Science topic

Nephrology - Science topic

Nephrology is a branch of internal medicine dealing with the study of the function and diseases of the kidney.
Questions related to Nephrology
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The development of the kidney begins with the formation of the nephrogenic cord, derived from intermediate mesoderm, which includes the sequential formation of three nephric systems: the pronephros, mesonephros, and metanephros.
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The nephrogenic cord, derived from the intermediate mesoderm, plays a fundamental role in the development of the kidney through the sequential formation of the pronephros, mesonephros, and metanephros. This process is essential for the formation of the mature kidney, with the metanephros being the permanent and fully functional kidney in humans.
The nephrogenic cord serves as the foundation for nephron development, guiding the differentiation of cells into the nephric systems that ultimately lead to the formation of nephrons and the collecting duct system. According to research, the reciprocal interactions between the ureteric bud and the metanephric mesenchyme are key for nephron differentiation and ureteric bud branching, processes critical for proper kidney formation (Khoshdel Rad et al., 2020).
In addition, advances in kidney organoid technologies have provided significant insights into nephrogenesis, demonstrating the complex cellular and molecular interactions that occur in the nephrogenic cord. These organoids mimic the architecture of the developing kidney, helping researchers study the differentiation signals that regulate the formation of the nephric systems (Gupta & Morizane, 2022).
References:
  • Khoshdel Rad N., Aghdami N., Moghadasali R. Cellular and Molecular Mechanisms of Kidney Development: From the Embryo to the Kidney Organoid. Frontiers in Cell and Developmental Biology, 2020.
  • Gupta N., Morizane R. Kidney development to kidney organoids and back again. Seminars in Cell & Developmental Biology, 2022​(GenesisoftheKidney_Insi…).
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international journal of urology and nephrology
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Unfortunately, many clients with chronic kidney disease don't have enough vitamin K. This allows calcium buildup to form more easily.
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Please share experience with Archives of Nephrology and Urology journal. Is it authentic or fake/predatory.
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I will repeat my answer as I gave in a related question here on RG
“The journal “Archives of Clinical and Biomedical Research” is published by (as you indicated yourself) “Fortune journals” a publisher mentioned in the updated version of the Beall’s list (https://beallslist.net/#update). This is a red flag that you are dealing with a potential predatory publisher (and consequently journal). There are more red flags:
-Contact info (https://www.fortunejournals.com/) 11355 Richmond Ave #507, Houston, TX 77082, USA is fake or at best a virtual office. The same is true for the Delaware address (frequently used by predatory publishers for misleadingly suggesting an US origin while they are not)
-Same Delaware address is used by https://inter-publishing.com/index.php/ijbde published by Academic Journal INC a predatory publisher for sure numerous so-called misleading metrics are prominently mentioned on their website (https://beallslist.net/misleading-metrics/)
-Looking at https://www.fortunejournals.com/archives-of-clinical-and-biomedical-research-home-acbr.php I see a prominently mentioned impact factor, which is false and misleading since this journal is not indexed in Clarivate’s SCIE (you can check here https://mjl.clarivate.com/home )
-Mentioning PubMed is also misleading since ALL papers published by authors with a NIH grant are indexed in PubMed irrespective of the journal where the paper is published in. This has nothing to do with being a PubMed indexed journal (which they are not)
-APC (https://www.fortunejournals.com/article-processing-charges.php) is ridiculously high for an essentially non-indexed journal
Overall, I would say avoid this one.
Best regards.”
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Can you please suggest as soon as possible potential research topics on diabetic or cardia or nephrology pharmacotherapy , i need something retrospectively and drug related
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Belumosudil (KD025) is a specific inhibitor for ROCK2, which has been used for lung fibrosis and some other diseases. It may also be a potential drug in renal diseases.
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Kindly. Looking for s medical journal indexed Scopus, with Nephrology and Biochemistry subspeciality. Any suggestions?
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Hello Dr Abdulla Abdulla
For this purpose, I particularly like:
Nature Reviews Nephrology
Kidney International
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Need Expert opinion, how nephrology is running their HD machines on covid-19 patients even on heparin without getting clogged!
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What we faced COVID19 affect on cardiovascular system which has effect the blood stream of clots of blood
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I found a wide range in different papers or company websites ranging from 40 uM to 100 uM. Does using 100 uM will have cells in clumps and using 40 uM we may loose bigger cells? However, I found on Research Gate discussion that the size of cells of spleen vary in the range from 5-10 uM only. So getiing confused why we need 100 uM strainer.
Thanks.
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I believe that 100 uM is too big. Although, some papers and companies recommended 70 um, I found an article using 40 um. So I combined both 70 and 40 um, and I got way better results.
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Right ureter is maked by gases, for further assessment by CT. What does the previous indicate and mean?
Medical History:
53 Y Female with uterine prolapse.
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From what i understood you mean to say what does this mean ?
Ultrasound sometimes is unbale to diagnose the cause of hydronephrosis at it may not be seen in due to bowel gases or sometimes in nig obese individuals , to overcome such scenario patinets are usually advised CT abdomen which will help is diagnois of cause of level of obstruction .
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Which dose of vitamin C is the risk of forming oxalic stones? above 3 gm?
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Thank you for your comment, I see your point.
But there is no need to consume abundant citrus fruits or even citric acid. It seems that trisodiumcitrate works as well in lowering the risk of oxalate urolithiasis
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The US abdomen and pelvis of 65 Years old male report says: Both kidneys are normal in size, shape and position. They show normal echogenicity with preserved interfaces and parenchymal thickness. No masses or cysts could be detected, apart from left lower pole simple cyst measuring 10 mm in diameter.
Will this need a follow-up by a CT scan, or there is no need?
Images of US attached
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It looks like a simple cyst
No hurry repeat ultrasound in 3 to 6 months
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65 Y male who underwent Prostatectomy (weighing about 85 gm - 70 CC) got a urinary tract infection (As shown in the images attached) following the operation.Bothersome Symptoms following the operation (Hematuria that lasted more than a month but stopped) and another symptom that appeared 10-14 days after removal of the catheter (The catheter was removed two days after surgery) Burning urination (Still exists). Which antibiotic would you choose? And would you combine more than one antibiotic or monotherapy is just sufficient?
The urologist (Who did the surgery) recommended Cefepime 1 gm IM twice daily monotherapy. Is this the best choice? Or what would you choose/recommend based on this sensitivity test and history?
Also: The surgeon prescribed levofloxacin 750 mg after the surgery for 21 days. The surgery took place 7-8-2019
Past medical history:
Acetylsalicylic acid (Aspirin): 100 mg once daily
Rosuvastatin calcium: 10 mg once daily
Candesartan cilexetil: 4 mg once daily
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We can use combination of both cefipim and amikacin for infection according to C/S results as well as finasteride to decrease post prostatectomy bleeding for one month, and then repeat the urine culture to confirm the cure of infection
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53 Y F has 3rd degree uterine prolapse associated with bladder prolapse (Will under hysterectomy) but there are some urological problems that arose on examination. Initially Right grade 2 Hydronephrosis on US scan (Abdomen and Pelvic), thus she did CT scan to know the cause as directed by the Urologist and the findings are presented as follow (Image attached - CT image). So my Q is how would you manage the renal stones, Kinks, angiomyolipoma, Hydronephrosis? Will you just observe/wait and see the results after hysterectomy or you will try the ureter stent?
Medical History:
Atrial Fibrillation (Bisoprolol 2.5 mg once daily)
Chronic venous insufficiency (Daflon 500 mg one tablet daily)
Allergic Rhinitis (Cetirizine 10 mg once daily)
Non-Alcoholic Fatty liver disease
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It's your decision
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Is it necessary to give a daily IV furosemide blus when using CARRESS-HF protocol for cardiorenal syndrome type 1?
The details of the protocol are sometimes confused, this came as a question during a discussion with the Nephrology residents at my hospital.
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I agree that the protocol in the supplementary data of the NEJM paper is confusing. However, using pharmacokinetic principles, a ONCE-OFF intravenous bolus seems reasonable on the first day ONLY if the maintenance infusion runs uninterrupted for 24 hours. Also, keep in mind that the protocol also recommends the use of the potent thiazide, metolazone (incorrect spelling in the suppl. data) , for patients using loop diuretics in doses greater than 80 mg per day.
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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.
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I wonder if this case can tolerate the surgery.?
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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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I am a paediatrician b with special interest in nephrology.  
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what is the indication for nephrectomy you needs, I have many cases
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Does anyone have continuous quantitative bioimpedance data of intracellular changes during dialysis?  I am also interested if anyone has the same type of data regarding the deconvolution of extracellular bioimpedance data into its interstitial and intravascular components.
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What are the inputs and expected outputs for bioimpedance measurement?
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Are symptoms in patients with advanced chronic kidney disease related to Glomerular filtration rate and comorbidities? Less GFR means more symptoms and more severity of symptoms? more comorbidities means more symptoms?
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The symptoms which appear with advancing renal failure are due in the large part to the accumulation of metabolites and to changes in renal physiology. A good example is the reduction in excretion and then accumulation of phosphorus and the development of secondary hyperparathyroidism. Another example is the development of metabolic acidosis. Decrease in the excretion of several other metabolites may result in symptoms depending on their role in normal physiology. It is the development of the accumulation of metabolites and the physiologic response which results in the symptoms and development of comorbidities. Thus the development may be different in different diseases and in different individuals. For instance a diabetic with diabetic nephropathy and nephrotic syndrome, will develop symptoms early on. Although one should follow the guidelines in treating patients with CKD, the actual follow-up should be individualized to the patient, his symptomatology and speed of decrease in eGFR. In practice, a patient with an eGFR of 20 to 30 ml/min, should be followed closely for symptomatology and treatment of comorbidities. Below 20 he should be referred to a pre-dialysis clinic to investigate his condition, to ascertain the best method of treatment (hemodialysis, peritoneal dialysis, pre-emptive transplantation)  and to start to prepare them. Some patients show very slow progression and may thus be treated in a slower fashion, whereas others may require more intensive treatment.
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Estimated glomerular filtration rate ( eGFR ) is the basis for the classification of chronic kidney disease (CKD)?How.
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In the lead poisoning normal urine color but produces red
fluorescence when urine is examined with an ultraviolet (Wood’s) lamp normal urine color but produces red fluorescence when urine is examined with an ultraviolet (Wood’s) lamp
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How to perform it ? 
Once per week, twice per week, once every 2 weeks?
The idea is : patient is already having UOP, of-course with exclusion of totally anuric, oliguric or HF patients.
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Candidates that may benefit from incremental hemodialysis
Good residual renal function with urine output > 0.5 L/d (or KRU>3 ml/min)
Limited fluid retention between two conservative HD treatments with fluid gain < 2.5 kg (or < 5% of ideal dry weight) without HD for 3-4 days
Limited or readily manageable cardiovascular or pulmonary symptoms without clinically significant fluid overload
Suitable body size relative to renal residual kidney function
Hyperphosphatemia (P> 5.5 mEq/L) is infrequent or readily manageable
Good nutrition status
Lack of profound anemia
Infrequent hospitalizations and easily manageable comorbid conditions
Satisfactory health-related quality of life
Use of the criteria on 2x/week HD therapy patients should be re-evaluated once a month.
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Hi everyone!
I am conducting a research in drug-induced nephrotoxicity. In your opinion, what would be the most suitable standard to define drug-induced nephrotoxicity case? Is it KDIGO Clinical Practice Guideline for AKI or NCI-CTCAE v4.0? Or maybe you have another preference.
Please see the attachment for more details.
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Thank you for the response, Daniel & Michaela
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The question is addressing the use of SGLT2 inhibitors in a T2DM patient with past history of renal transplant provided his or her eGFR>60 and there are no other contraindications.  Please state:
Is there any trial evidence for efficacy and safety?
Do you have any personal experience?
Would you dare do it (personal view)?
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We are running a trial i RenalTx patents using an SLGT2 inhibitor and it looks to be safe in the interim analysis.
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creatinine increased up to 4 milligrams in 5 days after IV contrast and starting hydration and antioxidant treatmnet
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Contrast-induced AKI is generally reversible and non-oliguric.  SCr peaks typically 2 or 3 days after PCI and returning to baseline within 2 weeks in most cases. Although rare, persistent elevation of SCr may develop and last for several months. All that depends on several factor that increase the risk for permanent kidney dysfunction including basal renal function, comorbidities (i.e. diabetes, MM), age, injected volume of radiocontrast, dehydration, medications (NSAIDs, ACE-I/ARBS, SGLT-2 inhibitors) and recent colonoscopy.
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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.
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Hi Sal,
PAE for symptomatic patients with BPH has been widely performed with low complication rates, however, there is a potential for severe complications, including technical and clinical treatment failures. Long catheter time after the procedure and repeated catheterization are seen frequently due to failed trials of voiding without catheter. We have experienced such worse outcome during conducting a comparative RCT between PAE and green light laser prostate ablation.
Furthermore, PAE has many limitations, including  lack of significant improvement in IPSS or Qmax in 25% of patients,  unknown long-term durability,  need for high dose ionizing radiation dose and contrast material for procedural guidance, can not be technically achieved on one or both sides as a result of  atherosclerosis, small artery size, and/or tortuosity and  collateral circulation may be present, and maintains vascularity.
To date, no high-quality multi-center RCTs have been published on safety, efficacy, and cost-effectiveness of PAE for BPH.  Most of the studies are of low quality due to their case series design. Therefore, advantages of PAE must be weighed against the risk of technical and clinical failures requiring a second intervention. 
Regarding your question, bladder neck will not be affected by a selective technique done by an expertise.
Regards
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Thank you
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It refers to an epidemiologic study. You can choose the groups of individuals (cohorts)  from more than 2 centers (multiple centers) on the bases of factors that you want to investigate. Then, you follow up the cohorts over a period of time (prospective) to find out  the incidence rates of the outcomes.  As Emmadi points out observational study means there is no intervention, you just observe the outcomes.
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Is there any guideline or published papers regarding the use of maintenance IV fluids in patients with fluid overload (eg. CKD or HF) who are already using diuretics to relive symptoms of pulmonary congestion?? 
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I agree with all the authors comments. Inferior venacava diameter in echo or usg might help to guide fluid therapy in such conditions. Thanks... 
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Lupus nephritis may present with abnormal urinary findings (overt lupus nephritis) or be apparent only upon renal biopsy (silent lupus nephritis).
I would like to know the pathophysiology of silent lupus nephritis, especially, the reason why it has pathological findings of immune complex-mediated glomerulonephritis but does not have abnormal urinalysis findings of proteinuria and hematuria.
Any suggestions will be greatly appreciated.
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Usually, severe forms of lupus nephritis, e.g., DPGN would present with an active urine sediment, with the presence of red cell casts, and proteinuria; often, these patients are also hypertensive, and may have an increased serum creatinine. Pure membranous lupus nephritis would present with significant proteinuria and nephrotic syndrome, however, with a normal serum creatinine. Mixed forms like membrano-proliferative lupus nephritis would have nephrotic and nephritic components, and the urine findings would likely be abnormal in most if not all cases. For the precise histopathologic findings, including the latest WHO classification, including electron microscopy, you may want to consult a pathology book, 
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We were not able to detect elevated EDP in mice using miller pressure catheter. But we see a clear increase in EDV in same mice using MRI scanning? What would be a possible explanation for this?  
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why
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Hyponatremia is a frequent finding in the critically ill; most of these patients are euvolemic.
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Sreenivasa,
From what I'm reading, it appears to occur in about a third of all ICU admissions. Septic patients are statically more like to develop SIADH. Please see references below.
Regards,
Christopher
Pasha, S. A., Pasha, S. A., Prabodh, V. S., Vidya, S. D., & Suhasini, T. (2016). Frequency of Hyponatremia in Critically ill Patients. Indian Journal of Applied Research, 6(6).
Padhi, R., Panda, B. N., Jagati, S., & Patra, S. C. (2014). Hyponatremia in critically ill patients. Indian Journal of Critical Care Medicine : Peer-Reviewed, Official Publication of Indian Society of Critical Care Medicine, 18(2), 83–87. http://doi.org/10.4103/0972-5229.126077
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During research in urolithiasis, my team has found a few apparently healthy adults with extreme (>50%) variation in creatinine excretion, compared day and night 12-hour sample (from the same day). Obviously, we suspected inadequate collection with >12 hours in the sample with higher creatinine excretion, but those volunteers insisted in a correct collection and seemed to be reliable. The volume excretion was also quite higher in the sample with more creatinine, which was the diurnal one.
Thus, we have been thinking about alternative explanations. We have thought of a possible creatinine clearance variance. Water and other fluids overload should not change significantly glomerular filtration, as this could be usually managed by ADH supression and urine dilution in a rapid way (unless >10 litres/day, which does not seem likely). Protein overload is a well-known cause of increased glomerular filtration, in clinical and experimental settings. But could this be enough for such a different creatinine excretion in a day?
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Please consider also the intake of meat at lunch or dinner that increase creatinine excretion in the following hours.
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IVIG treatment for GBS is not cost effective.There is circumstantial evidence that standard IVIG dose (2 g/kg bodyweight) is not, or not sufficiently, effective in some GBS patients because a proportion of GBS patients continues to deteriorate after a standard course of IVIG [1]. Recently a girl of 17 yrs died in spite of IVIG treatment in a hospital with ICU support in Bangladesh. So is there any alternate cost effective treatment available for GBS? 
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Iv IG is one if the traetment modaluties for GBS,  after the 1St Dose if there was no response or even the patient showed deterioration another dose of 2gm per kg can be given,  Plasmapharesis is another option but should be done by qualified personelle in qualified centers.  There is a category in GBS Response to treatment called Treatment Related Flactuation in GBS 
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Kidney injury by contrast 
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Thank you Jasenko
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Should we worry and what is our strategy 
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We must worry. The world kidney day is just for this
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Antidiabetic drugs limitations according to GFR, a presentation from French society of Nephrology conference 2015
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There was a fear of using antidiabetic drugs especially in the dialysis patients earlier.
In our institution we use oral hypoglycemic agents modified to the renal function and according to the sugar control achieved
We do use dextrose can containing 100 milligram per decilitre but have not found episodes of hypoglycemia in such patients
Actually planning to study them prospectively
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We give pirfenidone at dose of 100 mg/kg/d in three devided doses, by oral gavage
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They have more than expected weight loss
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I and many other researchers published papers pointing out the advisability to leave the indexation of row data using BSA, fundamentally based on many different aspects : a) the used BSA is not a direct measure of the  body surface but only an estimate based on formulae derived by measures to be evaluated inadequate for the selection of measured subjects and the method of measuring ; b) the selection of formulae to use is casual, often simply due to the  easiness to remember it - c) the formulae used very often can be quite different from those used in  studies  whose results have to be compared each other d)  the change in time of the body weight, a variable on which are based the most used formulae, will induce the size of the indexed value respect to the previous value,  this causing a misinterpretation of the comparison of data in time, even the measured data remained the same. e)  the coefficient to index  data is based on the formula 1,73/BSA the same since 1928  : taking into account the average  BSA increased very much respect to 1,73 square meters in time, the indexation will excessively correct the measured value.
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I am really happy to know new and different reasons to leave the normalization of biological data on BSA
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I am going to attempt using PDGFRB tagged PE antibodies to attempt to isolate these cells from mice kidneys and to culture these cells ( if successful). Would appreciate some advise on this if you have some experience in this. 
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I have some experience with MACS but not with PDGFRB. My advice would be to make sure your cells will stain for IF with the same antibody you are using for the sorting. If the antibody doesn't bind well on IF, you won't get adequate binding for associating your cells with the beads. I believe there are Rabbit, Mouse and Streptavidin conjugated heads available so this might broaden your options.
I use the MS columns and find any more than 25 million cells takes a long time to pass (the PI says 50 million but I add another column if sorting more than 25 million - I'm also sorting kidney cells). Keep everything on ice and work fast and smart. Finally the Miltenyi Biotech protocol says to plunge the plunger into the column after it is removed from the magnet and MACS buffer added. I use chilled media instead (whatever I'm planning on culturing them in) which obviates the need to spin them down again prior to culture. Also, I apply gentle pressure only with the plunger and it is clear that the cells come out in the first few drops so no need to be aggressive with flushing them out in my opinion.
Ultimately the quality of the MACS will be determined by the quality of the dissociation and you will need single cells. I use Accutase and a 20um vacuum cell strainer to maximise separation and yield.
Best of luck!
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To the Renal Transplant/Nephrological Specialists on RG
Our renal transplant programme here is Sydney Australia is faced with an unusual problem which we have not encountered before.
We have a female recipient aged 54 years of a blood group incompatible live donor renal allograft (transplanted in April 2014), who required a prolonged course of blood filtering via columns post transplantation due to persistingly high Ab levlels to the donor blood group. This was associated with two confimred epsisodes of Ab mediated rejection. Ultimately a splenectomy was performed mid June of this year in order to help alleviate the situation.
Now she has represented with what appeared to be a long segment stenosis of the mid aspect of the transplant ureter this last week. A ureteric stent was inserted via cystoscopy and the renal allograft function has stabilised. What is now apparent on CT scan imaging is that there is marked dystrophic calcification of the renal pelvis as well as the transplant ureter (such that the ureter has the appearances of a calcified blood vessel).
Any suggestions on how best to manage this patient now?
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There is mural calcification but is there an actual ureteric stricture as demonstrated by either contrast studies or functional radionuclide studies? 
If so, I would attempt a stricture dilatation with a period of stenting in the first instance. If, however, re-stricturing or encrustations were to be bothersome, I would consider using a metallic ureteric stent such as the Memokath.
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The impact of dystrophic calcification in pressure injury management for client with a spinal cord injury
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Regardless of the etiology, the presence of calcium deposits in soft tissues may lead to chronic wounds that do not respond to conservative local wound care. For healing to occur it is well established that the solid calcific deposits and surrounding devitalized tissue must be removed from the wound sites. The mechanism for nonhealing is thought to be similar to that of a foreign body reaction caused by calcified tissue leading to chronic inflammation that does not allow granulation tissue to form.
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what is the role of 99mTc-DTPA exercise renogram in the evaluation of renal disorders ?  
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Interesting perhaps, but as renal ptosis can cause hypertension, there is a differential diagnosis to consider, and it is not straight forward. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628267/ Thus, one should check kidneys position and BP supine, and then repeat that erect, prior to exercise. Especially since ptosis repair is easy, with few complications.
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Anyone can guide me on the
1. Method of GFR measurement using Iothalamine
2. Protocol of measurement
3. Analyzer / Equipment needed for analysis
4. Average cost of the equipment and reagents?
Thanks in advance.
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Thanks mate
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The boy has received treatment with steroids, cyclophosphamide and cyclosporine A, without a good response.
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Plasma pheresis would not be our choice. Rituximab has probably the best effects, depending on the degree of glomerulosclerosis. We use rituximab even in children at very young ages (e.g. Kawasaki Disease in infants) with excellent results.
Best Chris
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Hi
I need some help for time consuming methods. I have to calculate estimated Glomerular filtration rate (eGFR) for my study patients. These are 700 patients and I have calculate eGFR for each patient. Problematic thing for me is that I have to take 5 readings of eGFR during their followup (it means I have to take 3500 readings for all patients). Can anyone suggest me any online calculator which could provide me GFR all all patients once I enter required data. Or anyone share some spreadsheet made by himself or herself so I could use it to save my time.
I shall be very thankful to you.
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Please, attached is eGFR syntaxis of CKD-EPI equation...SCr_1 (serum Creatinine measurement 1). Please, change the name Scr-1 for your current creatinine name of each measurements. Then, run the syntaxis and the eGFR will be calculated on your database.
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Sepsis, Nephrology, Internal Medicine.
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There is no proven role of low dose dopamine as renoprotective agents. A mata-analysis  reviewing 21 trials in 970 patients showed no added advantage of low dose dopamine. Instead, higher adverse events were recorded in patients who were give low dose dopamine for renoprotective effect.
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Hi
I am evaluating renal recovery pattern among non-dialysis dependent AKI patients especially among patients with AKIN-I and AKIN-II stage of AKI. I am bit confuse because my outcome is renal recovery but available literature has vast variation for definition of renal recovery.
Most of the studies have been done on critically ill patients requiring dialysis. But in my case, patients have mild to moderate severity of AKI. There is no patient with dialysis in my study. So definition of dialysis independence will be excluded. On the other hand, as in my study patients are not critically ill and have less severe stage of AKI, so defining AKI as +/-25% of baseline will show that all patients have full recovery. However, most of the patients have elevated levels of Serum creatinine as compared to baseline. and I am confuse to declare them as fully renal recovery patients because I can not ignore the findings of previous studies that "small increase in serum creatinine is associated with high morbidity and mortality"
Please guide me in this regard, with appropriate reference
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Recovery process in patients followed-up due to acute kidney injury
K Magden,1 I Yildirim,1 ME Kutu,2 MC Ozdemir,2 S Peynir,2 A Altas,2 G Yildiz,3 and E Hur1
Abstract
Introduction: Acute kidney injury (AKI) may result in complete recovery in some of the patients and partial recovery in others. AKI episodes may accelerate the progression to chronic kidney disease and end-stage renal failure, while risk for morbidity and mortality is high following AKI. Discharge of patients from the hospital, independently from dialysis is a crucial outcome. Many patients without a need for dialysis, require follow-up for various durations and different treatments. The objective of this study was to compare mean recovery time of the patients followed-up due to prerenal, renal and postrenal AKIs.
Method: In this prospective observational study, a total of 159 patients hospitalized in Bulent Ecevit Hospital, clinic of nephrology or monitored in the other wards and intensive care unit due to AKI, between June 2011 and January 2012, were enrolled. The cases were divided into three groups as prerenal, renal and postrenal, and monitored with the daily visits and renal function testing.
Results: Prerenal AKI was seen by 54%, while renal AKI was observed by 34% and post-renal AKI by 12%. Incidence of chronic kidney disease was 17.6%. Totally 43 patients required hemodialysis (27%). Of these patients, 23 were in the prerenal AKI (53.4%), 15 in the renal AKI (34.8%) and 5 (11.6%) in the postrenal AKI group. Blood urea nitrogen (BUN) and creatinine levels were dropped to the basal values only in the prerenal AKI group, on the seventh day of treatment. These levels remained higher in the postrenal and renal groups on the 7th day of treatment compared to the basal values. BUN levels decreased to the normal values on average 7th day in the postrenal, while remained higher in the renal group.
Conclusion: Prerenal AKI patients recovered in seven days with a proper treatment, although AKI patients due to other reasons should be followed-up for a longer time.
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Hello. I have a population of 500 subjects with 100 cases of MGUS. I would calculate the rate of cases over population among age-class (e.g. 20-29, 30-39, 40-49 etc). My problem is that these cases have been gathered during a follow-up of 14 years. Should I divide population in age -class of 14 years? Thanks.
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Before this can be properly answered some key questions need answering:
(i) "how were the subjects selected?" 
(ii) "was the diagnosis at the time of recruitment or at some later time point?"  (it is not clear to me that "follow-up" means follow up time of individual patients or simply the time period over which you have recruited patients).
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Hi! I am new to RT-qPCR and I have the following question.
We are planning to measure some miRs in plasma in a longitudinal cohort. As far as I know, there aren't any generally accepted reference genes to use as endogenous controls for plasma. 
We are thinking using absolute quantification with synthetic miR standards and report results as copies/ul of plasma. 
If we use AQ, do we still need to normalise against eg. cel-miR-39, to account for variability in extraction? What would be the best method for normalisation in this case? Thank you in advance!
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I will suggest you to try with RUN48 as endogenous control for RT-qPCR. We worked with this and is fine with human samples. You will get the universal primer from kit that you will use for cDNA conversion.
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He has hypothyroidism, diabetes, and hypertension. Last summer he was admitted to the ICU for severe hyponatremia (after a 4 day period of febrile illness). Several investigations we done, no specific cause was found (no infection, no malignancies and no adrenal insufficiency). It was decided it was caused by malnutrition and colonic irrigation that was done 4 days in a row.
This summer he has been complaining of fatigue for 4 days associated with worsened back pain. Routine investigations were done, including electrolytes. His Na is 132 mEq/L. 
The patient complains frequently that he feels cold. He is always overdressed. The past few days have been extremely hot, temperatures ranged between (33-36C). According to his family he has been overdressed, and covers himself with heavy blankets. The bed and blankets are wet with sweat. He almost drinks 2.5L of water daily.
*40 days ago his Na level was 134 mEq/L, his water intake was restricted and his Na levels became within normal range within a few days.
*His antihypertensive medication has no diuretic. He has a sessile colonic polyp discovered almost a year ago.
Could his hyponatremia possibly be caused by excessive sweating and high water intake? (Mimicking Exercise-Associated hyponatremia in athletes).
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Urine sodium in this patient is ~ 50 mMol/L. In presence of hyponatremia a urine Na of > 20 mMol/L is suggestive of relative excess of volume due to Inappropriate secretion of Antidiuretic hormone or Hypothyroidism, or Glucolorticoid deficiency or Stress.
In this patient hypothyroidism is already present. Stress also may be a factor. SIADH can't be ruled out at the moment.
If it is purely due of sweating (extrarenal losses) Urine Na should be < 20 mMol/L.
Water restriction to < 1 liter per day should correct hyponatremia in this patient. Also, correction of hypothyroidism will be needed.
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A 28 year old male presented with high grade fever with jaundice with severe pancytopenia, positive for Leptospira serology, deterorating further even after i/v antibiotic therapy. Later bone marrow was suggestive of HPS with high level of serum ferritin and triglyceride. He was started with pulse dose of i/v solumedrol (methyleprednisolone), and there was dramatic response with disappearance of fever and improvement of blood parameters.
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Pulsed solumedrol would likely be most effective for HLH when treating a causative auto-immune disorder, such as the above article on Still's Disease or MCTD.
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Many researchers here mentioned not to use HEK293 as it is transformed cell line and it is not really attaching the surface and easily detach even washing with pbs. I also faced the same issue with this HEK293 cells. I would like to check with you guys which human kidney cell is better to test cytotoxicity tests. Will it be valid if I choose to test from other spp kidneys? e.g. Canine kidney MDCK, Feline kidney CRFK, Vero (ATCC® CCL-81™)~monkey kidney, mouse and rat? 
So appreciate if someone know the best human kidney cells for cytotoxicity test?
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Don't use HEK293 for cytotoxicity test with MTT or other dye. Cell are not attached well. Finally dye will be gone with aspiration out MTT before adding Solvent. So, never give actual results at all. I have tried many times. It is crazy. Just sharing. 
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On our center our patients on CCPD plus do not connect to the cycler to do the daytime dwell, they do a manual exchange, many times due to personal constraints. We should add a sample of that dialysate to the sample of the cycler the patient collects to calculate a precise kt/v.
How should we do the ratio of volume of that manual dwell to add to the sample they bring of the night dwell from the cycler, in order to calculate the correct kt/v? How many mL should the patient collect of that bag and of the nighttime dwell?
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Thank you! That's a new idea to solve this problem, we are asking 2 separate samples and then trying to do a proportional mixing, but as you understand it's not easy and it is prone to error... I will present that option to the team, thank you.
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His Na on discharge from the hospital (11 days ago) was 138mEq/L. 9 days ago it was 139mEq/L. Today it is 133mEq/L. 
Is it worrisome, should the patient be admitted to the hospital? Is conservative management (fluid restriction & higher salt intake) enough? Are there any other investigations to be done? 
His SIADH was attributed to drugs (Thiazide Diuretics, Alprazolam, Escitalopram), Hypothyroidism (his thyroid meds were stopped for 3 days during which SIADH developed, Infection (Suspected Sepsis from Gastroenteritis). Paraneoplastic syndrome was suspected because of elevated CA 19.9, and CEA. After thorough investigations, a .77cm sessile polyp was found in the sigmoid colon. It is to be removed and evaluated 3 months later.
The patient has had fleet enemas (colonic irrigation) six times in five days immediately before symptoms of hyponatremia first began to show.
He has HTN, DM, & Hypothyroidism. His blood pressure was controlled (130/90mmHg) but after hospital discharge his blood pressure ranges between (120-110/75-55). 
His appetite is excellent, he didn't take Glimipiride(1mg) for the first 7 days after discharge, he has been back on it for 3 days now. His fluid intake is normal (no fluid restriction). 
The patient complained of dysuria for the past 4 days.
Other: He has vetiligo, and has bouts oral HSV.
EXTRA INFO: 
He was on Thiazide Diuretics until he had SIADH.
His Na when he had SIADH (20 days ago) was 103mEq/L.
He didn't have diarrhea when he had SIADH, nor does he have it now. But he had fleet enemas from tap water (colonic irrigation) five days in a row immediately before he developed SIADH because he was constipated and had abdominal pain.
What should be done for this patient? 
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The following investigations might help in treatment of this patient - measurement of urine Na & osmolarity .  A low urine Na & high urine Osm would suggest hypovolemia as a cause of Hyponatremia . A normal urine Na & high urine Osm with euvolemic status would suggest SIADH . A similar urine Na & Osm status can also occur in hypervolemic status , such as cardiac failure .
   The fact that he had thiazide diuretics & enema suggest that he would have had hypovolemia as a cause of hyponatremia & in addition , his anti - depressant might have also contributed to hyponatremia . The improvement of hyponatremia from 103 to 139 mEq suggest that the restricted water & high salt intake has worked  His 133 mEq , at present might also suggest hypovolemia which needs evaluation . Please continue the same protocol of treatment as this has corrected his hyponatremia during his previous admission .
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Is there prognostic or predictive significance in those approximately 5% dialysis patients who experience repeat exaggerated responses to even a single administration of modest doses of intravenous iron? [much higher than expected and more prolonged elevations of TSAT (serum iron/TIBC) and ferritin]?
Sometimes, the labs remain elevated for months after a modest IV iron administration.
While these labs are not perfect, they are currently the most commonly used markers to aid prescribing of iron therapy in dialysis.
This observation presents challenges for the treating prescriber.
It would be nice to know what is the significance to help guide therapy.
I'm not familiar enough with the use of soluble ferric pyrophosphate (SFP) to know if SFP would be a better choice for treatment of these patients.
I do not have full access to the below referenced article. While the focus may be different from the question above, I wonder if the authors noticed any significance for the observations referenced above.
Nephrology (Carlton). 2016 Jan 29.
Characterisation of hepatic and cardiac iron deposition during standard treatment of anaemia in haemodialysis.
Holman R1, Olynyk JK1,2, Kulkarni H3, Ferrari P4,5.
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Thank you kindly Dr. Gillain-Martin for the resource.  It is an excellent read.
I am uncertain if these patients are truly iron deficient or functionally iron deficient.  I was hoping that prior research might have already answered this question of significance.
Is an exaggerated change a clinically significant finding and how would "exaggerated change" be best defined? 
On a deeper level, I wonder about mitochondrial iron metabolism especially in this subset of dialysis patients.
I am revisiting the data on these patients looking for any patterns or clues.  However, I was hoping that large data base analysis would have already offered useful insight.
Does the three month testing as suggested by the article reduce the chances of capturing these patients?
In the US, electronic decision support protocols suggest dosing and frequency of parenteral iron prescribing for the overwhelming majority of dialysis patients using the surrogates of ferritin, TSAT and also commonly using elevated hemoglobin cutoff levels.  The testing frequency is usually every 30 days with the exception of at least a week post last administration of parenteral iron (which might not be long enough ?)
Also, as mentioned in the article, other markers may not be as practical for broad use.  To my knowledge, IV iron prescribing in the US HD population does not usually consider exaggerated response to IV iron (exaggerated change in parameters/markers) beyond the cutoff parameters as set by the algorithm.    
_______________________________________
Excerpts from the referenced article:
"Combined use of CHr and high-fluorescence reticulocyte count allowed for very high accuracy in the early prediction of the response to intravenous iron therapy in hemodialysis patients, with a sensitivity of 96% and a specificity of 100% (10). However, neither CHr nor the percentage of hypochromic RBC has the ease of use, cost-effectiveness, and widespread availability of the traditional tests, such as ferritin and TSAT (34)."
"Diagnosis of iron deficiency and guidance of iron supplementation should be made in stable patients with ESRD by ferritin and TSAT measurements at 3-mo intervals."
Clinical Aspects of Iron Use in the Anemia of Kidney Disease
Walter H. Ho ̈rl
Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria
J Am Soc Nephrol 18: 382–393, 2007. doi: 10.1681/ASN.2006080856
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We are injecting collagenase NB8 to the pancrease,
17 minutes in 37 bath,
Washing twice,
Filter the suspension through a 425um diameter wire mesh
Use Histopaque to seperate the cells 
and wash twice.
Do self sedimentation 6 times..
and yield only 300 islets.
How can I improve the method?
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Dr. Yael,
Manishma!
Selection of enzyme and species is important. It is important to choose an enzyme and species it pairs well with. For Rats (Wistar, Lewis, SD) we have found Collagenase XI (Sigma) at 1.5 mg/mL in HBSS works well. 
Some common steps to check:
1. Pancreas distension is full, indicating injection was into common bile duct not hepatic artery. Hepatic artery injection will result in islet being preferentially digested instead of the exocrine.
2. Digestion time optimization (12-15 mins). You will probably due 3 rats at once. So, the first one at 12 min digestion, take out conical tube and with one hit about 80-100% of the pancreas should fall apart. If it does not, then digest a little and then stop reaction. You will know to extend your digestion time for the other tubes.
-You can also take dithiozone, and take a sample of the digested pancreas extract to see if intact islets are staining purple. If small fragments are staining, then you have overdigested. If you see trapped islets, then you are not digesting enough. Dr. Nunemaker's comments about islet roughness also apply.
3. Gradient purification tips. Following washing cells, pour out wash into gradient beaker. Then place conical tube, inverted, onto paper towel and let drain for about 30 sec. This will help remove excess water from tissue and help your purification.
4. Did gradient purification work as intended. Following gradient purification with histplaque, collect "other" supposedly non-islet fraction. Stain with dithizone to see where islets are ending up.
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Oncology ; Nephrology ; Intensive Care ; Hematology
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It depends on indications and clinical conditions (fist of - all hemodynamic stability). What is the cause of renal failure? For example - sepsis - CRRT (hemo- or hemodiafiltration) 12-24 or more hrs. Pre-renal failure after massive blood loss and risk of haemorrhage - short-term dialysis may be better, and so on. Can anybody compare such different patients in a trial?
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What is the best way to measure urine bicarbonate (HCO3-)?
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we have measured urine pH and PCO2 using a clinical laboratory blood gas analyzer and calculated urine HCO3 from these results. The blood gas analyzer can be re-calibrated to a lower pH of the urine to give more accurate results; however there are some extremes of urine pH ie 4 or 9 not seen in blood and even with re-calibration, the blood gas analyzer results will not be close to these values giving some error. Also the warranty for the blood gas analyzer does not extend to testing urine samples with extreme pH deviation. So you might be best to use specific electrodes for pH and PCO2 that can be calibrated to the pH range of your samples rather than clinical grade blood gas analyzers.
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patients with tx glomerulopathy have been seen commonly recently. management of tx glomerulopathy is diffucult.
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Agree with previous opinions, not sure if increasing immunosupression will be of any benefit. Try to rescue the remaining viable tissue and buy some time before it fails. Would suggest keeping TACROLIMUS blood level around 5, rule out BKV associated nephropathy " although it is less likely giving the remote time of transplant and the low level of Tacrolimus in blood, follow renal diet " Salt and Protein restriction". Would starting counseling for re-transplant. One last option would be a single run of steroid pulse " if no other contraindication" - won't hurt.
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CECT is one of the most frequently performed radiological investigations in emergency settings. Though, unquestionably, in certain circumstances, the benefit of CECT outweighs the risk of CIN in patients at risk. However, in all patients where CECT may be helpful should not form a basis for routine practice. The nephrology residents often just act to "clear" the patient for contrast study without actually knowing the patients' condition (save S.ur/ S.cr levels!). The standard line written is CECT may be undertaken if clinically indicated.
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Hi Pankaj,
I view this nephrology "clearance" in two parts, depending on the source of the referral. Firstly and more commonly, is the expectation that nephrologists will identify the relevant risk factors for contrast-induced nephropathy in order to help optimize the patient's condition and minimize the risk of CIN. Others have already provided suggestions as above. Secondly, there is also perhaps a medico-legal aspect to this "clearance" as it relates to procedural informed consent, particular regarding the possibility of AKI requiring renal replacement therapy (particularly in high risk patients and existing CKD). It also means that "clearance" implies that the nephrology team will then provide supportive RRT if the worse case scenario eventuates. In some cases of multi-morbid and elderly/frail patients, RRT may not be tolerated or possible and these issues need to be discussed beforehand.
So, I totally agree with your comments that nephrology residents "clearing" a patient for CECT without due diligence and consideration of the issues, is risky not just for the patient but also potentially from a medico-legal perspective (depending on the environment you work in).
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The Roche Ketorolac Package insert for Toradol tablets and the ketorolac package inserts from generic manufacturers state that ketorolac is contraindicated in advanced renal impairment, but the degree of renal dysfunction is not specified (i.e. moderate or severe), and specific values for serum creatinine or creatinine clearance are not given. Hospira Medical Information states that the package insert only states “advanced renal failure” as a contraindication, and the degree of renal dysfunction (i.e. moderate or severe) is left to the discretion of the clinician. Drug references such as the Lexicomp Drug Information Handbook and others interpret this as meaning that ketorolac is only contraindicated in severe renal failure, and can be dosed in moderate renal failure at the reduced dose of IV or IM 15mg q6hrs.
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Avoid using at all cost, esp in those with any stage of CKD or proteinuria, those on inhibitors of the renin ang system, in obesity, or anyone who may be predisposed to AKI. De novo oligiric AKI can occur even in young patients who have no CKD.
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Eight decades ago, Al exander Randall identified calcium phosphate deposits at the tip of renal papillae as the origin of renal calculi. The awareness that these “Randall’s plaque” promote renal stone formation has been amplified during the past years by the development of endoscopic procedures allowing the in situ visualization of these plaques. Recent studies based upon kidney biopsies evidenced that apatite deposits at the origin of these plaque originate from the basement membranes of thin loops of Henle and then spread in the surrounding interstitium. In addition, scanning electron microscopy examination of calcium oxalate stones developed on Randall’s plaque evidenced that plaque may also be made of tubules obstructed by calcium phosphate plugs. Hypercalciuria has been associated to Randall’s plaque formation. However, several additional mechanisms may be involved resulting in increased tissular calcium phosphate supersaturation and the role of macromolecules in plaque formation remains elusive. At last, apatite crystals are the main mineral phase identified in plaques, but other calcium phosphates and various chemical species such as purines have been evidenced, revealing thereby that several mechanisms may be responsible for plaque formation.
Urolithiasis August 2014 Date: 07 Aug 2014
Randall’s plaque as the origin of calcium oxalate kidney stones
Michel Daudon, Dominique Bazin, Emmanuel Letavernier
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Article gives good information. however, while investigating a Stone disease patient , a high Super-saturation index gives useful information whether individual is forming stone or not. This is irrespective of values of urinary calcium, oxalates etc.  I mean for example even if urinary calcium or other components are  abnormal and supersaturation is not high, then person is not forming stones
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Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. is the same efect in patients with familial glucosuria?
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http://www.medscape.com/viewarticle/812072_12      This might be of help.
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All I can find in the literature is intravenous injection followed be several timepoints of blood sampling.
Thanks
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So many better ways to measure or estimate GFR
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I have read that ATG is a cumulative drug and the life long dose that the patient can recieve should not exceed 25mg/kg - how true is that statement?
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I don't think anyone knows. . .
Just recently SRTR has started collecting the the number of doses (not the actual numer of mg/kg), so I think we may have a better idea in the future.
My bet is it is a continuous variable, like pack-yr in smoking, where you have higher index of suspicion for cancer, etc, as the lifetime dose increases.
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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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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.
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My patient was transplanted just 6 weeks ago, and has done very well. After her MAS she was treated with pulse solumedrol x 3 doses, followed by oral steroids 60mg q day and MMF in a dose of about 1000mg/m sq /day. She became remarkably well after going on the this treatment. She had been ill on hemodialysis for months without any diagnosable cause.  Oral Steroids were weaned completely as she was doing so well.
For the renal transplantation she was induced with Simulect and treated with Tacrolimus and MMF (our usual protocol), and she has been doing well except delayed graft function for 2 weeks. She is off dialysis now with almost normal renal function. Her MAS was not reactived during any of the surgeries.
Thanks for comments for my question
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A 69-year old woman was diagnosed primary amyloidosis with renal involvement and nephrotic syndrome in 2006. She was treated by another nephrologist with 9 cycles of prednisone, melphalan and Rituximab. NS underwent partial remission, renal function remained normal. After the 9 cycles, she developed tubercular cystitis. She now has no evidence of active infective disease, but present a NS, normal renal function. What treatment options can be considered?
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After all that, I would treat a 69-year old woman with normal renal function not specifically, because treatment may cause more harm.
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Seeking information on IPD intermittent peritoneal dialysis.
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Intermittend peritoneal dialysis (IPD) was used earlier in severe uremic patients to avoid a dialysis disequilibrium syndrome or as a longterm treatment. IPD has been replaced by short daily hemodialyses on the start of intermittent hemodialysis dialysis (IHD) or continuous ambulatory peritoneal dialysis (CAPD).
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dialyzer size - pump speed - dialysate speed - max Ultrafiltration and the relation with sex - age - BMI and cardiac health 
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There are some individual parameters which must be set for each particular patient (dialysis time, blood flow, heparin dose, sodium and bicarbonate concentration, substitution volume if you use HDF) or even for each dialysis session (volume to be ultrafiltered). There are a few "rules of thumb" with which you can start and later adjust according to the results:
Dialysis session time should not be less then 4 hours
Blood flow should be high enough to give total processed blood volume equal or higher than body weight
Sodium concentration about 3 mmol/l higher than patient predialysis plasma value
Bicarbonate concentration i dialysate - start with 30 mmol/l is safe.
UF rate should not generally exceed 10 ml/hour/kg of body weight
If you use unfractionated heparin you can start with bolus of 50 iu per kg of body weight and then 300 iu/hour as an infusion. This will certainly need adjustment - you have to look to bleeding time after removal of needles and to the dialyzer appearance (how many fibres are clotted) after rinse back.
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Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use  of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
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See the relevant chapter in my wonderful new book. CARDIORENAL CLINICAL CHALLENGES.  Eds Goldsmith, Covic, Spaak. Published by Springer Jan 2015.
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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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We have managed 2 cases. Both of them were diagnosed with SSNS at two years, responded to prednisolone, subsequently became steroid resistant, managed with methylprednisolone and cyclosporine. After stopping cyclosporine a recent relapse shows serum creatinine levels of 3 mg/dl. What should we do?
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Have you studied autoimmunity of  your patients?
the presence of anti-ANCA antibody, anti-PLA2R, anti-DNA ...?
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19 YRS,Male.Confirmed MCGN on biopsy,now in CKD 5 stage.His 2 Male,first cousins have renal failure(Children of his mothers 2 sisters) and on dialysis.
Is this an X-Linked inheritance pattern
Can his mother be a kidney donor for him.
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Thanks for your response Dr.Vellanki
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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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There are pro and contra opinions regarding the keeping of the AV Fistula or not after KTX. What is your experience?
Arteriovenous fistula after renal transplantation: utility, futility or threat? Nephrology Dialysis Transplantation 2006 21(2):254-257; doi:10.1093/ndt/gfi276
AV fistula closure reduces left ventricular volume and mass in renal transplant patients. Whether fistula closure will reduce the associated high cardiac morbidity and mortality is unknown. There are clearly insufficient data yet to promote systematic closure of AV fistulas in kidney transplant patients with stable renal function, unless symptoms are present. The balance might favour closure in selected asymptomatic patients, with a large AV fistula, a dilated left ventricle,a low probability of graft loss and a high risk of cardiac events. Randomized large-scale prospective studies are clearly needed and, potentially, will better define the protective role of fistula closure.
Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients Nephrol Dial Transplant (2001) 16: 368-372
Closure of the arteriovenous fistula in stablerenal transplant patients results in a decrease in LVMi, dueto a reduction in LVEDD. The change in LVMi is significantlyrelated to the LVMi and LVEDD before fistula closing. In patients with a well-functioning allograft and persistent LV dilatation,closure of the AV fistula might be considered.
Arteriovenous fistula closure after renal transplantation: a prospective study with 24-hour ambulatory blood pressure monitoring.  Transplantation. 2008 Feb 15;85(3):482-5.
Because the increase in diastolic blood pressure after arteriovenous fistula closure occurred regardless of the preoperative level of diastolic pressure, we suggest that blood pressure should be monitored after fistula closure, particularly when preoperative diastolic blood pressure is borderline or elevated.
Cardiac impact of the arteriovenous fistula after kidney transplantation: a case-controlled, match-paired study (Transplant International, Volume 21, Number 10, October 2008 , pp. 948-954(7))
In kidney transplant (KT) recipients, cardiac impact of the persistence of an asymptomatic arteriovenous fistula (AVF) for hemodialysis has not been fully elucidated.
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The number of vascular access sites for hemodialysis is limited to about 8 (3 in each upper extremity and 1 in each lower extremity).  Even the best kidney transplant grafts do not last forever.  The conclusions by Manca et al from almost a decade ago are still valid: " we conclude that the definite indications for AVF closure in well functioning renal transplanted patients are heart failure, high flow fistula, VA complications and important aesthetic reasons. Routine AVF closure is not indicated until prospective and randomized studies can demonstrate the ability of this procedure to reduce the high incidence of cardiac morbidity and mortality that is present, even after renal transplantation." From "The management of hemodialysis arteriovenous fistulas in well functioning renal transplanted patients: many doubts, few certainties" in Journal of Vascular Access (Oct-Dec 2005) Vol 6 Number 4:182-186 
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What is the role of anp on renoprotective and what is mechanism behind it?
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In 1995, the Ministry of Health and Welfare of Japan approved recombinant ANP (carperitide) for intravenous administration in patients with acute heart failure (AHF) and acutely decompensated heart failure (ADHF). However, the recombinant form of BNP (nesiritide) was not approved for therapeutic use in Japan. In contrast, in the USA, the Food and Drug Administration (FDA) approved nesiritide in 2001. Therefore, the clinical evidence for ANP has been compiled mainly in Japan, whereas the evidence for BNP is mainly from the USA. Several reviews and meta-analyses concerning BNP use were generated using data obtained in the USA. In this context, this review focuses on recent clinical data regarding ANP as a therapeutic agent in several diseases, as well as experimental data from genetically engineered mice which may rationalize the clinical usefulness of ANP.
google base data....
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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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I'm skeptical, especially as I have refereed a lot of low quality research. However, a conversation with a colleague led me to think that there may be some niche (maybe AKI or research in certain parts of the world?) not currently covered by journals. What do you think? Are there particular forms (e.g. online only, with discussion forums etc.) that you think could enhance nephrology journals?
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I feel there is no need for a new Journal, however the need of the hour is to get more data from countries like China. Being not so accomplished in English or other European languages many countries are not reporting interesting data. Instead of adding new Journal we should strive for bringing out more quality data from such countries. It will also be interesting to see if we can change the policies in dialysis particularly as the current data is heavily based on Caucasean population studies.