The Kidneys and Osmoregulatory Organs

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The Kidneys and Osmoregulatory Organs The Kidneys and Osmoregulatory Organs Bởi: OpenStaxCollege Although the kidneys are the major osmoregulatory organ, the skin and lungs also play a role in the process Water and electrolytes are lost through sweat glands in the skin, which helps moisturize and cool the skin surface, while the lungs expel a small amount of water in the form of mucous secretions and via evaporation of water vapor Kidneys: The Main Osmoregulatory Organ The kidneys, illustrated in [link], are a pair of bean-shaped structures that are located just below and posterior to the liver in the peritoneal cavity The adrenal glands sit on top of each kidney and are also called the suprarenal glands Kidneys filter blood and purify it All the blood in the human body is filtered many times a day by the kidneys; these organs use up almost 25 percent of the oxygen absorbed through the lungs to perform this function Oxygen allows the kidney cells to efficiently manufacture chemical energy in the form of ATP through aerobic respiration The filtrate coming out of the kidneys is called urine 1/11 The Kidneys and Osmoregulatory Organs Kidneys filter the blood, producing urine that is stored in the bladder prior to elimination through the urethra (credit: modification of work by NCI) Kidney Structure Externally, the kidneys are surrounded by three layers, illustrated in [link] The outermost layer is a tough connective tissue layer called the renal fascia The second layer is called the perirenal fat capsule, which helps anchor the kidneys in place The third and innermost layer is the renal capsule Internally, the kidney has three regions—an outer cortex, a medulla in the middle, and the renal pelvis in the region called the hilum of the kidney The hilum is the concave part of the bean-shape where blood vessels and nerves enter and exit the kidney; it is also the point of exit for the ureters The renal cortex is granular due to the presence of nephrons—the functional unit of the kidney The medulla consists of multiple pyramidal tissue masses, called the renal pyramids In between the pyramids are spaces called renal columns through which the blood vessels pass The tips of the pyramids, called renal papillae, point toward the renal pelvis There are, on average, eight renal pyramids in each kidney The renal pyramids along with the adjoining cortical region are called the lobes of the kidney The renal pelvis leads to the ureter on the outside of the kidney On the inside of the kidney, the renal pelvis branches out into two or three extensions called the major calyces, which further branch into the minor calyces The ureters are urine-bearing tubes that exit the kidney and empty into the urinary bladder Art Connection 2/11 The Kidneys and Osmoregulatory Organs The internal structure of the kidney is shown (credit: modification of work by NCI) Which of the following statements about the kidney is false? The renal pelvis drains into the ureter The renal pyramids are in the medulla The cortex covers the capsule Nephrons are in the renal cortex Because the kidney filters blood, its network of blood vessels is an important component of its structure and function The arteries, veins, and nerves that supply the kidney enter and exit at the renal hilum Renal blood supply starts with the branching of the aorta into the renal arteries (which are each named based on the region of the kidney they pass through) and ends with the exiting of the renal veins to join the inferior vena cava The renal arteries split into several segmental arteries upon entering the kidneys Each segmental artery splits further into several interlobar arteries and enters the renal columns, which supply the renal lobes The interlobar arteries split at the junction of the renal cortex and medulla to form the arcuate arteries The arcuate “bow shaped” arteries form arcs along the base of the medullary pyramids Cortical radiate arteries, as the name suggests, radiate out from the arcuate arteries The cortical radiate arteries branch into numerous afferent arterioles, and then enter the capillaries supplying the nephrons Veins trace the path of the arteries and have similar names, except there are no segmental veins As mentioned previously, the functional unit of the kidney is the nephron, illustrated in [link] Each kidney is made up of over one million nephrons that dot the renal cortex, giving it a granular appearance when sectioned sagittally There are two types of nephrons—cortical nephrons (85 percent), which are deep in the renal cortex, and juxtamedullary nephrons (15 percent), which lie in the renal cortex close to the renal medulla A nephron consists of three parts—a renal corpuscle, a renal tubule, and the associated capillary network, which originates from the cortical radiate arteries 3/11 The Kidneys and Osmoregulatory Organs Art Connection The nephron is the functional unit of the kidney The glomerulus and convoluted tubules are located in the ...J Occup Health 1998; 40: 264–269 Journal of Occupational Health A Review on the Cadmium Content of Rice, Daily Cadmium Intake, and Accumulation in the Kidneys Tomoyuki KAWADA and Shosuke SUZUKI Department of Public Health, Gunma University School of Medicine, Maebashi, Japan Abstract: A Review on the Cadmium Content of Rice, Daily Cadmium Intake, and Accumulation in the Kidneys: Tomoyuki K AWADA, et al. Department of Public Health, Gunma University School of Medicine—The body burden of cadmium primarily depends on the daily intake of the element in food, and thus the geographical differences in cadmium content in foods and the daily intake of cadmium should be studied. There is a food chain from soil through plant and animal foods to man. Estimation of daily cadmium intake according to the geographical region is important for monitoring environmental cadmium pollution and health effects. In the 1990s, the daily intake of cadmium and accumulation in the kidney were reported. Japanese have a relatively high daily intake of cadmium, although the percentage daily cadmium intake obtained from rice decreased from 50% in 1970 to 34% in 1994. This change is proportional to the change in average rice consumption from 261 g/day in 1970 to 182 g/day in 1994. These changes also indicate a reduced cadmium burden in the past twenty years, from 35–50 µ g/day to 30 µ g/day. The cadmium level in the renal cortex of Japanese is the highest in the world, but the cadmium in the kidney has been decreasing in most Japanese. ( J Occup Health 1998; 40: 264–269 ) Key words: Cadmium in rice, Daily intake of cadmium, Cadmium accumulation in the kidneys, General inhabitants In mammals cadmium is known to accumulate exclusively in the kidneys, and it has a long biological half-life in the human body, ranging from 10 to 33 years 1, 2) . The amount of cadmium that has accumulated in the kidneys is a function of age and/or daily cadmium intake, and the latter is mainly from food, beverages and smoking 2–5) . Cadmium in drinking water and in the atmosphere contributes little Received May 22, 1998; Accepted July 7, 1998 Correspondence to: T. Kawada, Department of Public Health, Gunma University School of Medicine, Showa, Maebashi 371-8511, Japan to the daily intake of cadmium 6) . Man is an element in an ecosystem. The cadmium pathways to man are soil-plant-animal-man and soil-plant- man. Cadmium-rich soil generally results in cadmium- rich food, and geographical differences have been reported in daily cadmium intake and cadmium accumulation in the kidneys 2, 4, 7, 8) . Earlier investigators reported finding that Japanese have the highest renal cadmium levels in the world, followed by rice-eating ethnic groups such as the people of Thailand, Hong Kong and Taiwan, with the lowest levels in people in the United States, Switzerland, India, Nigeria, and Rwanda-Burundi 2, 9) . Data for cadmium concentrations in the human renal cortex range from an average of 10 to 30 µ g/g wet weight for Europeans, Americans and Africans, but from 65 to 115 µ g/g wet weight for Japanese (Table 1) 10–16) . Renal De novo synthesis, uptake and proteolytic processing of lipocalin-type prostaglandin D synthase, b-trace, in the kidneys Nanae Nagata 1 , Ko Fujimori 1,2 , Issey Okazaki 1 , Hiroshi Oda 3 , Naomi Eguchi 1 , Yoshio Uehara 4 and Yoshihiro Urade 1 1 Department of Molecular Behavioral Biology, Osaka Bioscience Institute, Japan 2 Laboratory of Biodefense and Regulation, Osaka University of Pharmaceutical Sciences, Japan 3 Central Research Institute, Maruha Nichiro Holdings, Inc., Ibaraki, Japan 4 Health Service Center, The University of Tokyo, Japan Introduction Lipocalin-type prostaglandin D synthase (L-PGDS; EC 5.3.99.2) catalyzes the isomerization of prostaglan- din H 2 (PGH 2 ), a common precursor of various pro- stanoids, to produce PGD 2 , an endogenous regulator of sleep and pain [1–5]. L-PGDS was originally puri- fied from rat brain [6] and found to be a monomeric Keywords kidney; monoclonal antibody; renal disease; urine; b-trace Correspondence Y. Urade, Department of Molecular Behavioral Biology, Osaka Bioscience Institute, 6-2-4 Furuedai, Suita, Osaka 565-0874, Japan Fax: +81 6 6872 2841 Tel: +81 6 6872 4851 E-mail: uradey@obi.or.jp (Received 12 August 2009, revised 29 September 2009, accepted 6 October 2009) doi:10.1111/j.1742-4658.2009.07426.x Lipocalin-type prostaglandin D synthase (L-PGDS) is a multifunctional protein that produces prostaglandin D 2 and binds and transports various lipophilic substances after secretion into various body fluids as b-trace. L-PGDS has been proposed to be a useful diagnostic marker for renal injury associated with diabetes or hypertension, because the urinary and plasma concentrations are increased in patients with these diseases. How- ever, it remains unclear whether urinary L-PGDS is synthesized de novo in the kidney or taken up from the blood circulation. In crude extracts of monkey kidney and human urine, we found L-PGDS with its original N-ter- minal sequence starting from Ala23 after the signal sequence, and also its N-terminal-truncated products starting from Gln31 and Phe34. In situ hybridization and immunohistochemical staining with monoclonal antibody 5C11, which recognized the amino-terminal Ala23–Val28 loop of L-PGDS, revealed that both the mRNA and the intact form of L-PGDS were local- ized in the cells of Henle’s loop and the glomeruli of the kidney, indicating that L-PGDS is synthesized de novo in these tissues. However, truncated forms of L-PGDS were found in the lysosomes of tubular cells, as visualized by immunostaining with 10A5, another monoclonal antibody, which recog- nized the three-turn a-helix between Arg156 and Thr173. These results suggest that L-PGDS is taken up by tubular cells and actively degraded within their lysosomes to produce the N-terminal-truncated form. Structured digital abstract l MINT-7266187: L-PGDS (uniprotkb:P41222) and Cathepsin D (uniprotkb:Q4R4P0) colocal- ize ( MI:0403) by fluorescence microscopy (MI:0416) l MINT-7266176: L-PGDS (uniprotkb:P41222) and Cathepsin B (uniprotkb:Q4R5M2) colocal- ize ( MI:0403) by fluorescence microscopy (MI:0416) Abbreviations CSF, cerebrospinal fluid; DIG, digoxigenin; GST, glutathione S-transferase; KO, knockout; L-PGDS, lipocalin-type prostaglandin D synthase; MAb, monoclonal antibody; PG, prostaglandin; SPR, surface plasmon resonance. 7146 FEBS Journal 276 (2009) 7146–7158 ª 2009 The Authors Journal compilation ª 2009 FEBS protein with a molecular mass of approximately 26 000 [1], and was later Open Access Available online http://arthritis-research.com/content/7/3/R445 R445 Vol 7 No 3 Research article Expression of cytokine mRNA and protein in joints and lymphoid organs during the course of rat antigen-induced arthritis Dirk Pohlers 1 , Angela Siegling 2 , Eberhard Buchner 3 , Carsten B Schmidt-Weber 4 , Ernesta Palombo-Kinne 1 , Frank Emmrich 5 , Rolf Bräuer 6 and Raimund W Kinne 1 1 Experimental Rheumatology Unit, Friedrich Schiller University Jena, Jena, Germany 2 EUCODIS GmbH, Vienna, Austria 3 Pfizer GmbH, Karlsruhe, Germany 4 Swiss Institute for Asthma and Allergy Research (SIAF), Davos, Switzerland 5 Institute of Clinical Immunology and Transfusion Medicine, University of Leipzig, Leipzig, Germany 6 Institute of Pathology, Friedrich Schiller University Jena, Jena, Germany Corresponding author: Raimund W Kinne, Raimund.W.Kinne@rz.uni-jena.de Received: 4 Nov 2004 Revisions requested: 3 Dec 2004 Revisions received: 4 Jan 2005 Accepted: 11 Jan 2005 Published: 17 Feb 2005 Arthritis Research & Therapy 2005, 7:R445-R457 (DOI 10.1186/ar1689) http://arthritis-research.com/content/7/3/R445 © 2005 Pohlers et al.;licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/ 2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is cited. Abstract Cytokine expression was assessed during antigen-induced arthritis (AIA) in synovial membrane (SM), inguinal lymph node (LN), and spleen using competitive RT-PCR and sandwich ELISA. In the SM, early elevations of IL-1β and IL-6 mRNA (by 6 hours; 450- and 200-fold, respectively) correlated with the joint swelling; a 6-fold increase in tumor necrosis factor α (TNFα) was not significant. Not only IL-2 and IFN-γ (which increased 10,000-fold and 200-fold, respectively), but also IL-5 and IL-10, increased acutely (6 hours – day 1; 3-fold and 35-fold, respectively) in the SM. In general, the protein levels in the SM for IL-1β, IL-6, TNFα, IFN-γ, IL-4, and IL-10 (increase from 4-fold to 15-fold) matched the course of mRNA expression. In the inguinal LN, there were early mRNA elevations of IL-6 (a 2.5-fold increase by 6 hours, which correlated positively with the joint swelling) and IL-2 (4-fold by 6 hours), as well as later rises of IL- 4 and IL-5 (2.5- and 4-fold, respectively, by day 3). No significant elevations of the corresponding proteins in this tissue were observed, except for IL-1β (by day 6) and IL-10 (by day 1). In the spleen, there were significant mRNA elevations at 6 hours of IL- 1β (1.5-fold), IL-6 (4-fold; positively correlated with the joint swelling), IFN-γ (3-fold), and IL-2 (7- to 10-fold). IL-5 and IL-10 (2- and 3-fold, respectively) peaked from 6 hours to day 3 in the spleen. Increases of the corresponding proteins were significant in comparison with day 0 only in the case of IL-2 (day 6). By day 6 (transition to the chronic phase), the mRNA for cytokines declined to or below prearthritis levels in all the tissues studied except for IL-1β in the SM and IL-6 in the spleen. AIA is thus characterized by four phenomena: early synovial activation of macrophages, T helper (Th)1-like, and Th2-like cells; late, well- segregated Th2-like responses in the inguinal LN; late, overlapping Th1-like/Th2-like peaks in the spleen; and chronic elevation of synovial IL-1β mRNA and spleen IL-6 mRNA. Introduction CD4 + T helper (Th) cells and macrophages infiltrate the synovial membrane (SM) during the course of rheumatoid arthritis (RA) [1-3]. Both cell types, when activated, appear to play a central role in promoting and maintaining the dis- ease process [4,5], for example by producing certain sets of cytokines that influence the quality and extent of the inflammatory process [6]. Cytokines, in turn, can elicit the production of tissue-degrading enzymes, a mechanism eventually involved in tissue destruction and Open Access Available online http://ccforum.com/content/13/6/R182 Page 1 of 9 (page number not for citation purposes) Vol 13 No 6 Research Ventilator-induced endothelial activation and inflammation in the lung and distal organs Maria A Hegeman 1,2 , Marije P Hennus 2 , Cobi J Heijnen 1 , Patricia AC Specht 3 , Burkhard Lachmann 3,4 , Nicolaas JG Jansen 2 , Adrianus J van Vught 2 and Pieter M Cobelens 1,5 1 Laboratory of Psychoneuroimmunology, University Medical Center Utrecht, Lundlaan 6, Utrecht, 3584 EA, the Netherlands 2 Department of Pediatric Intensive Care, University Medical Center Utrecht, Lundlaan 6, Utrecht, 3584 EA, the Netherlands 3 Department of Anesthesiology, Erasmus Medical Center, Dr. Molewaterplein 50-60, Rotterdam, 3015 GE, the Netherlands 4 Department of Anesthesiology and Intensive Care Medicine, Charité Campus Virchow-Klinikum, Humboldt-University, Augustenburger Platz 1, Berlin, D-13353, Germany (current address) 5 Department of Intensive Care Medicine, University Medical Center Utrecht, Heidelberglaan 100, Utrecht, 3584 CX, the Netherlands Corresponding author: Cobi J Heijnen, c.heijnen@umcutrecht.nl Received: 11 Sep 2009 Revisions requested: 19 Oct 2009 Revisions received: 23 Oct 2009 Accepted: 16 Nov 2009 Published: 16 Nov 2009 Critical Care 2009, 13:R182 (doi:10.1186/cc8168) This article is online at: http://ccforum.com/content/13/6/R182 © 2009 Hegeman et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Results from clinical studies have provided evidence for the importance of leukocyte-endothelial interactions in the pathogenesis of pulmonary diseases such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), as well as in systemic events like sepsis and multiple organ failure (MOF). The present study was designed to investigate whether alveolar stretch due to mechanical ventilation (MV) may evoke endothelial activation and inflammation in healthy mice, not only in the lung but also in organs distal to the lung. Methods Healthy male C3H/HeN mice were anesthetized, tracheotomized and mechanically ventilated for either 1, 2 or 4 hours. To study the effects of alveolar stretch in vivo, we applied a MV strategy that causes overstretch of pulmonary tissue i.e. 20 cmH 2 O peak inspiratory pressure (PIP) and 0 cmH 2 0 positive end expiratory pressure (PEEP). Non-ventilated, sham- operated animals served as a reference group (non-ventilated controls, NVC). Results Alveolar stretch imposed by MV did not only induce de novo synthesis of adhesion molecules in the lung but also in organs distal to the lung, like liver and kidney. No activation was observed in the brain. In addition, we demonstrated elevated cytokine and chemokine expression in pulmonary, hepatic and renal tissue after MV which was accompanied by enhanced recruitment of granulocytes to these organs. Conclusions Our data implicate that MV causes endothelial activation and inflammation in mice without pre-existing pulmonary injury, both in the lung and distal organs. Introduction Critically ill patients in the intensive care unit often require mechanical ventilation (MV) to adequately oxygenate vital organs. Although artificial ventilation is lifesaving, the proce- dure itself may lead to serious damage in both healthy and dis- eased lungs [1]. Studies have revealed that the cyclic opening and collapse of alveoli during MV may provoke alveolar stretch and subsequently result in ventilator-induced lung injury (VILI) [2,3]. Important features of VILI are increased cytokine or chemokine production, alveolar-capillary permeability, protein- rich edema formation and, ultimately, impaired gas exchange [4-6]. ALI: acute lung injury; ARDS: acute ... nephrons and fuse together as they enter the papillae of the renal medulla 4/11 The Kidneys and Osmoregulatory Organs Capillary Network within the Nephron The capillary network that originates from the. .. tubule, and the associated capillary network, which originates from the cortical radiate arteries 3/11 The Kidneys and Osmoregulatory Organs Art Connection The nephron is the functional unit of the. .. region called the hilum of the kidney The hilum is the concave part of the bean-shape where blood vessels and nerves enter and exit the kidney; it is also the point of exit for the ureters The renal