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Hello, I am a postgrad student currently working on my dissertation. I am running a meta-analysis on R and I am looking at the effect of ACEI and ARBs on cardiovascular outcomes such as myocardial infarction, heart failure, and stroke, and renal outcomes such as doubling of serum creatinine and end-stage renal disease. Each outcome has several studies supporting it and so I would like to group those studies together to show an overall result. For example, heart failure outcome has 5 articles that support it, I would like to pool them together if possible. I am using a generic inverse variance meta-analysis (function on R is metagen). Thank you for your help!
The R code I used is: studymeta <- metagen(Log_of_HR, Standard_error, Outcome, data=dat, sm= "HR", random = gs("random"), method.tau = "DL", tau.common= TRUE)
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Not really sure what is the problem. There are different R packages available that can make you compare the different treatments and give the overall effects for treatments by inserting either the number of events or the overall effect.
I usually use the package "metafor" for metanalyses with the frequentist approach.
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Except for the heart failure and the renal disease edema cases
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Thank you very much. It will be easier to choose the right instrument now
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Many congratulations are extremely well deserved for the amazing role out of vaccinations in the world populations in the fight against the COVID-19 pandemic, at a speed intended to keep ahead of the mutability of the virus reducing and the possibility of more virulent and transmittable variants to emerge yet inhibiting transmission through mitigations and lock down. Were many convalescent patients included in the vaccination trials, who may have experienced thrombophilic events during their infection?
Should we, however, show some concern about individuals with abnormal mutations (factor V Leiden or prothrombin gene Factor V506 Arg to Gln mutation) as factors that predispose them to developing thrombosis even if there has not been an occurrence of thrombosis?
In a more general sense, it is recognised that extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation.
· Should we be more cautious of vaccinating convalescent patients, without first testing them for significant increases in D-dimer, fibrinogen, prothrombin time, hypercoagulation, and or disseminated intravascular coagulation that causes micro thrombosis?
· Should we add questions about family history to the current question in UK patient preparation to vaccination- ‘Do you have a bleeding disorder or have any issues with bleeding?’
· Should questioning about family history identify susceptibility to thrombosis and either test for underlying conditions or suggest aspirin as a prophylaxis against possible clotting?
· Should we be identifying heritable risk factors with genetic evaluation to inform the patient and help clinical decisions in managing these disorders in the light of thrombosis in COVID 19 convalescent patients and vaccination?
Thrombosis can simply occur due to immobility, particularly postoperatively and, although patients are regularly turned intensive care treatment, this level of activity may exacerbate blood-clotting complications. Clearly pre-existing cardiovascular conditions are an important factor such as arterial thrombi in MIs and Strokes.
Genetic factors that the human coagulation cascade are relatively common. Thrombophilia can be caused by a severe deficiency of inhibitors (type I) or a severe elevation of coagulation factors the can be congenital or acquired also arterial, venal or combined. Venal thrombosis can be portal, renal, hepatic, Paget-Schrotter disease (upper extremity) and Thoracic outlet syndrome (unrelated to trauma).
Of the congenital conditions 5% of the population have the Factor V Leiden thrombophilia condition, where 95% carrying this genetic mutation develop a blood clot during their life. By 50 years of age 25% of those affected genetically have a thrombophilic event. Some common types of thrombophilia create an imbalance in haemostatic and fibrinolytic pathways affecting the proteolytic clotting cascade thus leading to thrombosis include:
· Prothrombin mutation (G20210A, 5’UTR)
· High homocysteine levels due to MTHFR mutation
· (High homocysteine levels also due to vitamin deficiency B6, B12 and folic acid)
· Factor VIII promoter polymorphism (high FVIII levels)
· Other factors causing blood clotting are autoimmune disorders such as Anticardiolipid antibodies
· Lupus anticoagulants
· Renal disease (renal loss of thrombin)
· Budd-Chiari syndrome
· factor V Leiden
· protein C deficiency
· protein S deficiency
· antithrombin deficiency
· antiphospholipid syndrome
Some of these heritable thrombophilic disorders and clinical phenotypes are relatively common in the general population especially in Caucasian genotypes. For example is a polygenic autosomal dominant inheritance of protein C deficiency. Other examples of deficiencies involve Antithrombin (AT), Protein C and Protein S causing an increased generation of thrombin and a predisposition to thrombosis. Venous thrombosis in the population is less that 1 in 1000 on average but when we consider the number of vaccinations taking place this number adds up.
Currently, thrombophilia are treated prophylactically with low-molecular weight heparin, purified factor concentrate or warfarin. Many of the inherited thrombophilic disorders, such as, antithrombin, protein C, or protein S deficiency, factor V Leiden, and the prothrombin G20210A mutation are not usually anticoagulant resistant.
SARS-CoV-2 induces the cytokine storm that activates IL-6 that damages the microvascular system thus activating the coagulation system. It also inhibits fibrinolysis and anticoagulation process that induces thrombopoietin synthesis in the liver leading to thrombosis in microvessels. COVID-19 patients with high levels of D-dimers and conditions causing hypercoagulation are particularly susceptible to this process.
Khan, S., & Dickerman, J. D. (2006). Hereditary thrombophilia.Thrombosis journal, 4, 15. https://doi.org/10.1186/1477-9560-4-15
Thakur V, Ratho RK, Kumar P, et al. Multi-Organ Involvement in COVID-19: Beyond Pulmonary Manifestations. J Clin Med. 2021;10(3):446. Published 2021 Jan 24. doi:
10.3390/jcm10030446
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Dear Annwyne Houldsworth,
ITP also occurs wit influenza virus vaccine which do not use vector
and mostly live attenuated virus.
Of ours it doesn't cause VIPIT.
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For hepato or reno-protective effect of plant extract, is it OK to use long evan rat model? Why many prefer to use male rat model for renal disease?
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Males have higher metabolic rate when compared to female this t is the reason we choose male rats for hepatoprotective studies
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I think that as also some scientist suggest that liver dysfunction is the main cause of many diseases such as renal disease , atherosclerosis even some types of diabetes and failure in detoxification function of the liver may lead to accumulation of toxin and by aging of persons this waste will affect the normal function of the blood vessel and may lead to blood hypertension , then the healthy liver means no risk blood pressure , so I will ask you , how we are able to maintain healthy and powerful liver from 20 year old up to 90 years old ?
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Why so happens? What is the mechanism behind this?
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Beta-2 microglobulin (B2M) is a protein that is found on the surface of nucleated cells and functions as part of the human immune system. This protein is routinely shed by cells into the blood and is present in most body fluids, with highest levels in the blood, generally lower levels in spinal fluid, and trace levels in urine.
In the kidneys, B2M passes through blood-filtering units called the glomeruli and is then reabsorbed by the renal proximal tubules, structures that reclaim water, proteins, vitamins, minerals, and other vital substances. Normally, only small amounts of B2M are present in the urine, but when the renal tubules become damaged or diseased, B2M concentrations increase due to the decreased ability to reabsorb this protein. When the glomeruli in the kidneys are damaged, they are unable to filter out B2M, so the level in the blood rises.
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We are invited to write a special issue of a topic theme on "The role of ongoing biomarkers for increasing the predictability of renal diseases".
We invite every contribution from international scientists in this field to send papers under this topic.
We also need High H-index reviewers and coauthors. We share, contribute and cooperate in writing review articles and research papers together. Worldwide authors are invited without any exceptions.
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We also need High H-index reviewers and coauthors. We share, contribute and cooperate in writing review articles and research papers together. Worldwide authors are invited without any exceptions.
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The Kidney (Brenner and Rector eds. )
Oxford Textbook of Clinical Nephrology (Davison et al. eds. )
Therapy of Renal Diseases and Related Disorders (Suki and Massry eds. )
Clinical Physiology of Acid-base and Electrolyte Disorders (Burton Rose ed.)
Replacemrnt of Renal Function by Dialysis (Drukker et al. eds.)
etc...
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Could be because they only look to cite the efitirs who compiled the work, not the contributors who authored. This is not specific to our nephrology community either. You could share a different citation format to indicate which chapter you authored in the textbooks. I am only familiar with APA citation for this.
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Hi,
I have a data frame that includes people who developed end stage renal disease (ESRD) and those who didn't (controls). I want to match my cases with controls based on age, sex and ethnicity. my sample is 32000. I want to match 5 controls for each case (ratio 1:5). For age I want to match the cases over a range of +/- 5 years (not the exact match), while sex and ethnicity will be exact match (understandably).
Once I match the cases and control i will compare their clinical characteristics with each other to see how different cases are from controls.
I am performing the case control match in R using the package "MatchIt"
m.out=matchit(ESRD~Age+Sex1+Race,method="nearest",data=datamatch,ratio=5)
the above syntax gives me exact matching for age (I think).
Can you please advise me what command to use if I want to match over a range of age?
If there is an easy way of doing it in spss please let me know.
p.s. I am new to R, i mostly use spss.
Many thanks
Saima
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Why match at this point in the study. Why not run some regressions with age, sex, and ethnicity as covariates first to see if any of the 3 covariates change anything. If not why match? If they do change something then you know that there is some effect to be found. Best, David
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"Utilization of haemodialysis services by End Stage Renal Disease patients"
questionairre on above or related topic.
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Is the patients with pre-hypertension are at high risk for developing frank hypertension?
Of course in this case very important to focus on lifestyle modifications to reduce the risk of later hypertension.
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Yes, probably. It shows a 37.3 percent rate of progression from prehypertension to frank hypertension reported in the Framingham Study after four years of follow-up.
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I have a 50 y/o male patient who's with end stage renal disease pending renal transplant. He was diagnosed with complete intestinal metaplasia during pre-renal transplant OGDS surveilance, confirmed with pathology report.
His mother passed away due to gastric cancer at age of 60. He's a non smoker/teetotal. H.pylori test negative.
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Thank you, Dr Ali. Nice sharings.
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Treatment of Thrombosis With Fondaparinux (Arixtra) in a PEDIATRIC Pateint With End-stage Renal Disease Receiving Hemodialysis Therapy
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Fondaparinux (Arixtra) may be given for the prophylaxis of thromboembolism in patients with heparin-induced thrombocytopenia (HIT).  If the patient is not HIT positive one may consider other LMWHs.  Peter is absolutely right that the dose of Fondaparinux or for that matter any LMWH should be carefully titrated based on the CrCl and closely monitored by anti-Xa levels.
Omer
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Which kind of drug therapy or molecule class can be prescribed to the renal impaired diabetic patient?
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I'm not a specialist in the field of this question but think that the paper linked below might be a good reference for you.
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Symptoms assessment tools are very important to evaluate symptoms in end stage renal disease, but there are any symptoms assessment tool to evaluate symptoms in ACKD in spanish population?
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I agree with Dr. Aldallal, that a lot of - by itself - unspecific findings may occur. No single item is specific for chronic kidney disease, but the sum of many symptoms is indicative of progredient uremia.
As a comment, weight loss measured by kg or pounds may be misleading as muscle wasting may be "neutralized" by fluid retention and also body composition may change with loss of muscles and an increase in fat mass. Thus, the question on weight loss should always be accompanied by the question on loss of physical function and general strenght.
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Urinary angiostatin--a novel putative marker of renal pathology chronicity in lupus nephritis.
Wu T, Du Y, Han J, Singh S, Xie C, Guo Y, Zhou XJ, Ahn C, Saxena R, Mohan C.
Mol Cell Proteomics. 2013 May;12(5):1170-9. doi: 10.1074/mcp.M112.021667. Epub 2013 Jan 23.
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thanks!
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Is there an Arabic Validated versions of PedQL inventory for ESRD (for all ages)?
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I'm afraid this is an area I am not an expert in.
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I read about the CKDKAT-N but I can´t find the format, does anyone have an idea where can I download it?
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hi 
attached is  a questionnaire adapted from a bit older reference. 
Adapted from: Caroll J et al, Journal of Renal Nutrition, 14,1, pp:36-44, 2004                   
i have modified it and used it in a study i conducted
 moreover, attached is a PDF of the article that i published explaining the scoring method of the questionnaire in addition to other questionnaires use  in our study 
feel free to ask more questions if needed. 
regards
Mirey 
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Hi everyone
I am working on a rat model of uremia with high adenine feeding. The aim is to induce arterial calcification using this model. From the literature I have gathered, it seems to take a time of 8-10 weeks for the calcification to be initiated. We need it to be sooner than that. Have any one of your worked on this model before and how were your results?
There is one publication by Paul Price and his group which modifies the diets to achieve calcification earlier. Other groups have used this model ad libitum. Has anyone used this model before? What are the various ways to ameriolate mortality that is caused by this model?
Thanks
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Try a high phosphate diet (1.2%) and if that is not enough, adding a calcitriol shot three times a week will work.
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I am trying to measure Beta-2-Microglobulin concentration in urine samples from patient with renal disease, so the concentration is expected to be high. I first used abcam SimpleStep ELISA kit then R&D Quantikine to confirm. But the inter-assay variation is so big (>100%) leaving me no idea which is the right result. Can anyone suggest how to make these result more reproducible and reliable? Thanks
Attached is some of the results on a spreadsheet.
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There is a lot of variation in data when you used R&D kit. Usually R & D kits wont give such values. Abcam kits are coming with much more senstivity these days. hence the values are higher in Abcam. Neverthless it also depends upon how old is your sample. Is there any precipitate formation in your sample?? Did you centrifuge your sample properly and take out the supernatant before going for the assay. 
If you use fresh sample or centrifuged properly.. then still I would suggest to go for the Abacam kit as your data looks more stable there.
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Could anyone could suggest the reference of prevalence of ESRD patients on dialysis with HIV infection for the recent years? 
The last updated data that I found was in 2010. I would appreciate if anybody can suggest me references for recent data.
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You could find the answer in pubmed search itself with the key "Prevalence of End stage renal disease with HIV infection". However, the following few references may be helpful for you. But I don't know whether they are on dialysis or not. You need to go through the article:
1. Clin Infect Dis. 2015 Mar 15;60(6):941-9. doi: 10.1093/cid/ciu919. Epub 2014 Nov 18.
End-stage renal disease among HIV-infected adults in North America.
2. Clin Infect Dis. 2015 Feb 15;60(4):627-38. doi: 10.1093/cid/ciu869. Epub 2014 Oct 30. Comparison of risk and age at diagnosis of myocardial infarction, end-stage renal disease, and non-AIDS-defining cancer in HIV-infected versus uninfected adults.
3. J Acquir Immune Defic Syndr. 2014 Oct 1;67(2):177-80. doi: 10.1097/QAI.0000000000000291. End-stage kidney disease and kidney transplantation in HIV-positive patients: an observational cohort study.
4. Br J Hosp Med (Lond). 2014 Apr;75(4):197-201.
HIV and the kidney: a UK perspective.
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This will be done in renal disease patients.
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We have used NBT from Sigma, Himedia, Merck, SD-Fine chemicals etc. NBT from all these sources worked equally well.
As far as NBT assay is concerned for measuring oxidative stress is concerned, I have reservations. NBT can be reduced by number of biological events, almost all dehydrogenases can reduce Tetrazolium. I am attaching a good publication, wherein researchers reported that NBT can even generate superoxide anion radicals (many of us use it for measuring superoxide anion radicals).
It is not clear, what exactly you want to measure (what aspect of oxidative stress)? Are you interested in measuring total antioxidant capacity or lipid peroxidation or levels of enzymatic & non-enzymatic antioxidants?
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In Nephrovit (the multivit tablet for dialysis patients ) there is only 500 micro gr to 800 micro gr folic acid but in some paper they recommend 5 to 15 mg folic acid per day . is there any need to add tab folic acid 5 mg to nephrovit or the folic acid in nephrovit is enough ?
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5 and up to 10 mg/day should be sufficient to treat the deficiency.
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The intensity of proteinuria is an important element to define the degree of chronic renal failure. As a clinician, what importance do you attribute to the type of protein (low/high molecular weight) detected?
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The interpretation of proteinuria is based on amount (heavy indicates glomerular disease), type (glomerular disease primarily albumin; tubular disease b2 micro globulin, light chains etc), and transient/persistent. The former can be orthostatic (benign) and the latter more likely to indicate a disease state. It is a risk marker for progressive disease: the higher the value more likely the disease will progress. It is also used as a surrogate marker to assess treatment efficacy: angiotensin blocking agent dosage is titrated per proteinuria, with the largest of bringing it down to less than 1 g/day. There are issues around measurement of proteinuria as well (spot measurement vs 24 hr values vs ACR). A good source is the 2012 KDIGO CKD Guidelines (Free download: http://www.kdigo.org/clinical_practice_guidelines/pdf/CKD/KDIGO_2012_CKD_GL.pdf).
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ESRD (End Stage Renal Disease) prevalence is increasing in Oman and worldwide. The difference is that, the western world has an update system of documentation and statistics for everything. In Oman and the developing countries, where are we now? How many dialysis-treated end renal disease at present? If you know the answer, how many females and males? Why they end up with ESRD? Do we have guideline in operation now and is it successful?
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Dear Mr. Salah,
Yes I have the information I need now because I went to Oman last summer and gathered the necessary data. In fact Dr. Nabil is one of the collaborative team of this project and am really proud about having him. I should say thanks for your consideration.
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Several studies indicated urine flow and Bowman's capsular space were increased/dilated in diabetic nephropathy. Is it possible that the  Bowman's capsular space declined in severe diabetic nephopathy (because mesangiolysis, tuft-capsule adhesion or hyalinosis) while urine flow remains high?
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There is no cause effect relationship between urine flow and bowman space volume.Urine flow increases due to osmotic duresis. Bowman space may be dilated due to initial hyperfiltration or later, because of increases in intracapsular pressure due to incomplete proximal water reabsorption due to the glucose overload. Of course in advanced stages adhesions, fibrosis etc may limit Bowman space expansion and diuresis can persist.
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The use of pre-blood fluid in the reduction of filter clotting in dialysis is well known, but it is also known to reduce the efficiency of the dialysis abilities.
Could you please explain how your unit overcomes the drawback of the use of pre-blood fluid, and how the use of Filtration Fraction determines the use of pre-blood fluid? Some units determine that pre-blood fluid is not needed if the Filtration Fraction is below 30%. 
Does this not then save the unit money if pre-blood fluid is not used? Also, it has been stated that in the use of Heparin in Dialysis, the APTT is irrelevant in the ability to stop the filter clotting off. What APTT therapeutic range does your unit run at?
Any information provided would be appreciated.
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Thank you Ali for your input on this subject, I will read them with interest.
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Let's suppose hsa-miR-320 was found to be deferentially expressed in ESRD (end stage renal disease) - how can we predict its exact gene in the renal cortex?
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you may try mirtarbase 
Generally, the collected miRNA-target interactions are validated experimentally by reporter assay, western blot, microarray and next-generation sequencing experiments. 
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There is no unanimous agreement in the literature on prescribing Asprin for the above renal pathology.
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I agree - no evidence, but aspirin in a low dose is not bad for the kidney. I would recommend it for that reason and its potential benefits in heart disease.
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Renal transplantation and JC & BK polyoma virus induced nephropathy
How effective are these therapies?
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No antiviral is really effective "in vivo"...the only treatment  is reducing immunosuppression until T-cell immunoreactivity against  BKV  (monitored by means of Elispot or a similar assay) develops.
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Is one protein for each activity enough?
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Thanks Vivekanand for your reply. 
I am looking markers for both formation and resoprtion and also for chondrogenic phenotype only. I understand that Bone Specific ALP is for bone formation. Any markers that will be expressed in in vitro cultured cells such Runx-2/cbfa-1, smad, BMPs etc will be great that could be detected with western blotting or Elisa.
Thanks Again. 
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Recently we had a patient candidate for CABG who was alert and oriented. The first K after induction was 8 mEq/L. This number was confirmed by recheck. Two measurements on CPB were 6.5 (with low potassium cardiopledgia) and 7 (at the end of CPB). off pump K was 6.5 after giving insulin for BS=190 and NaHCO3 for acidosis (BE= -10). First postoperative K was 6.5 too. There was no EKG sign in perioperative period.
The patient had no Hx of renal problem with Cr=0.95 mg/dl. preop drug Hx included Aldacton 25 mg BD. however, last preop K was 4.8.
What's your opinion about this case?
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One may not find ecg change many a times. 
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Cadmium is said to be an important cause of chronic kidney disease of uncertain aetiology in Sri Lanka. It would be very beneficial that if there is a non invasive screening tool to detect cadmium induced early renal damage.
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I think that  protein of  low MW like alpha1microglobulin  would be an early test of renal damage  but it is a very sensitive test and therefore not specific; some are orientated towards new test as KIM-1 but this test is more expansive
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Based on the evidence can any one suggest the best treatment option for this group of patients?
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elderly females with PPP will do better with phototherapy using Narrow band UVB.
Topical steroid with salicylic combination.
It may be difficult to consider methotrexate, but fatty liver should not be a problem, if The LFT is within normal limits and it may be tried for a short duration.
but yes Phototherapy helps. 
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Trying to do a write up on SCA and renal papillary necrosis.
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Loads of thanks to Ranella and Jha, your suggestions are surely on point.
 
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In nephrologists' clinical experience, the overactivation of the complement alternative pathway (AP) is acquiring more and more importance in kidney failure etiopathogenesis. Indeed AP is involved in membranoproliferative glomerulonephritis, in atypical hemolytic uremic syndrome, in post-infectious glomerulonephritis, and now we are debating about a role of AP complement overactivation in ANCA associated vasculitis, in MGUS related nephrophaties.....Often patients with an AP dysregulation simulate Lupus without Lupus antibodies (SLE without SLE) and we observed some patients that overlaps with hypocomplementemic cutaneous vasculitis and/or cryoglobulinemic vasculitis
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Yes it's true. But the question is about AP overactivation/dysregulation without any infectious or immunocomplexes trigger. This pathogenetic pathway was clearly showed in atypical haemolitic uremic syndrome, in dense deposit disease, in C3 glomerulonephritis. In ANCA associated vascultiis is described that ANCA primed neutrophils are able to activate the AP, and so on...
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A 65 year old woman with CKD (urate nephropathy) with severe chronic asymptomatic hyponatremia (S-Na 121 mmol/L), elevation of creatinin kinase (7 ukat/L), polyuria (3600ml/day), polydipsia. No episodes of seizures, no clinical signs of dehydration, no medications affecting diuresis or natriuresis.
Serum Na 121, K 4, Cl 82, P 1.31, Ca 2.5, urea 9.2 mmol/L, OSM 254 mmol/kg, creatinine 97 umol/L, CK 7 ukat/L.
Urine Na 36, K 9, Cl 26 , P 3.7, Ca 0.21, urea 59, creatinine 1.28 mmol/L, OSM 147 mmol/kg.
Fractional excretion of Na 2.25%, OSM 4.4%, water 7.6%, urea 48.6%.
pH 7.41, pCO2 5.9 kPa, HCO3 28 mmol/L. Creatinine clearance 0.56 ml/s.
After 4 hours of fluid restriction diuresis was 400ml, increased urine osmolality from 147 to 265 mmol/L, increased urine sodium from 36 to 57 mmol/l, slightly decreased serum osmolality from 254 to 252 mmol/kg, serum sodium remained unchanged.
What is the diagnosis?
Is it water diuresis? Serum osmolality is higher than urinary, but fractional excretion of osmolal substances is high.
Could be primary polydipsia - urine osmolality increased after water restriction, so probably it is not diabetes insipidus, ADH should be present, at least partially.
Why did serum sodium not increase after fluid restriction? Could it be the combination of primary polydipsia and decreased tubular reabsorption of sodium (urate nephropathy)? Why is CK elevated without episodes of seizures?
Thank you for your opinions.
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In this patient the primary problem is polyuria . Is the polyuria due to water diuresis or solute diuresis . Chronic Interstitial nephritis can produces both nephrogenic diabetes insipidus as well as salt losing nephropathy . The evidence for nephrogenic DI is low urinary Osm , which is partial , as there is improvement with water restriction . The increase in urinary sodium is probably due to correction of hypovolemia , due to salt wasting nephropathy . The hypontremia is probably due to excess water consumption , with restricted salt intake causing hypovolemic hyponatremia . I would treat this patient with salt & water or IV 0.9% Nacl of about 2.5 - 3 litres / day . Francois Brivet used to state that decreased renal function is a sign of volume depletion , even if there are no clinical signs . Whether , this is CKD or AKI or AKI on CKD would be determined by recovery of renal function after correction with saline .
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It is very important to have a surveillance system for early diagnosis of HCV infection in dialysis centers and for control of it we should attend to some strategies, such as:
1. Less transfusion, more use of erytropoithin.
2. More education for the nurses in dialysis centers.
3. Treatment of HCV infected patients.
Do you agree with dedication of HCV infected from non-infected patients in dialysis centers?
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I strongly agree with this statement, but let me underscore that HCV infected patients are to be considered only those with HCV-RNA detectable. Indeed a lot of my patients have HCV antibody with undetectable RNA and I think no isolation is required
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We have been looking at a blood marker in transplantation. This marker is present in normal humans at about 50pM in blood, and increases in ESRD to about 1000pM. After transplantation the marker decreases again. Renal disease is not our primary focus and I figured, there may be some specialists with a opinion out there.
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Hello Bruno. Nice graph. Is the difference because CAF is no longer being generated post transplant whereas creatinine is? Do CAF levels in non DGF patients decrease more rapidly b than those in DGF patients? (clinical relevant)
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I am searching for a good control set to verify the specificity of a putative new renal cancer biomarker that I have isolated in urine of RCC patients. I am particularly looking at urine samples from patients affected by prostate cancer or bladder cancer. Any suggestions?
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You could use two control groups for testing your potential marker: healthy people at the same age as your RCC patients, and a mixed control group consisting of patients with no RCC but other urological disease (e.g. urolithiasis, BPH, urinary tract infection). This could show if your putative marker is biased by other diseases.