Questions related to Renal
I am currently quantifying damage in renal histological sections of AKI model. I found EGTI scoring system during the literature search. However, I did not find the detailed protocol of it. Does anybody help me with the step-by-step protocol of this scoring system?
I really appreciate any help you can provide.
I am studying the hepatoprotective activities of beta caryophyllene therefore i need to know about the route of clearance of beta caryophyllene
There seems to be much previous interest in developing haemodynamic monitoring equipement, espcially non-invasive ones, for haemodialysis. However, there is not much over the last decade.
Can anyone give my an update on current practices and development?
I would like to measure the inner diameter, the outer diameter, and then a measure of the thickness between the inner and outer diameter. I have created several regions of interest (ROIs) but am not certain about the output from ImageJ. Someone, please assist me.
Transperitoneal laparoscopic pyelolithotomy was done for a young patient with a big (4*3.5cm) renal pelvic stone. The stone was escaped into the peritoneal cavity and was not found. Post-op X-ray shows a big radiopaque structure (retained stone) near the pelvis.
I was unsuccessful to find anything in the literature about proteins that are not reabsorbed (efficiently) in the renal tubule. Maybe it was the way I searched or it doesn't occur or no one has looked for it. Sure, it's unlikely and I assume the uptake mechanisms are so "generic" that any protein/peptide will be fished out of the filtrate and taken up by tubular cells. But maybe there are some proteins that escape this?
I am having trouble interpreting some pharmacokinetic data. I work with mice. I have two groups of animals all given with the same drug in the same route at the same dosage. There were statistically significant differences in the AUC, Clearance, and Cmax between groups. However, the half-life was the same for all groups. Two of these groups were infected with a virus that replicates in the kidneys, so we expected them to have impaired renal clearance of the drug. If that were the case, wouldn't we see a prolonged t1/2? I am concerned that even though there are differences in the AUC and Clearance, without changes in T1/2, we can't conclude that the variation in PK parameters is due to changes in renal function.
HI everyone! I am going to start culturing RPTEC/hTERT renal proximal epitelial cells and I have several questions about it. First of all I want to know when the cells are proliferating and when differentiating. I have cultured immortalized podocytes previously and these cells proliferate at 33ºC and differentiate at 37ºC, so i have clearly differentiated the two populations. But in the case of RPTEC/htert cells I dont know how to know it, because I think they dont have the SV40 T antigen to thermoswitch them. So, are cells proliferating and differentaiting joint? How to know which are mature cells? And if I want to treat them with something, I will treat proliferating and differentiating cells?
Another question is the appropiate culture medium for these cells. I have read that the supplied medium from evercyte or ATCC in some cases didn't work very well, and as well the mixture of DMEM/HAMs F12 . So the best option is to buy DMEM (low glucose with glutamine?) and F12 separately, plus glutamax, EGF, ITS, Penicillim/Streptomycin and hydrocortisone? and FBS is necessary or not?? Because I have read the two options
I would appreciate any answer from peolple working with this cell line.
Thank you in advance
I want to develop renal cell carcinoma in C57BL/6J mice preferably by chemical method.
Kindly pour in some suggestions if any one have an experience in this field.
I am looking at studying patients with chronic renal disease and their preception on their fertility.
Over the past two years, our understanding of anti-hyperglycemic medications used to treat patients with type 2 diabetes (T2D) has fundamentally changed. Before the EMPA-REG OUTCOME trial, agents used to lower blood glucose were felt to prevent or delay the development of microvascular complications, but were not known to definitively reduce cardiovascular risk or mortality. Previous studies with then novel sodium-glucose cotransport-2 (SGLT2) inhibitors demonstrated improvements in several cardiovascular and renal risk factors, including HbA1c, blood pressure, weight, renal hyperfiltration, and albuminuria. However, as with other antihyperglycemic drugs, it could not be known if these salutary effects would translate into improved cardiorenal outcomes. In the EMPA-REG OUTCOME trial, SGLT2 inhibition with empagliflozin reduced the primary outcome of major adverse cardiovascular events (MACE), while also reducing mortality, hospitalization for heart failure, and progression of diabetic kidney disease. In the CANVAS Program trials using canagliflozin, the rates of the 3-point MACE endpoint, the risk of heart failure and the renal composite endpoint were also reduced, albeit with an increased risk of lower extremity amputation and fracture. As a result, clinical practice guidelines recommend the consideration of SGLT2 inhibition in high-risk patient subgroups for cardiovascular risk reduction. Ongoing primary renal endpoint trials will inform the cardio-metabolic-renal community about how to optimally treat patients with chronic kidney disease – including those with and without diabetes.
Coffee farmers in the Philippines have had a tough time over the past few decades with the decline of coffee plantations across the archipelago. This has driven them oftentimes to sell their best beans and consume the damaged or scrapped ones.
I'm currently looking into studying the effects of this by analyzing the blood of renal disease-afflicted coffee farmers from different regions of the Philippines for Ochratoxin A, which is produced by Aspergillium and Penicillium species that grow on damaged coffee beans.
As far as my research has shown, the correlation between ochratoxin A and renal disease in humans or primates is yet to be studied. Any help finding pre-existing research regarding this topic would be much appreciated.
My protocol for the staining seems to be working, except the localization of the protein in the kidney cross section is not clear to me. I see a stronger staining near the renal cortex, whereas, I was under the impression that it should be near the medulla. Can anyone comment or help me with the localization?
For my research I’m culturing renal epithelial cells and wanted to observe the primary cilia formed by the microtubules, however a curtain subpopulation does not stain positive (or greatly reduced expression) for alpha-Tubulin.
Does anybody know what could be going on?
I’ve added a picture of the staining.
I was thinking that the epitope could be post-modified and the antibody no longer binds.
The antibody I’m employing is the ab18251 from Abcam, I still have to receive answer of Abcam if post-modification could explain the negative population.
However is it then possible that all microtubules are post-modified and no longer visible? Or is something else going on?
In my clinical practice I have seen many nephrologist ordering renal usg in AKI patients, but current literature does not support it.
What do you practice in your ICU ?
It is often observed that in many cases it if found written on prescribing information that the drug is contraindicated in breast feeding mothers, while if you see the route of excretion for that particular agent is either renal, bile etc. What is the logic behind ?
56year old male presented to his local physician for dry cough,clinical exam was nil significant.CBC is N except ESR 40,blsugar ,urea,creatinine, LFT were N,X Ray chest N,U/S mass in the R lobe of liver.when he was ref to our hospital.viral markers are N so as AFP and PT INRAny other investigation.A high resolution cect was reported as HCC in segments 6 and7.Rest of the study was N.Anyother investigation will be of any help before proceeding for surgery or straight away go ahead with surgery.I have once again repeating AFP and
viral studies and PFT.
Efferent as afferent renal sympathetic nerve fibers have a important relevance in the development of cardiovascular disease.
Thyrosine hydroxylase is a marker for sympathetic fibers. Is there a way to distinguish afferent and efferent nerve fibers from each other by dyeing?
How does the walk distance vary after renal transplantation from other patient groups i.e. Cardiac rehabilitation ; Do we have established reference values in renal population
Nowadays people due to some musculoscletal problems such as osteoarthritis and osteoprosis, overuse calcium resources ever over the counter(OTC). Some renal stones consist of calcium carbonate or calcium oxalate... Is there any relation between mentioned subjects? Can anyone introduce some useful case-control and clinical trial articles?
I have found a new predictive model for renal outcome among IgAN patients using the MESC score. I want to validate it by using my own data set that is around one hundred patients. May I able to conduct an internal validation or cross validation study among 100 patients?
Thank you all
want to study ceramide toxicity on cultured renal cells. Any special condition (serum-free medium, etc...) would be necessary?
My study is time to event study. I have determined cutoff points by logistic regression model in association with renal outcome. Is it correct to run cox model using the cutoffs determined by logistic regression? if not how can I determine cutoffs using cox model in stata or spss?
Hypertensive patients with diabetes mellitus 2 type have more often and early renal dysfucntion due to negative influence of 2 diseases. There is a cut-off of kidney function according to GFR - lower then 60 ml/m2/1.73. But what about hypertensive patients with diabetes with 60-89ml/m2/1.73 - with mildely decrease GFR?
In patients with this GFR level can we declare about kidney organ damage?
67 years old man presented with hematuria 2 years ago. ultrasound show just few small renal stones. Now presented with gross intermittent (nearly every week) hematuria, no pain and no fever.
Lab data no pus in urine, no stone or mass by ultrasound.
ESR is 10 mm/hr and Hb is 14.7.
What is the possible cause of such a case?
I want to quantify acute renal injury, myocardial injury, brain insult, liver injury and eye insult from nocturnal hypertension.
In my experiments I measure different renal parameters (urea, creatinine, proteinuria, etc) in two groups (control and ischemic) in four different time points.
My aim is to assess whether the difference between each group is statistically significant or not. I would like to compare the time point 0 (baseline) to every other time point for each parameter.
My guess is that I should use a one way ANOVA, but I don´t know if my parameters follow a normal distribution or not and my sample size is not very large (n=6-8).
Does anyone know how I can know if my parameters have normal distribution? Is my guess right about the one way ANOVA?
The software that I´m using is GraphPad Prism.
Thank you very much in advance!
Basal septal thinning, sarcoidosis,, CAD.. Possibilities... Over the last 1year I have seen five patients who have thinning of basal septum.. They are mildly dyspoenic and doing well in followup.. CAG were normal.. No obvious evidence of sarcoidosis were present.. One patient was on pacemaker..
In normal tubular tissue, renal tubular cells contain both functioning apical and basolateral membrane transporters. However, I am not sure in the cell culture model study that cells attach with the polyvinyl vehicle, their basolateral membrane transporters still works on exchange ions/organic substrates with the media or not. For example Na+ is rebsorbed into cells and transports back into bloodstream. Though cell culture contains not interstitial tissue or blood vessels, reabsorbed Na+ will be stagnant in the cell or secretes back to environment using basolateral Na transporters? I appreciate for every comments
I want to evaluate the results of kidney transplantation in patients with Alport syndrome and what about the percentage of rejection ?
I have developed an algorithm to identify the best HLA matched donor- recipient pair from the available HLA data bank, with parameter named as Tissue Matching Index.
This method can be used to select the best HLA matched donor/recipient.
This parameter can be easily incorporated with existing donor/recipient selection criterion.
Prostatic artery embolism is an interventional radiological procedure which can be done on TURP-NON eligible patient for BPH, it involves entrance to Prostatic Artery through the femoral artery- and embolizing w/small bubbly material.
My question is- Due to ischemic necrosis of Hyperplasic prostatic tissue there will be some kind of erosion of that tissue from rest of prostate--is it possible to see that necrotic tissue can block flow of urine- leading an obstruction of urine outflow?
My other question is-- perfusion of pelvic structures are quite complicated and involves lots of small anastomosis'-- after disabling flow of the Prostatic artery, what are the chances of getting bladder neck into an ischemic necrosis--due to possible anastomosis'?
I thank you all for your answers and your comments.
I have a 17 yrs old medically free male patient having facial scleroderma,without any manifestations in any other parts of his body.He has a tight perioral fibrous band causing severe limitation in his mouth opening.He has a history of previous attempts to restore the mouth opening surgically,but a relapse had taken place after each attempt.
N.B: the patient started to suffer limitation in his mouth opening since he was six years old.
A 54-year old man had an episode of acute pancreatitis 4 years ago (drug related). He developed an obstruction of main pancreatic duct about 3 cm from the ampula of Vater. Since then the Wirsung is increasing. Now is 11 mm. He developed a type 2 diabetes and mild atrophy of the pancreas. He is not alcoholic. Should we leave this obstruction till develop pain or other symptoms or should we operate and perform a Roux-en-Y lateral pancreato-jejunostomy?
we have 2 patients presented with confusion and quadrihyper reflexia. they completely recovered except for hyper reflexia. MRI was suggestive of osmotic demyelination. but sodium was normal through out. can any other condition mimic osmotic demyelination in MRI
One part of my work includes state of osmoregulatory function in patients with urolithiasis. But I only find one paper "Pre- and postoperative osmoregulatory renal function in urolithiasis" V. N. Tkachuk 1982. Maybe anyone know someting new?
i am doing research in diabetes complications regarding oxidative damages in kidney tissues so please inform the answer in my question
Traditionally, in patients with bilateral stones, more symptomatic side had been operated initially, but in the past few years much effort has been done to operate both sides simultaneously. My question is about your experiences in bilateral single session PCNL. Do you recommend it to your patients?
What is the clinical importance of the testicular artery emerging from renal artery in case of renal transplantation ?
Typically, clear cell renal cell carcinoma (CCRCC) is characterized by epithelial cells with clear cytoplasm and a well-defined cell membrane. Are there any software or methods we could use to quantify the transparency of the cytoplasm?
I am planning a population PK/PD study for a drug with 80% unchanged renal excretion. Can serum and urine samples be combined in NLME analysis for making a PK model followed by an exposure - response analysis? As an extension - for drugs with such high renal excretion can urine be used as a primary specimen for calculation of AUC? It will be useful to me as my sample size can increase enormously if I can find a way to use urine samples from subjects for whom even a single serum sample is not available.
Hello! I'm searching for a protocol to measure dopamine, epinephrine and norepineprhine in pig renal cortex and renal medulla. I have only performed HPLC in rodents brain, which simply consisted of a homogeneization in perchloric acid and centrifugation followed by a filtration. The organic solvent used for mobile phase was acetonitrile. Thanks a lot.
I've been using rat tissue with KHS as the primary buffer and ultimately attempting a percoll gradient of 48%. I cannot achieve good separation and end with a band entering the gradient by 1cm. I've also attempted a gradient of 45%. I aim to propagate the cells and do some toxicity studies. Thank you in advance for your help.
The question bases on the wide criticism by which measuring and estimating the body surface area (BSA) are questioned. Within the many doubts, it was emphasized the inadequate methods to measure and to estimate the body surface, the frequent change of the weight, on which are based practically all the formulae stated to estimate the body surface, and the criteria followed for indexation according to the equation : variable N x 1,73/BSA, where the standardized measure of 1,73 square meters was the average body surface in 1927 , a measure that increased very much during the past years, at present attaining 1,97 square meters, this inducing an underestimation of the measure function, being 1,73/1,97 = 0,878, that is to say a reduction of about 12 %.
I´m a PhD student, and I have been trying with silver clips, but it doesn´t works, because or is to tight and the kidney dies or is to loose and nothing happens.
I have a 15yo girl with HD dependent ESRD over the last 2 years. We don’t know her underlying diagnosis, but we think she has Wegener's. She has no symptoms, other than pos p and c anca antibodies and recurrent severe jaw pain. A recent bone biopsy has just shown chronic inflammation, kidney biopsy at presentation showed 90% globally sclerosed glomeruli.
We were planning to list her for a renal tx last month, but she got very sick. We now know she had macrophage activation syndrome (ferritin 40000) and she has responded well to high dose steroids. Our Rheumatologist thinks it is her underlying autoimmune dz that provoked the macrophage activation, as her bone marrow biopsy is without signs of malignancy and she is EBV negative.
We are now trying to find someone with experience in doing solid organ tx after macrophage activation syndrome. How should we treat the macrophage activation syndrome, and when is she safe to undergo Tx?
We can’t seem to find anything in the literature.
In earlier research we realized a high index of obese adolescentes. At the moment we are considering the possibility of kidney damage in these patients
I want to characterize renal progenitor population derived from human amniotic fluid, for this I want to know about minimum requirement of renal progenitor markers for the inclusion of a cell in renal progenitor population.
Can anyone recommend me some papers related to the risk factors of the Haemorrhagic Fever with Renal Syndrome caused by Apodemus flavicollis?
Looking at the literature on the clinical value of monitoring the volume output on a very frequent basis/second by second, I haven't found much. Are there a couple of luminary papers or experts who could help me out?
From 2 year experience in a transplant center I've seen only one pt survived with severe cavitary pneumonia.
The ideal timing of nephrectomy after embolization is unclear.