protective effect and mechanism of Baicalin on acute kidney injury in septic mice

To observe the protective effect and mechanism of different doses of Baicalin (BAI) on acute kidney injury (AKI) in septic mice. According to the random number table, 100 mice were divided into sham operation group (Sham group), cecal ligation and perforation (CLP) induced sepsis model group (CLP group) and BAI pretreatment groups. The mice in BAI pretreatment groups were divided into low-, medium- and high-dose groups (BAI-L+CLP, BAI-M+CLP, BAI-H+CLP groups), with 20 mice in each group. A murine sepsis associated-acute kidney injury (SA-AKI) model was reproduced using CLP. The mice in the Sham group were only opened and closed the abdomen, without ligating or perforating the cecum. The mice in the BAI pretreatment groups were given BAI 25, 50 and 100 mg/kg daily for 3 days, and CLP was performed at 6 hours after administration of BAI at the 3rd day to reproduce sepsis model. The mice in the Sham group and CLP group were given the same amount of distilled water as control. Ten mice were sacrificed at 24 hours after operation to collect orbital blood for renal function determination [serum creatinine (SCr), blood urea nitrogen (BUN), plasma neutrophil gelatinase-associated lipocalin (pNGAL) and plasma kidney injury molecule-1 (pKIM-1)] by enzyme linked immunosorbent assay (ELISA). The kidney tissue was collected to observe the kidney tissue injury under light microscope after hematoxylin-eosin (HE) staining. The TdT-mediated dUTP nick-end labeling (TUNEL) was used to detect the apoptosis of renal tubular epithelial cells. Western blotting was used to detect the expression of cell FLICE like inhibitory protein (c-FLIP) in renal tissue. The remaining 10 mice in each group were used to calculate the survival rate of 7 days after operation. The renal tubular epithelial cells in the CLP group were massively degenerated with necrosis, the renal tubular lumen was significantly expanded, and inflammatory cells were widely infiltrated in the renal interstitium. Furthermore, the renal function deteriorated rapidly. Compared with the CLP group, the renal function of mice pretreated with low dose of BAI was improved, but the difference was not significant. Compared with the CLP group, the renal function in the mice pretreated with medium and high doses of BAI was significantly improved, the SCr, BUN, pNGAL and pKIM-1 were significantly reduced [SCr (μmol/L): 135.16±5.18, 125.70±5.26 vs. 170.42±5.42; BUN (mmol/L): 33.59±1.77, 27.29±1.61 vs. 45.68±1.39; pNGAL (μg/L): 91.29±4.68, 73.40±3.77 vs. 131.50±6.55; pKIM-1 (μg/L): 6.34±0.30, 5.51±0.35 vs. 8.03±0.29; all P < 0.01], the pathological injury of renal tissue was significantly decreased, the apoptotic number of renal tubular epithelial cells was significantly reduced (cells/HP: 16.20±0.49, 13.10±0.66 vs. 29.60±0.49, both P < 0.01), and the expression of c-FLIP protein in renal tissue was significantly increased [c-FLIP protein (c-FLIP/GAPDH): 0.35±0.02, 0.46±0.02 vs. 0.21±0.01, both P < 0.01]. No mouse in the Sham group died within 7 days. Compared with the CLP group, the average survival time of the mice within 7 days in the BAI-L+CLP, BAI-M+CLP and BAI-H+CLP groups was significantly prolonged with a dose-dependent manner (days: 3.5±2.5, 5.4±2.2, 5.9±1.9 vs. 2.1±1.2; Log-Rank test: χ2 = 73.410, P < 0.001). Pretreatment with medium and high doses of BAI can significantly improve the renal function in mice with SA-AKI, decrease the pathological damage and increase the survival of mice, and its mechanism may be related to promoting the increase of c-FLIP protein expression and inhibiting cell apoptosis.

Short-time Effects of Malathion Pesticide on Functional and Histological Changes of Liver and Kidney in Female Mice.

The malathion is one of the most important organophosphorus pesticides used in Iraq. The present study was designed to investigate the short-time effects of the malathion on the biochemical parameters of AST, ALT, ALP, urea, creatinine, total cholesterol, triglycerides and total protein as well as histological changes of the liver and kidneys of female laboratory mice for an interval of 6 days. The animals were divided into 3 groups, each group included 8 mice. They were injected with the pesticide in the intraperitoneal region. The 1st group (the control group) was injected with 0.1 mL of distilled water, the 2nd group (the low dose group) was injected with 0.1 mL of the pesticide solution at 3 mg/body weight while the 3rd group (the high dose group) was injected with 0.1 mL of the pesticide solution at a concentration of 6 mg/body weight. The biochemical tests of the liver and kidney showed significant elevation in serum AST, urea, creatinine and cholesterol concentrations in mice compared to control group (p<0.05). In addition, the results showed a significant decrease in the ALP, triglycerides and the total protein in serum of the treated mice. Also, the results of histological sections of the liver and kidneys included congestion, necrosis, degeneration of cytoplasm, blood congestion, apoptosis, bleeding and sloughing of epithelial cells to the renal tubular lumen. Finally, the results indicated that malathion pesticide has the ability to induce hepatic and renal toxicity in mice within 6 days.

Curcumin Prevents Renal Dysfunction, Proteinaceous and Granular Cast Formation in Tubular Lumen in Kidney of Mice Exposed to Formaldehyde Inhalation

Formaldehyde is a volatile chemical compound that is commonly used in the chemical industry. Formaldehyde inhalation exposure has been associated with cancer, respiratory diseases, digestive and neurological disorders. Oxidative stress is one of the potential mechanisms by which formaldehyde inhalation induces toxicity. Curcumin is a natural compound endowed with antioxidant properties and my thus prevent formaldehyde-induced toxicity. This study aimed to examine the effects of formaldehyde inhalation on renal function and kidney structure of mice; the potential protective effects of curcumin administration against kidney dysfunction, renal damage and oxidative stress were also investigated. Formaldehyde inhalation induced renal dysfunction and damage, as shown by the increase of serum creatinine and blood urea nitrogen levels, and caused histological damage associated with proteinaceous and granular cast formation in renal tubular lumen. The activity of antioxidant enzymes remained unchanged and malondialdehyde levels increased in a discrete and statistically non-significant way. Curcumin treatment prevented the above-described alterations by preventing an increase in renal dysfunction and changes in the kidney structure of mice. Therefore, curcumin can be a potentially useful treatment against the effects induced by exposure to gaseous pollutants such as formaldehyde in distal organs.

Temporal changes in urinary excretion of liver-type fatty acid binding protein (L-FABP) in acute kidney injury model of domestic cats: a preliminary study.

Liver-type fatty acid–binding protein (L-FABP) is a biomarker for the early detection of renal diseases in humans. It is secreted along with cytotoxic oxidation products from proximal tubular epithelial cells under conditions of ischemia and/or oxidative stress. This study examined urinary L-FABP excretion under renal ischemia in feline acute kidney injury (AKI) model. L-FABP excretion increased immediately after renal ischemia/reperfusion, despite the absence of obvious structural damage to the kidneys, in the two AKI model cats studied. L-FABP was detected in the renal tubular lumen immediately after renal ischemia/reperfusion in the two cats, but not in a sham surgery cat. These results suggested that high L-FABP excretion is a pathophysiological response associated with antioxidant defense in proximal tubules with renal ischemia and/or oxidative stress in a feline model.

Functional roles of Grainyhead-like transcription factors in renal development and disease.

Proper renal function relies on the tightly regulated development of nephrons and collecting ducts. This process, known as tubulogenesis, involves dynamic cellular and molecular changes that instruct cells to form highly organized tubes of epithelial cells which compartmentalize the renal interstitium and tubular lumen via assembly of a selective barrier. The integrity and diversity of the various renal epithelia is achieved via formation of intercellular protein complexes along the apical-basal axis of the epithelial cells. In recent years, the evolutionarily conserved family of Grainyhead-like (GRHL) transcription factors which encompasses three mammalian family members (Grainyhead-like 1, 2, 3) has emerged as a group of critical regulators for organ development, epithelial differentiation, and barrier formation. Evidence from transgenic animal models supports the presence of Grainyhead-like-dependent transcriptional mechanisms that promote formation and maintenance of epithelial barriers in the kidney. In this review, we highlight different Grhl-dependent mechanisms that modulate epithelial differentiation in the kidney. Additionally, we discuss how disruptions in these mechanisms result in impaired renal function later in life.

Multidrug resistance protein 4 (MRP4) is expressed as transcript variants in both Gallus domesticus and Gyps himalyanesis

The non-steroidal anti-inflammatory drug (NSAID) diclofenac, known to cause hyperuricemia and concomitant visceral gout in Gyps vultures is suggested to be a result of interference with renal uric acid excretion. Three species of Gyps vultures are on the verge of extinction due to nephrotoxic veterinary diclofenac having entered the food chain, notwithstanding the fact that the toxicity of different avian species to the NSAIDs like diclofenac varies. The multidrug resistance protein 4 (MRP4), an organic anion transporter in birds has unique role in unidirectional efflux of urate into proximal renal tubular lumen for excretion and maintenance of homeostasis. We characterized MRP4 channel at molecular level to predict its structural based ligand binding activity in Gallus domesticus (Indian domestic chicken) and Gyps himalayensis (Himalayan griffon vulture). MRP4 gene was amplified using reverse transcribed cDNA from renal tissue sample in overlapping fragments. The obtained amplicons were cloned, sequenced, assembled and analyzed. Multiple alignment and blast analysis revealed point variations and presence of additional stretch of 57 bp towards the 3′ end which was confirmed in Real time PCR. Predicted MRP4 polypeptides revealed presence of characteristic 12 transmembrane helices (TMH) with two nucleotide binding domains (NBD). Additional 19 amino acids in transcript variant was found to be localized in NBD2 that might influence the transporter function. The homology modeling and pocket identification throws ample light on varying transport efficacy and paves the way for depicting its role of these amino acids in effect of diclofenac on urate transport in further studies.

The Relationship between the Intrarenal Dopamine System and Intrarenal Renin-angiotensin System Depending on the Renal Function

Objective The mechanisms underlying the intrarenal renin-angiotensin system (RAS) activation depend on the conditions of kidney diseases. In angiotensin II (AngII) infusion models, the circulating AngII is filtered into the renal tubular lumens, activating intrarenal RAS. However, in the chronic kidney disease (CKD) models, plasma angiotensinogen (AGT) is filtered into the tubular lumens because of glomerular injury, activating intrarenal RAS. The intrarenal dopamine system activation reduces intrarenal AGT expression and suppresses the intrarenal RAS activity in AngII infusion models. However, the relationship between the intrarenal dopamine system and intrarenal RAS has not been elucidated. Therefore, this study was conducted to determine that relationship in CKD patients. Methods We recruited 46 CKD patients (age: 51.1±20.0 years; 16 men; causes of CKD: chronic glomerulonephritis, 34; diabetic nephropathy, 2; nephrosclerosis, 4; and others, 6) not undergoing dialysis or taking RAS blockers. The urinary dopamine (U-DOPA) level, an indicator of intrarenal dopamine activity, and the urinary AGT (U-AGT) level, a surrogate marker of intrarenal RAS activity, were measured. Results As the CKD stages progressed, the U-DOPA levels decreased while the U-AGT levels increased. The U-DOPA levels were significantly and negatively correlated with the U-AGT levels but significantly and positively correlated with the estimated glomerular filtration rate (eGFR). A multiple regression analysis revealed that the U-DOPA levels were associated with the U-AGT levels after adjusting for age, sex, body mass index, and blood pressure (β=-0.38, p=0.045). However, no correlation was observed when eGFR was also adjusted (β=-0.17, p=0.29). Conclusion The negative correlation between the intrarenal dopamine system and intrarenal RAS in CKD patients may be affected by the renal function.

Kidney stone formers have more renal parenchymal crystals than non-stone formers, particularly in the papilla region

BackgroundWe investigated the renoprotective ability of healthy people against kidney stone formation. To clarify intratubular crystal kinetics and processing in human kidneys, we performed a quantitative and morphological observation of nephrectomized renal parenchyma tissues.MethodsClinical data and pathological samples from 60 patients who underwent radical nephrectomy for renal cancer were collected from June 2004 to June 2010. The patients were retrospectively classified as stone formers (SFs; n = 30, kidney stones detected by preoperative computed tomography) and non-stone formers (NSFs; n = 30, no kidney stone history). The morphology of parenchymal intratubular crystals and kidney stone-related gene and protein expression levels were examined in noncancerous renal sections from both groups.ResultsSFs had a higher smoking rate (P = 0.0097); lower red blood cell, hemoglobin, and hematocrit values; and higher urinary red blood cell, white blood cell, and bacterial counts than NSFs. Scanning electron microscopy revealed calcium-containing crystal deposits and crystal attachment to the renal tubular lumen in both groups. Both groups demonstrated crystal transmigration from the tubular lumen to the interstitium. The crystal diffusion analysis indicated a significantly higher crystal existing ratio in the medulla and papilla of SFs and a significantly higher number of papillary crystal deposits in SFs than NSFs. The expression analysis indicated relatively high osteopontin and CD68, low superoxide dismutase, and significantly lower Tamm–Horsfall protein expression levels in SFs. Multivariate logistic regression analysis involving the above factors found the presence of renal papillary crystals as a significant independent factor related to SFs (odds ratio 5.55, 95% confidence interval 1.08–37.18, P = 0.0395).ConclusionsRegardless of stone formation, intratubular crystals in the renal parenchyma seem to transmigrate to the interstitium. SFs may have reduced ability to eliminate renal parenchymal crystals, particularly those in the papilla region, than NSFs with associated gene expression profiles.

Mori cortex prevents kidney damage through inhibiting expression of inflammatory factors in the glomerulus in streptozocin-induced diabetic rats.

Objective(s):It has been widely reported that Mori cortex extract (MCE) is used for the treatment of diabetes mellitus in traditional medicine. The present study was designed to investigate its mechanism of action in the treatment of diabetic nephropathy (DN). We assessed whether MCE preventive treatment ameliorates kidney damage in high-fat diet and streptozotocin (STZ)-induced type 2 diabetic rats.Materials and Methods:Rats were fed a high-fat diet and injected with STZ. MCE was given to rats daily at 10 g/kg. Fasting blood glucose (FBG) and postprandial plasma glucose were measured. Blood and urine biochemical parameters, renal tissue morphology, and inflammation were investigated.Results:Prevention with MCE significantly decreased FBG and homoeostasis model assessment (HOMA) of IR (HOMA-IR) levels and increased insulin levels in diabetic rats. MCE prevention significantly decreased levels of KW/BW, BUN, Cr, and 24 hr urinary protein. MCE inhibited glomerular basement membrane thickening, tubular epithelial cell hypertrophy, and glomerular capillary dilation. MCE also prevented the disappearance of bowman’s space and renal tubular lumen and decreased collagen deposition in rat kidney. Moreover, MCE reduced the levels of inflammatory factors (MCP-1 and TNF-α) and fibrosis factors (collagen IV and fibronectin).Conclusion:MCE prevents DN through inhibition of inflammation and fibrosis in a rat model. It might provide a safe and effective way to prevent DN.

Histopathological and biochemical evaluations of the kidney inbroiler chickens under acute heat stress conditions.

The purpose of the present study was to investigate the correlation between acute heat stress and relevant histopathology and biochemical parameters of kidney function. A total of 80 healthy Arbor Acer (AA) broiler chickens were randomly divided into two groups: CT (Control Temperature; 22±1°C) group and HT (High Temperature; 38±1°C) group. Histopathological images revealed alteration in kidney (renal tubular lumen dilation with tubular necrosis, especially after 10h of heat stress) of broiler chickens in HT group leading to disturbance of acid base balance. Blood urea nitrogen (BUN) and creatinine (CREA) as serum markers of renal dysfunction were elevated significantly (p less than 0.05) after 5h, and especially, after 10h of heat stress (p less than 0.01) as compared with CT group. These results indicated that the evaluation of morphological and functional parameters in kidney is required, in order to monitor broiler chickens exposed to heat stress.

A Review of the Efficacy and Safety of Sodium-Glucose Cotransporter 2 Inhibitors: A Focus on Diabetic Ketoacidosis.

Diabetes is a complex, chronic medical condition affecting 29.1 million people in the United States (9.3% of the population) and is projected to affect one in three Americans by 2050 if the current trend continues (1). Diabetes management can be challenging, often requiring multiple therapeutic agents as the disease progresses. Current guidelines recommend metformin as first-line pharmacological therapy for the treatment of type 2 diabetes. Multiple second-line options are available for patients whose A1C goal is not achieved with monotherapy, and selection should be based on patient- and drug-specific factors. Sodium–glucose cotransporter 2 (SGLT2) inhibitors, the newest U.S. Food and Drug Administration (FDA)–approved oral antidiabetic agents, are among these options for patients with type 2 diabetes. Canagliflozin, dapagliflozin, and empagliflozin are the currently available SGLT2 inhibitors in the United States (2,3). Sodium–glucose cotransporter 1 (SGLT1) is predominantly located in the small intestine, but is also expressed in the kidneys, trachea, heart, and colon (4,5). In the kidneys, SGLT1 is primarily located in the S3 segment of the proximal convoluted tubule (PCT) (4). SGLT2 is expressed in the kidneys and primarily located in the S1 and S2 segments of the PCT (4,5). In normoglycemic adults, about 180 g of glucose (Figure 1) is filtered per day in the glomerulus, and most is reabsorbed (4,6). In people with diabetes, reabsorption of glucose is increased compared to people without diabetes (7,8). SGLT1 and SGLT2 are located in the apical membrane and facilitate the transport of glucose with sodium from the renal tubular lumen into the cells (Figure 2) (4). FIGURE 1. Structures of glucose, phlorizin, canagliflozin, dapagliflozin, and empagliflozin. FIGURE 2. Cotransport of glucose and sodium by SGLT1 and SGLT2 in the PCT. Phlorizin (Figure 1), an O -glucose derivative/ O -glycoside, was discovered in …

Preventing and Managing Toxicities of High-Dose Methotrexate.

High-dose methotrexate (HDMTX), defined as a dose higher than 500 mg/m2, is used for a range of cancers. Although HDMTX is safely administered to most patients, it can cause significant toxicity, including acute kidney injury (AKI), attributable to crystallization of methotrexate in the renal tubular lumen, leading to tubular toxicity. When AKI occurs despite preventive strategies, increased hydration, high-dose leucovorin, and glucarpidase allow renal recovery without the need for dialysis. This article, based on a review of the current associated literature, provides comprehensive recommendations for prevention of toxicity and, when necessary, detailed treatment guidance to mitigate AKI and subsequent toxicity.

MP58-13 THE MECHANISM OF RENAL STONE FORMATION AND RENAL FAILURE INDUCED BY MELAMINE AND CYANURIC ACID; LONG-TERM EXPERIMENT RESULTS

You have accessJournal of UrologyStone Disease: Basic Research & Pathophysiology I1 Apr 2016MP58-13 THE MECHANISM OF RENAL STONE FORMATION AND RENAL FAILURE INDUCED BY MELAMINE AND CYANURIC ACID; LONG-TERM EXPERIMENT RESULTS Takahiro Kobayashi, Atsushi Okada, Ryossuke Ando, Keiichi Tozawa, Kenjiro Kohri, and Takahiro Yasui Takahiro KobayashiTakahiro Kobayashi More articles by this author , Atsushi OkadaAtsushi Okada More articles by this author , Ryossuke AndoRyossuke Ando More articles by this author , Keiichi TozawaKeiichi Tozawa More articles by this author , Kenjiro KohriKenjiro Kohri More articles by this author , and Takahiro YasuiTakahiro Yasui More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.811AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Recently, cases of renal stones and acute renal failure have been increasingly reported among Chinese children who were fed infant formula contaminated with melamine. According to a 2008 World Health Organization report, of the 294,000 babies identified after drinking melamine-contaminated milk, 51,900 were hospitalized, and 6 died from renal failure. We investigated the mechanism by which melamine and cyanuric acid induce renal stone formation and renal failure in animal models. METHODS Ten-week-old F344 rats were administered both melamine and cyanuric acid (each at 6, 12, 18, 24, 36, 48, 60 mg/kg/day). Blood, 24-h urine samples, and kidney sections were evaluated on days 14, 28, and 90. Resected kidney specimens were stained with hematoxylin and eosin (HE), Oil Red O (ORO) stain for lipid and plastics, and Von Kossa stain for phosphates, carbonates, and oxalates of calcium. For each rat, one kidney was processed for optical microscopy, while the other was processed for Scanning Electron Microscope. RESULTS Serum and urine biochemistry showed no significant differences in serum creatinine levels at doses of 6 and 12 mg/kg/day. Higher doses were associated with serum creatinine levels higher than those of control group. In rats given 6 mg/kg/day melamine/cyanuric acid combination, crystals were not detected, but body weight was lost. Crystal formation was observed in the renal distal tubular lumens and collecting ducts of rats administered 12 mg/kg/day melamine/cyanuric acid, with crystal numbers increasing along the experimental course. In rats administered over 24 mg/kg/day melamine/cyanuric acid combination (24–60 mg/kg/day), crystals were found in the proximal tubular lumens of the renal cortexes on day 3, and acute renal failure resulted in death by day 28. The upper regions of occluded tubes were expanded and the epithelium was thin.(Fig.1) There were some crystals on the surface of the renal papilla of the same form as those found in the renal tubular lumens. CONCLUSIONS Melamine and cyanuric acid in combination, but not melamine alone, induced crystal formation and affected renal function. Renal failure due to melamine cyanurate crystals appears to occur via tubular occlusion. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e781 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Takahiro Kobayashi More articles by this author Atsushi Okada More articles by this author Ryossuke Ando More articles by this author Keiichi Tozawa More articles by this author Kenjiro Kohri More articles by this author Takahiro Yasui More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Histopathological and biochemical changes in the liver, kidney, and bloodof amphibians intoxicated with cadmium

The worldwide decline in amphibian populations has made heavy metal pollution a subject of interest. The aim of this work was to analyze the effect of sublethal doses of cadmium (Cd) on the liver, kidney, and blood of Rhinella arenarum specimens. Serum markers indicative of hepatic injury (gamma glutamyltransferase, alkaline phosphatase, pseudo cholinesterase, and total cholesterol) and markers of renal dysfunction (blood urea nitrogen, serum creatinine, calcium, and glucose) showed variation in animals treated with a 0.5 mg/kg dose compared to controls. Histopathological images revealed alterations in the liver (hepatocyte ballooning and hyperplasia of Kupffer cells) and kidney (renal tubular lumen dilation with tubular necrosis) of animals with abnormal serum markers. The above-mentioned lesions were more evident with the 5 mg/kg dose. With the 0.5 mg/kg dose, hematological values remained normal with the exception of the leukocyte formula. Animals treated with 5 mg/kg showed a significant decrease in both white and red blood cell counts and hematocrit and hemoglobin values. Differential leukocyte counts showed neutrophilia, monocytosis, and lymphopenia. Morphological aberrations were found in white and red blood cells. Results indicated that the evaluation of morphological and functional parameters in kidney, liver, and blood is required in order to monitor amphibian populations exposed to chemical contaminants.

Protective effect of Angelica sinensis polysaccharides on subacute renal damages induced by D-galactose in mice and its mechanism

To explore the protective effect of Angelica sinensis polysaccharides(ASP) on subacute renal damages induced by D-galactose in mice and its mechanism. Male C57BL/6J mice were randomly divided into 3 groups, with 10 mice in each group. The D-galactose model group was subcutaneously injected with D-galactose (120 mg x kg(-1)), qd x 42; the ASP + D-galactose model group was intraperitoneally injected with ASP since the 8th day of the replication of the D-galactose model, qd x 35; and the normal control group was subcutaneously injected with saline at the same dose and time. On the 2nd day of after the injection, the peripheral blood was collected to measure the content of BUN, Crea, UA, Cys-C; paraffin sections were made to observe the renal histomorphology by HE staining; senescence-associated β-g-alactosidase (SA-β-Gal) stain was used to observe the relative optical density (ROD) in renal tissues; transmission electron microscopy was assayed to observe the renal ultrastructure; the renal tissue homogenate was prepared to measure the content of SOD, GSH-PX, MDA; the content of AGEs and 8-OH-dG were measured by ELISA. According to the result, compared with the D-galactose model group, the ASP + D-galactose model group showed obviously decreases in the content of BUN, Crea, UA, Cysc, AGES, 8-OH-dG, the number of hardening renal corpuscle, renal capsular space and renal tubular lumen, ROD of SA-β-Gal staining positive kidney cells, mesangial cells, basement membrane thickness, podocyte secondary processes fusion and MDA and increases in the number of normal renal corpuscle, ribosome and rough endoplasmic reticulum in podocytes, the activity of SOD and GSH-PX. In Conclusion, A. sinensis polysaccharides can antagonize kidney subacute damages induced by D-galactose in mice. Its protective mechanism may be correlated with the inhibition of the oxidative stress injury.

Oxalate nephropathy in free-living American bullfrog tadpoles.

In February 2014, wild American bullfrog Lithobates catesbeianus tadpoles from an artificial pond in the Kyusyu region, Japan, presented with coelomic and subcutaneous edema and erythema within the skin. A pathological examination of 57 tadpoles of American bullfrogs in the region was conducted to evaluate the disease. Crystal deposition of varying degrees was found in the kidneys of 35 tadpoles (61.4%). The crystals were transparent, pleomorphic in shape, highly birefringent in polarized light, and arranged in a radial pattern within the renal tubular lumen. Using Alizarin Red S stain and liquid chromatography, these crystals were identified as calcium oxalate. Severe coelomic and subcutaneous edema was observed in 7 of these 35 tadpoles (20.0%). Ammonia levels in coelomic fluid were extremely elevated (>1000 µg dl(-1)) in 4 tadpoles examined. These findings suggest that oxalate deposition in kidneys causes metabolic disorder with renal nephropathy. The source of the oxalate could not be determined; however, the presence of calcium oxalates in pond sediments, as revealed by liquid chromatography, suggested that the deposition was most likely due to ingestion of oxalate materials from the environment. This is the first report of oxalate nephropathy in free-living amphibians.

Tetracapsuloides bryosalmonae infection affects the expression of genes involved in cellular signal transduction and iron metabolism in the kidney of the brown trout Salmo trutta.

Tetracapsuloides bryosalmonae is an enigmatic endoparasite which causes proliferative kidney disease in various species of salmonids in Europe and North America. The life cycle of the European strain of T. bryosalmonae generally completes in an invertebrate host freshwater bryozoan and vertebrate host brown trout (Salmo trutta) Linnaeus, 1758. Little is known about the gene expression in the kidney of brown trout during the developmental stages of T. bryosalmonae. In the present study, quantitative real-time PCR was applied to quantify the target genes of interest in the kidney of brown trout at different time points of T. bryosalmonae development. PCR primers specific for target genes were designed and optimized, and their gene expression levels were quantified in the cDNA kidney samples using SYBR Green Supermix. Expression of Rab GDP dissociation inhibitor beta, integral membrane protein 2B, NADH dehydrogenase 1 beta subcomplex subunit 6, and 26S protease regulatory subunit S10B were upregulated significantly in infected brown trout, while the expression of the ferritin M middle subunit was downregulated significantly. These results suggest that host genes involved in cellular signal transduction, proteasomal activities, including membrane transporters and cellular iron storage, are differentially upregulated or downregulated in the kidney of brown trout during parasite development. The gene expression pattern of infected renal tissue may support the development of intraluminal sporogonic stages of T. bryosalmonae in the renal tubular lumen of brown trout which may facilitate the release of viable parasite spores to transmit to the invertebrate host bryozoan.

Recurrent 2,8-Dihydroxyadenine Nephropathy: A Rare but Preventable Cause of Renal Allograft Failure

Adenine phosphoribosyltransferase (APRT) deficiency is a rare autosomal recessive enzyme defect of purine metabolism that usually manifests as 2,8-dihydroxyadenine (2,8-DHA) nephrolithiasis and more rarely chronic kidney disease. The disease is most often misdiagnosed and can recur in the renal allograft. We analyzed nine patients with recurrent 2,8-DHA crystalline nephropathy, in all of whom the diagnosis had been missed prior to renal transplantation. The diagnosis was established at a median of 5 (range 1.5–312) weeks following the transplant procedure. Patients had delayed graft function (n = 2), acute-on-chronic (n = 5) or acute (n = 1) allograft dysfunction, whereas one patient had normal graft function at the time of diagnosis. Analysis of allograft biopsies showed birefringent 2,8-DHA crystals in renal tubular lumens, within tubular epithelial cells and interstitium. Fourier transformed infrared microscopy confirmed the diagnosis in all cases, which was further supported by 2,8-DHA crystalluria, undetectable erythrocyte APRT enzyme activity, and genetic testing. With allopurinol therapy, the allograft function improved (n = 7), remained stable (n = 1) or worsened (n = 1). At last follow-up, two patients had experienced allograft loss and five had persistent chronic allograft dysfunction. 2,8-DHA nephropathy is a rare but underdiagnosed and preventable disorder that can recur in the renal allograft and may lead to allograft loss.