Objective: Estimation of glomerular filtration rate (GFR) is an important tool in the diagnosis and management of chronic kidney disease. Today creatinine is the most frequently used marker for kidney function though several studies indicate that cystatin C is a superior marker. The purpose of this study was to validate Abbott Diagnostics turbidimetric cystatin C assay and enzymatic creatinine assay. Methods: The validation was performed by studies of CV for the two methods and correlations between the two and other available methods for assessing GFR. The stability of cystatin C at room temperature was also evaluated. Results: Both methods showed good precision. The Abbott cystatin C assay generally gave lower values and thereby higher estimated GFRs than the correlated Gentian method. The Abbott enzymatic creatinine assay gave higher values than the correlated Jaffe method. Those results are generally unexpected, but in this study the cause is an automatically applied negative intercept used together with the Jaffe method. Cystatin C showed high stability when stored at room temperature. Conclusions: Estimated GFRs tend to differ depending on the choice of method for analyzing cystatin C or creatinine and this study gives an overview of the range of variation. The study also enlightens the need for an international calibrator for the cystatin C methods presented by different manufacturers.

Att ge bort en del av sig själv för att förbättra livet för en annan människa, är att ge gåvan till liv. Levande njurdonatorers upplevelser kommer ofta i skymundan eftersom studier ofta fokuserat på mottagarens upple-velse av njurtransplantationen. Donationen beskrivs med både positiva och negativa upplevelser. De negati-va upplevelserna förknippas med fysiska och psykiska komplikationer efter donationen. De positiva upplevel-serna beskrivs som ökad livskvalitet och glädje inför att hjälpa en människa till ett bättre liv. Syftet med denna litteraturstudie var att beskriva levande donatorers upp-levelser av att donera en njure från beslutsfattandet till tiden efter donationen. Studien genomfördes som en lit-teraturstudie, där 13 artiklar granskades och analysera-des. Resultatet visar att det finns flera faktorer, såsom oro inför mottagarens situation och oro inför sin egen framtid som påverkar donatorernas beslutsfattande. Det framkom även att både fysiska och psykiska upplevelser förekommer efter donationen. De fysiska upplevelserna var framförallt smärta, illamående samt ömhet och obe-hag runt operationssåret. Donatorns psykiska upplevel-ser efter donationen var vanligen oro inför mottagarens tillfrisknande, stress, depression samt nedstämdhet. Överlag upplevde donatorerna donationen positivt och var nöjda med sitt beslut. Mer forskning kring levande njurdonatorers upplevelser kan bidra till att sjuksköters-kor lättare kan stödja donatorer i donationsprocessen samt att blivande donatorer kan få en inblick i hur dona-tionen upplevs.

Bakgrund: Antalet patienter i behov av njurtransplantation per år är cirka 400-500, varav endast cirka 350 kommer att bli transplanterade. Bristen på organ är tydligt framträdande. I väntan på transplantation behöver patienten dialysbehandling, vilket ofta upplevs vara tidskrävande och utmattande. Sjuksköterskor bör ha kunskap om patienters upplevelser i samband med väntan på transplantation för att kunna utvecklas i sin roll som sjuksköterska och få en djupare förståelse för deras situation. Syfte: Syftet var att beskriva kroniskt njursjuka patienters upplevelser av att leva med dialysbehandling och väntan på transplantation. Metod: Studien är en litteratursammanställning av tio kvalitativa och kvantitativa vetenskapliga artiklar inom området, vilka har granskats, analyserats och sammanställts. Resultat: I resultatet framkom flera olika upplevelser, så som längtan efter frihet, utmattning, höga förväntningar, frustration och rädsla inför framtiden i samband med dialysbehandlingen och väntan på transplantationen. Slutsats: Kroniskt njursjuka patienters upplever sin situation som psykiskt, fysiskt och socialt påfrestande. En av sjuksköterskans viktigaste uppgifter i samband med bemötandet av patienter under dialysbehandling är att vara tillgänglig. Med en tillgänglig och öppen inställning till patienterna blir sjuksköterskan mer mottaglig för patienternas individuella behov. / Background: The number in need of kidney transplants per year is approximately 400-500, of which only about 350 will be transplanted. The shortage of organs is clearly prominent. In anticipation of the transplant patient needs dialysis, which is perceived to be time consuming and exhausting. Nurses should have knowledge of patients' experiences in connection with awaiting transplantation to be able to evolve in her role as a nurse and get a deeper understanding of the patients’ situation. Aim: The aim of this study was to describe patients’ experiences of living with chronic kidney failure with dialysis and awaiting transplantation. Method: The study is a literature compilation of ten qualitative and quantitative scientific articles in the field. The articles have been reviewed, analyzed and compiled. Results: The results revealed several different experiences, such as yearning for freedom, fatigue, high expectations, frustration and fear for the future in connection with the dialysis treatment and awaiting transplantation. Conclusion: Chronic kidney disease patients perceive their situation as mentally, physically and socially stressful. One of the nurse's most important tasks in connection with the treatment of patients in dialysis is to be available. With an accessible and open approach to the patient in general, a nurse becomes more responsive to patient's individual needs.

The incidence of chronic kidney disease (CKD) is increasing. CKD is characterized by a gradual decrease in renal function leading to end stage renal disease (ESRD). Damage to the glomerular podocytes, is one of the first hallmarks of CKD. We hypothesized that podocyte prostaglandin E2 (PGE2) receptors contribute to the progression of glomerular injury in models of CKD. To test this hypothesis, transgenic mice were generated with either podocyte-specific overexpression or deletion of the PGE2 EP4 receptor (EP4pod+and EP4pod-/- respectively). Mice were next tested in the 5/6 nephrectomy (5/6 Nx) or angiotensin II (Ang II) models of CKD. These studies revealed increased proteinuria and decreased survival for EP4pod+ mice while EP4pod-/- mice were protected against the development of glomerular injury. Furthermore, our findings were supported by in vitro studies using cultured mouse podocytes where an adhesion defect was uncovered for cells overexpressing the EP4 receptor. Additionally, our investigations have demonstrated a novel synergy between angiotensin II AT1 receptors and prostaglandin E2 EP4 receptors. This was revealed by in vitro studies using isolated mouse glomeruli. There we were able to show that Ang II stimulation leads to increased expression of cyclooxygenase 2 (COX-2), the enzyme responsible for synthesis of PGE2, in a p38 mitogen activated protein kinase (MAPK) dependent fashion. Moreover increased PGE2 synthesis was measured in response to Ang II stimulation. We confirmed the presence of this synergy in our cultured mouse podocytes and showed an adhesion defect in response to Ang II stimulation which was COX-2 and EP4 dependent. These findings suggest that Ang II AT1 receptors and PGE2 EP4 receptors act in concert to exacerbate glomerulopathies. Studies using mice with either podocyte-specific overexpression of a dominant negative p38 MAPK or mice with global deletion of the EP1 receptor did not provide conclusive results as to their respective signaling involvement in podocyte injury. Altogether our findings provide novel insight for podocyte PGE2 EP4 and Ang II AT1 receptor signaling in models of CKD. These studies provide novel avenues for pursuing therapeutic interventions for individuals with progressive kidney disease.

The “miracle” success of transplant technology, alongside the commercialization of health care, and the increasing polarization between rich and poor have created the conditions for an illegal but thriving trade in human body parts. Based on 15 months of challenging fieldwork, my research examines the ethics of the organ bazaar, particularly the experiences of 33 kidney sellers living in Bangladesh. On the underground bazaar, not only human kidneys but also livers and corneas are advertised for sale. Recipients, sellers, and brokers regularly post newspaper advertisements to buy and sell organs. The average price for a kidney is US $1,500 in Bangladesh, a country where 78% of people live on less than $2 a day. My research examines serious ethical questions, such as these: Is it right to purchase an organ, even if the organ sought provides longevity? Is the sale of one’s organ a justifiable means of fighting poverty? These questions allow me to examine the ethics of harvesting organs, particularly from the bodies of impoverished people. Narrating the victims’ deeply moving testimonies, my ethnography reveals how organ buyers (both recipients and brokers) tricked and pressured Bangladeshi poor into selling their kidneys. In the end, these sellers were brutally deprived and deceived, and their suffering was extreme. In the post-vending period, sellers’ health, economic, and social conditions significantly deteriorated, yet none of them received the promised post-operative care—not even one appointment. My research therefore concludes that organ commodification is serious structural violence against the poor, at the terrible cost of harm and suffering to them. Examining the organ market proposition, I argue that the resulting violence and injustice against the poor provide a hefty reason to rebut this trade. Bangladeshi kidney sellers also stood up against organ commodification, speaking out about their suffering, and about various detrimental and unethical outcomes incurred in this deal. My research aims to offer insights to bioethics and to broaden the debate on human rights by exposing how technological advancement, structural violence, and grinding poverty intersect in the violation of justice to the poor, turning them into “living cadavers.”

The “miracle” success of transplant technology, alongside the commercialization of health care, and the increasing polarization between rich and poor have created the conditions for an illegal but thriving trade in human body parts. Based on 15 months of challenging fieldwork, my research examines the ethics of the organ bazaar, particularly the experiences of 33 kidney sellers living in Bangladesh. On the underground bazaar, not only human kidneys but also livers and corneas are advertised for sale. Recipients, sellers, and brokers regularly post newspaper advertisements to buy and sell organs. The average price for a kidney is US $1,500 in Bangladesh, a country where 78% of people live on less than $2 a day. My research examines serious ethical questions, such as these: Is it right to purchase an organ, even if the organ sought provides longevity? Is the sale of one’s organ a justifiable means of fighting poverty? These questions allow me to examine the ethics of harvesting organs, particularly from the bodies of impoverished people. Narrating the victims’ deeply moving testimonies, my ethnography reveals how organ buyers (both recipients and brokers) tricked and pressured Bangladeshi poor into selling their kidneys. In the end, these sellers were brutally deprived and deceived, and their suffering was extreme. In the post-vending period, sellers’ health, economic, and social conditions significantly deteriorated, yet none of them received the promised post-operative care—not even one appointment. My research therefore concludes that organ commodification is serious structural violence against the poor, at the terrible cost of harm and suffering to them. Examining the organ market proposition, I argue that the resulting violence and injustice against the poor provide a hefty reason to rebut this trade. Bangladeshi kidney sellers also stood up against organ commodification, speaking out about their suffering, and about various detrimental and unethical outcomes incurred in this deal. My research aims to offer insights to bioethics and to broaden the debate on human rights by exposing how technological advancement, structural violence, and grinding poverty intersect in the violation of justice to the poor, turning them into “living cadavers.”

The incidence of chronic kidney disease (CKD) is increasing. CKD is characterized by a gradual decrease in renal function leading to end stage renal disease (ESRD). Damage to the glomerular podocytes, is one of the first hallmarks of CKD. We hypothesized that podocyte prostaglandin E2 (PGE2) receptors contribute to the progression of glomerular injury in models of CKD. To test this hypothesis, transgenic mice were generated with either podocyte-specific overexpression or deletion of the PGE2 EP4 receptor (EP4pod+and EP4pod-/- respectively). Mice were next tested in the 5/6 nephrectomy (5/6 Nx) or angiotensin II (Ang II) models of CKD. These studies revealed increased proteinuria and decreased survival for EP4pod+ mice while EP4pod-/- mice were protected against the development of glomerular injury. Furthermore, our findings were supported by in vitro studies using cultured mouse podocytes where an adhesion defect was uncovered for cells overexpressing the EP4 receptor. Additionally, our investigations have demonstrated a novel synergy between angiotensin II AT1 receptors and prostaglandin E2 EP4 receptors. This was revealed by in vitro studies using isolated mouse glomeruli. There we were able to show that Ang II stimulation leads to increased expression of cyclooxygenase 2 (COX-2), the enzyme responsible for synthesis of PGE2, in a p38 mitogen activated protein kinase (MAPK) dependent fashion. Moreover increased PGE2 synthesis was measured in response to Ang II stimulation. We confirmed the presence of this synergy in our cultured mouse podocytes and showed an adhesion defect in response to Ang II stimulation which was COX-2 and EP4 dependent. These findings suggest that Ang II AT1 receptors and PGE2 EP4 receptors act in concert to exacerbate glomerulopathies. Studies using mice with either podocyte-specific overexpression of a dominant negative p38 MAPK or mice with global deletion of the EP1 receptor did not provide conclusive results as to their respective signaling involvement in podocyte injury. Altogether our findings provide novel insight for podocyte PGE2 EP4 and Ang II AT1 receptor signaling in models of CKD. These studies provide novel avenues for pursuing therapeutic interventions for individuals with progressive kidney disease.

Thesis (Ph.D.)--University of Alabama at Birmingham, 2007. / Title from PDF title page (viewed on Feb. 19, 2010). Includes bibliographical references.

Kronisk njursvikt ökar varje år och vid terminal njurinsufficiens ses njurtransplantation som förstaval av behandling. Behovet av donerade njurar är större än tillgången, vilket leder till en lång väntan för individen. Studiens syfte var att beskriva individers upplevelser i väntan på en njurtransplantation. Metoden var en litteraturstudien där tio vetenskapliga artiklar granskades och analyserades. I analysen framkom tre teman som utgjorde resultatet: behandling för att överleva där dialysbehandlingen sågs som en begränsning i livet och gjorde det svårt att leva som dem gjort tidigare, känna hopp där en transplantation var något att hoppas på, ett sätt att ta sig ur dialysen och få tillbaka sitt gamla liv, samt känna hopplöshet där rädsla för att njurtransplantationen aldrig skulle bli av och känslor av att vara på is i väntan uppkom. Slutsatsen är att behandlingen påverkade upplevelsen av väntan och ledde till att livet var på is, det centrala i livet var att få en transplantation som skulle förbättra livet. För att underlätta situationen för individer i väntan på transplantation finns det ett behov av att det forskas på hur sjuksköterskans bemötande kan stötta individer i väntan. / Chronic kidney failure is increasing every year and at end-stage renal disease kidney transplantation is seen as the first choice of treatment. The need for donated kidneys is greater than the supply, leading to a long wait for the individual. The study aimed to describe individuals' experiences while waiting for a kidney transplant. The method was a literature study where ten scientific articles were reviewed and analyzed. The analysis revealed three themes that formed the result: treatment in order to survive where the dialysis treatment was seen as a limitation in life and made ​​it difficult to live as they did before, feel hope where the transplantation was something to hope for, a way to get out of dialysis and regain the old life, and feel hopelessness where fear that the kidney transplant would never happen and feelings of being on hold while waiting arose. The conclusion is that the treatment affected the experience of waiting and it led to the feeling of being on hold, the central focus of life was the transplant that would improve their lives. To improve the situation of people waiting for a transplant, there is a need for research on how nurse's attitude can support individuals in anticipation.

The incidence of chronic kidney disease (CKD) is increasing. CKD is characterized by a gradual decrease in renal function leading to end stage renal disease (ESRD). Damage to the glomerular podocytes, is one of the first hallmarks of CKD. We hypothesized that podocyte prostaglandin E2 (PGE2) receptors contribute to the progression of glomerular injury in models of CKD. To test this hypothesis, transgenic mice were generated with either podocyte-specific overexpression or deletion of the PGE2 EP4 receptor (EP4pod+and EP4pod-/- respectively). Mice were next tested in the 5/6 nephrectomy (5/6 Nx) or angiotensin II (Ang II) models of CKD. These studies revealed increased proteinuria and decreased survival for EP4pod+ mice while EP4pod-/- mice were protected against the development of glomerular injury. Furthermore, our findings were supported by in vitro studies using cultured mouse podocytes where an adhesion defect was uncovered for cells overexpressing the EP4 receptor. Additionally, our investigations have demonstrated a novel synergy between angiotensin II AT1 receptors and prostaglandin E2 EP4 receptors. This was revealed by in vitro studies using isolated mouse glomeruli. There we were able to show that Ang II stimulation leads to increased expression of cyclooxygenase 2 (COX-2), the enzyme responsible for synthesis of PGE2, in a p38 mitogen activated protein kinase (MAPK) dependent fashion. Moreover increased PGE2 synthesis was measured in response to Ang II stimulation. We confirmed the presence of this synergy in our cultured mouse podocytes and showed an adhesion defect in response to Ang II stimulation which was COX-2 and EP4 dependent. These findings suggest that Ang II AT1 receptors and PGE2 EP4 receptors act in concert to exacerbate glomerulopathies. Studies using mice with either podocyte-specific overexpression of a dominant negative p38 MAPK or mice with global deletion of the EP1 receptor did not provide conclusive results as to their respective signaling involvement in podocyte injury. Altogether our findings provide novel insight for podocyte PGE2 EP4 and Ang II AT1 receptor signaling in models of CKD. These studies provide novel avenues for pursuing therapeutic interventions for individuals with progressive kidney disease.