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Clinical Nephrology - Science topic

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I am preparing to conduct a study to investigate the association between periodontal status and Kidney health in Saudi patients.
Is it logic to examine randomly selected patients in dental clinics (with unknown systemic diseases) to check periodontal health (1st variable), and then send the patients to nephrology unit to check kidney health (second variable)?
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Hello Dr Hassan H Kaabi.
we have done an extensive study on the relation between periodontal disease and many systemic diseases and we found that periodontal disease affects kidneys
Periodontitis had a significant direct effect, an indirect effect through diabetes, on the incidence of Chronic Kidney disease. Awareness about systemic morbidities from periodontitis should be realized
The American Academy of Periodontology (AAP)
has published a statement on kidney disease and tooth loss (periodontal disease)
Researchers Caution that Tooth Loss May Increase Risk of Chronic Kidney Disease in U.S. Adults
as for your questions about the selection of patients
dr Grubb Vanessa Grubbs, MD, an assistant professor and neprology specialist in the UC San Francisco's School of Medicine who is determined to advance this research as part of her commitment to preventing the chronic health problems associated with kidney disease.
you might want to contact he she can tell you how she selected patients
Dr Grubbsince 2013 has published that paper and i have attached it, it really shows you how she selected her patients and you might want to look at it even copy the method
the title of the paper is The association of periodontal disease with kidney
function decline: a longitudinal retrospective analysis
of the MrOS dental studyin Nephrol dial transplant 2016 31;466-472
i also attached a 2021 paper on the topic, good luck in your study that is a very important topic
sincerely
Dr.K.A.Galil.Professor of Medicine and Professor of Dentistry DDS.,D.Oral & Maxillofacial Surgery ,PH.D,FAGD.,FADI.,Cert.Periodontist(Uof Michigan) (Royal College Dent Surg.Ont) Departments of Periodontics,Orthodontics and Clinical Anatomy Schulich School Of Medicine and Dentistry. University of Western Ontario, London,Ontario.
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A young patient attempted suicide by taking 63 tabs of carbamazepine 200 mg. she was managed with CRRT - CVVH and discharged 10 days later well and couscous.
data supporting the use of hemodialysis in managing carbamazepine poisoning is increasing, so I am not sure if it is worth publishing or not ( if it has a chance to get accepted for publishing)
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you must publish your findings
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Does this report indicate any malignancy and what are your recommendations based on these reports?
Transrectal Ultrasonography of the pelvis report:
The prostate is enlarged weighing about 85 gm with apparently intact capsule. The median lobe is hypertrophied indenting the bladder base and mildly projecting within its lumen. Heterogenous parenchymal echogenicity is noted however no definite evidences of focal lesions...BPH...For correlation with PSA level.
Both seminal vesicles are bulky showing tiny cystic changes.
Past Abdomen and Pelvis US report:
Mild circumferential wall thickening of the urinary bladder, with prominent trabeculations and with echofree lumen and no mural lesions..features of chronic obstruction uropathy...for clinical and lab correlation.
Full volume= 315 cc3
Post-voiding volume= 20 cc3
The prostate is enlarged in size (70 cc) seen identing the bladder base with prominent median lobe with intact capsule
Normal size and echogenicity of both seminal vesicles
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Based on the ultrasound report, this patient has BPH (with median lobe enlargement) and features of obstructive uropathy. The heterogeneity of the prostate only indicates there should be further evaluation.
Usually you have to correlate this finding with DRE findings as well as the PSA. Based on these, patient may thereafter need prostate biopsy (ultrasound/MRI guided preferably) before a diagnosis of prostate cancer can be made or ruled out.
So as a stand alone, this report does not indicate prostate cancer.
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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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from where we can get the value of PK?
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Depends upon the human variability and other factors that is determined by the expert toxicologist. There is no "cookie cutter approach." Go to https://goo.gl/dGrSqo for a large catalog of PDE/ADE monographs. BTW - you're not going to get this information for free. Occupational toxicologists expect to get paid and don't give away their expertise for free.
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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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Why do almost all the guidelines (WHO) choose urinary iodine to define iodine deficiency but not blood iodine?
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reply of Ken Andrew Sikaris is absolutely right. Spot Urinary Iodine excretion is utilized for epidemiological study which cannot be translated into individual iodine status.UIE is determined for assessment of IDD in a given population who reside in a defined geographical location.
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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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I have a group of subjects on supplement A for 3 years. Their blood pressure (BP) and kidney function, as measured by creatinine clearance (eGFR) were monitored at 1-, 2- and 3-year. In unadjusted models, BP decreased and eGFR increased significantly over time. It is well regonised that those who has a better kidney function (higer eGFR) will have a lower BP.
I would like to assess whether the changes in BP remained significant after controlling eGFR (to evaluate whether supplement A has direct effect on BP reduction or indirectly through eGFR improvement). Is it appropriate to use LMM with time-varying covariate for such analysis?
Thank you.
#edit: part of my text went missing earlier
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I noticed BP reduced and eGFR improved over time, however I would like to know whether Supplement A directly improved eGFR or indirectly improved it (mediated through BP reduction). In this case, is it feasible to use LMM with time-varying covariates? Thank you very much!
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Looking for some information on the effect of high intensity exercise on serum creatinine levels and potential false positive eGFR results?
I'm also interested if an individual with increased muscle mass would effect the serum creatinine levels and eGFR?
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Hi, perhaps this can be useful for you! 
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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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I have some incomplete data regarding creatinine in mouse urine that I would like to use to evaluate proteinuria. I would like to know what is the usual quantity of creatinine found in 24h urine to compare it to my results, does anyone know it?
Thank you!
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Thank you for your answers! Apparently, in human there is a fixed quantity (not concentration) of creatinine that can be found in 24h-urine samples. I think it is around 1 to 1.5 g so I was expecting something similar for mice. Thank you again
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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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I am conducting a meta-analysis for renal function as outcome. On of them is albuminruia/proteinuria. Some studies have reported albumnuria while other have reported proteinuria. Can I combine both in same meta-analysis?
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A meta-analysis on this subject is very interesting, but you must absolutely record the discrepancies between the two parameters and know the reason for these discrepancies. This will allow you to highlight some analytical errors due to the inaccuracy of the total protein assay , but also the many cases where the urine contains other proteins (high and low molecular weight proteins, monoclonal component...) than albumin
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Some books say ACE inhibitors are contraindicated in renal failure while some say they are first line for treatment of renal failure..I wanna know if they are indicated in renal failure when GFR is going down and creatinine is rising up whats the underlying mechanism by which they improve renal failure.? 
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The use of ACE inhibitors or  angiotensin receptor blocking drugs are indicated in nephropathy with proteinuria, includind those with chronic renal failure.
Hou and colleagues (China) (1) presented data indicating that the use of benazepril, an angiotensin-converting–enzyme (ACE) inhibitor, is feasible and beneficial in patients with advanced chronic kidney disease, demonstrating that ACE inhibitors can be administered in generous doses, even in patients with stage 4 chronic kidney disease, as defined by a glomerular filtration rate (GFR) of 15 to 29 ml per minute per 1.73 m2 and a serum creatinine level of approximately 3.0 to 5.0 mg per deciliter (265 to 442 μmol per liter).
Their findings also indicated that ACE inhibitors may provide renal benefit even if a patient's serum creatinine level continues to increase. Patients with hyperkaliemia and inordonate decining of renal function were excluded from the study. Diuretic use protects against hyperkalemia by shifting sodium reabsorption to the distal nephron, where increased sodium–potassium exchange occurs, resulting in increased renal potassium excretion.
Metabolic acidosis correction by using of bicarbonate oral supplementation can also minimize the risk of hyperkaliemia induced by those medications. and stopping decline of kidney function in CKD patients. (2)
But I agree with the opinions of my colleagues on the regular monitoring of kidney function and ionogram before and after the initiation of ACE inhibitors or angiotensin receptor blocking drugs.
 (1) Hou FF, Zhang X, Zhang GH, et al. Efficacy and safety of benazepril for advanced chronic renal insufficiency. N Engl J Med 2006;354:131-140
(2) Cochrane Database of Systematic Reviews Correction of chronic metabolic acidosis for chronic kidneydisease patients (Review)Roderick PJ, Willis NS, Blakeley S, Jones C, Tomson CRoderick PJ, Willis NS, Blakeley S, Jones C, Tomson C.Correction of chronic metabolic acidosis for chronic kidney disease patients.Cochrane Database of Systematic Reviews 2007, Issue 1. 
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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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I have used Intravital multiphoton microscopy for capillary rarefaction in disease states in rodent models. One also can use this tookit for glomeruli capillary function in health and disease in your particular rodent disease models. One noticeable examination of diseased superficial cortex capillaries is endothelial dysfunction and interstium leakage.
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I am trying to impute a continuous variable prior to running logistic regression and having trouble with it. Multiple imputation of the continuous variable works perfectly, however, when I categorize it, after imputation but prior to adding to the logistic model, somehow my results change. It appears to be significant loss of power for some reason such that my highly significant variable falls out of significance. For instance, when trying to impute blood sugar values and then running a logistic model against a binary outcome, the parameter estimates are very comparable for all covariates including blood sugar with or without imputed data. However, when I categorize the blood sugar into 4 categories in the imputed dataset and then run it, the variable falls out of significance. If I run the logistic model excluding patients with missing value (pre-imputation) with blood sugar categories, I get very plausible, logical results (comparable to results from an entirely different dataset). Is it wrong to categorize the imputed variable in the imputed dataset?
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Shveta -
Imputing within categories would help make nonignorable nonresponse, more "ignorable;" that is, you would account better for the mechanism of nonresponse.   If you are having a "significance" 'problem,' please note that p-values are sample size dependent, and your smaller sample sizes by category, if I understand your problem correctly, is what is giving you bigger p-values.   That is why you need to pay attention to effect size, or a type II error analysis, and not set the same "significance" threshold for every case.  (Note that confidence intervals and prediction intervals are less open to serious misinterpretation.) 
Please see the following:
Press release for the American Statistical Association:
My letter in The American Statistician:   
Hope I did not misunderstand your question.
Cheers - Jim
PS - Actually, however, even though you are using multiple imputation to avoid artificially reducing variance, it still depends on the original data, so the standard errors you estimate for the above should not include imputed data, as that would still artificially increase the sample size.  Breaking up by categories is good.  That helps with "representativeness," but too much missing data is still a problem.   -   If you are imputing in the case of multiple independent variables and have missing data that varies in the number and/or identity of missing cases, and doing multiple imputation on each, so that sometimes for a given "i" you have one regressor, but not another, you might look at the prediction interval with and without imputed regressors, to get bounds on the 'true' prediction interval for each category.  That's what I think I'd do with ordinary or weighted least squares regression.  I suppose analogously with logistic regression, with which I have not worked, however.  
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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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A 84 year old woman with hypertension, 2 type diabetes mellitus and chronic renal failure (GFR 30-50 ml).
2005 NSTEMI: LAD and LCX PCI
2006 angina pectoris: distal RCA PCI. LAD and LCX stents no changes
2014 UA: RCA ISR. 1 BMS implantation. Other stents without ISR 
Echocardiographia all the time showed good systolic ejection fraction with good wall motions. 
In 2014 starts: in ECHO showed a non siginificant pericardial effusion. After coronarographia seen hematuria and anemia. 
An urological examination was negative for tumor, but an pelvis CT was done, whith some negative result.
2014.07 gastroscopia: duodenitis erosiva and chronic erosive gastritis was.
              colonoscopy: negative
2015.08.03-04 was admited with melena.  Gastroscopy and colonoscopy was not showed a point of bleeding. 3 U of blood was transfused.
An echo showed a significant pericardial effusion and a pericardiocentesis was performed. 1200 cc. straw-yellow liquid evacuated. And other day 100 cc.
2015.08.05-12 admited to hospital with anemia for blood transfusion. Colonoscopy was done again.  The source of bleeding was not found. A polyp of the  Bauchin valve was cut of.
The histology result of the colonoscopy sample not confirmed malignancy.
2016.01.05 Admited agin with huge pericardial effusion and symptoms of HF. 1500 cc straw-yellow liquid evacuated. A pleural effusion was this time and a diagnostic thoracocentesis was done.
The results from the pleural fluid showed a sigillocellulare cc. cells
The CA 125 was elevetad.  (95 the normla range upper limit is 35 at our lab)
Pericardial fluid: eosinophil cells, mesothel and lymphoid cells was seen.
An cardiac MR was done with negative result for a  autoimmune disease or primer cardiac malignancy.
An chest CT was done: negative for cc.
An abdominal and pelvis MR was done: at the point of obturator in both side an 6 mm diameter  lymphaticus nodus was detected. In the corpus of uterus an 8 mm myoma detected (T2)
Tuberculosis negative.
The hemoculture results is negative
2016.04.20 was admited with huge pericardial effusion. 1200 cc bloody liquid was evacuated. 
And now 2016.05.31. Again was admited with effort dyspnoe and not a very huge pericardial effusion.
The pericardial effusion sizes was 30-35 mm mostly left side and 25 mm from apex and right side.
The gastroentereologist, onkologist, gynecologist and urologyst do not know the reason of chronic pericardial effusion. Please help, what is the diagnostic option which can use to find the cause of pericardial effusion.
Thank you that you read and help.
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I think a partial pericardiectomy and biopsy will both help symptomatically and will probably give the diagnosis.  Malignancy should be high in the differential especially sonce the last effusion was bloody. You can also do a mammography and a thorough skin examination. Please let us know of the progress. 
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I often find it challenging to clear patients with ESRD to proceed with renal transplant who also have asymptomatic moderate degree of aortic stenosis (which could progress to severe/critical AS within unpredictable period of time while awaiting for renal transplant).
1): Shall we clear those patients for renal transplant since they have acceptable surgical risks?
2): What are the possible clinical outcomes or best management strategy in case those patients became symptomatic from severe/critical AS within 1-2 years after renal transplant?
Any experience or suggestion?
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1. Yes. Ideally AVR prior to RT would make their surgical risks very low. But the anti coagulation would make logistic issues in a deceased donor transplant. The ebst would be to offer the transplant and then AVR.
2. From 2nd year post RT, they are "normal" individuals, other than for immunusuppressed status. They would benefit from AVR.
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The patients with chronic renal failure have to undergo hemodialysis. These patients usually have AV fistula. The question is if the blood can be collected from this AV fistula on the beginning, during or after the end of hemodialysis in order to avoid further puncture of vein. I suppose that values like mineralogram or pH will be completely different between these two approaches. But what about drug levels? Does anyone know any study dealing with this issue?
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There is no difference of drug levels known between venous blood and blood from an arteriovenous fistula or av-shunt in hemodialysis patients. However, there can be a difference between the arterial and venous line during hemodialysis because of extracorpororeal drug elimination by hemodialysis or plasmapheresis.
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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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Most of the patients with chronic renal failure suffer from a decline in the level of the hormone Erythropoietin. Are there cases where the hormone levels rise in patients with renal failure? and whether research supports this opinion?? and why this increase there?
I hope the physiological explanation for this phenomenon
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there is no simple answer. As CKD progresses, epo levels increase almost as expected (about 2-3 fold) until a eGFR of ~35 to 40 is reached. At this point, Hb on average is ~ 12-13 g/dL and the anemia is mild. With further progression, epo levels fall but even in ESRD average levels are about 50% higher than in normal individuals without anemia and no kidney disease. These levels however are only 1/10 of those which would have been expected in anemic patients with Hb levels of 8 without kidney disease.
so what causes the mild "increase: in epo. probably output from the liver. However epo produced by the liver has a different glycosylation pattern and may be less active at the EpoR .
The issue whether cystic disease of the kidney increases epo levels is controversial. some studies have shown no increase . Similarly in acquired cystic disease of the kidney, epo levels do not differ from those of patients without cysts
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what is the differences in complications of Isolated UF and Hemodialysis ?
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Hi Jahanzaib
Mainly pass water so solutes concentration increases. 
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In studies monitoring tenofovir-associated kidney impairment either in HIV-positive patients on ART or negative patients on PrEP, a common test is serum creatinine levels, which are used to estimate glomerular filtration rate (GFR). However, some studies have shown that an alternative, cystatin C estimated GFR is more closely associated chronic kidneys disease outcomes. What is the state of the science for most accurately monitoring kidney function in patients on ART or PrEP? Thanks.
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Two articles wil help you to answer to this question. However, cystatin C may be a good marker for risk prediction, cardiovascular events, and  long term decrease in GFR in HIV-infected  patients, but data are lacking.
Gagneux-Brunon A, Delanaye P, Maillard N, Fresard A, Basset T, Alamartine E, et al. Performance of creatinine and cystatin C-based glomerular filtration rate estimating equations in a European HIV-positive cohort. AIDS. 2013 Jun 19;27(10):1573–81.
Inker LA, Wyatt C, Creamer R, Hellinger J, Hotta M, Leppo M, et al. Performance of Creatinine and Cystatin C GFR Estimating Equations in an HIV-positive population on Antiretrovirals. Journal of acquired immune deficiency syndromes (1999) [Internet]. 2012 Jul 26 [cited 2012 Aug 3]; Available from: http://www.ncbi.nlm.nih.gov/pubmed/22842844
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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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HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.
Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.
Thanks
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No studies of lipid-lowering agents (statins or fibrates) in patients with NS have reported patient-centred outcomes including all-cause mortality, cardiovascular mortality, or non-fatal myocardial infarction; only single studies reported cholesterol (HDL, LDL and total cholesterol), There is no data on second-line agents (incl. ezetimibe) and outcomes in NS. 
There is also little evidence that secondary hyperlipidemia in NS has the same effect on cardiovascular outcomes. Bring the NS into remission and hyperlipidemia will resolve without the need of treating dylipidemia.
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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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I am looking for the latest algoritm in ESA's anaemia treatement in CKD
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Good morning
The attached file may be helpful
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A middle aged man presented with nephrotic syndrome (>10 gm protein/24hrs with sev dyslipidemia) with severe thrombocytopenia of almost one year duration. His auto immune profiles are negative, renal biopsy could not be done because of sev thrombocytopenis (Plat 5000). He was started on steroid (Pulse solumedrol follwed by oral prednisone), but there was no improvement. Any suggestion regarding further evaluation and management?
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The co-existence of the two diseases is very rare and therefore one can not find any trials of therapy. We have reported a case with co-existence of the two disorders. We treated the patient with Rituximab with good result. Please find the reference below:
Coexistence of immune thrombocytopenic purpura and idiopathic membranous glomerulonephritis successfully treated with rituximab. Pathare A, Alkindi S, Khan S, Riyami D, Farooqi M. Platelets. 2010;21(7):575-7
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Please do provide references as well. Many thanks!
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Dear researcher
Hope these article will solve your problem please see the attched articles.
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dengue fever in kidney patients
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It depends on the stage of CKD . Stage 5 needs renal replacement therapy . The major complications of severe Dengue are hypotension due to capillary leak , Bleeding & organ dysfunction such as AKI , hepatitis & encephalitis . Adequate fluid therapy is the cornerstone of therapy of severe dengue . The main aim of treatment in CKD stage 1 - 4 , with Dengue is to prevent AKI in CKD by adequate fluid therapy . Stage 5 CKD patients are already on dialysis , but caution should be used on use of anticoagulants .
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60 year old man presented with chronic renal failure and hyperurecemia but he developed allergy to allopurinol.
Serum creat.= 2.6 mg/dL 
Serum uric acid= 9.4 mg/dL 
What will be you plan of management?
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You didn't mention if your patient has symptoms like gout. If so you have to think about pseudo-gout too. So you have to look for Ca x Phosphate. If doubts remain that allergy to allopurinol is present you may test for HL-A B*5801.
Another approach: If the patient is obese he has to reduce his intake of carbohydrates strictly, since it is likely that his polyol-pathway is activated and he generates fructose by himself. Intake and degradation of fructose are the most common causes of hyperuricemia since the pool of ATP intracellularly is reduced rapidly and purins are broken down.
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I am trying to measure Beta-2-Microglobulin concentration in urine samples from patient with renal disease, so the concentration is expected to be high. I first used abcam SimpleStep ELISA kit then R&D Quantikine to confirm. But the inter-assay variation is so big (>100%) leaving me no idea which is the right result. Can anyone suggest how to make these result more reproducible and reliable? Thanks
Attached is some of the results on a spreadsheet.
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There is a lot of variation in data when you used R&D kit. Usually R & D kits wont give such values. Abcam kits are coming with much more senstivity these days. hence the values are higher in Abcam. Neverthless it also depends upon how old is your sample. Is there any precipitate formation in your sample?? Did you centrifuge your sample properly and take out the supernatant before going for the assay. 
If you use fresh sample or centrifuged properly.. then still I would suggest to go for the Abacam kit as your data looks more stable there.
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Thanks in advance for your replies.
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Dear Shankhajit,
The exosomes or the extracellular microvesicles from the blood cannot pass through the GBM with normal kidney function. Mostly all the cells excrete exosomes for cellular signaling or trafficking. Hence all the body fluids will be having exosomes. But the size of these exosomes (30-150 nm) are bigger than that of normal glomerular pore size (approximately 10 nm). Hence it cannot pass through. However, exosomes from kidney tubular epithelial cells will normally be excreted in urine. These urinary exosomes are nowadays used to monitor kidney function. 
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ILCs have important role in inflammatory diseases, newly there connections with tumors detected.
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thanks for everything,you were  very helpful.....if anything else i would like to ask i will let you know...thank you very much....
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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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published article, RCT, PROSPECTIVE STUDY
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please have a  look on this address 
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Schaeffner ES, Ebert N, Delanaye P, Frei U, Gaedeke J, Jakob O, Kuhlmann MK, Schuchardt M, Tölle M, Ziebig R, van der Giet M, Martus P. Two novel equations to estimate kidney function in persons aged 70 years or older. Ann Intern Med. 2012 Oct 2;157(7):471-81
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Hi, thank you for the publication!!!
Actually there was a mistake on the http://touchcalc.com/bis2.html. By "Different results" I meant discrepancy between results made within the calculator and within the original formula ( calculated by excel). I was mailing with prof Fade- the author of the BIS, and the mistake was corrected.  
Best regards
Marta
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when  an  eGFR is 15 - 29 ml/min/1.73 mwhich part of treatment, either clinical action alone or Nutrition part- is really works to get back to 30-59 ml/min/1.73 m2 or the actions for preceding stages? or increase the ca absorption, lipoprotein activity or develop the metabolic consequences?
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Nutrition is fundamental to:
a) avoid malnutrition and MIA syndrome
b) Give adequate caloric support
c) Limit unuseful proteic intake
d) don't give phoshorous
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Could you please introduce me paper(s) which describe peritoneal dialysis rats well?
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The peritoneal equilibration test (PET) is used to determine peritoneal transport in peritoneal dialysis patients.
References
1. Pannekeet M, Imholz A, Struijk D, Koomen G, Langedijk M, Schouten N, de Waart R, Hiralall J, Krediet R (1995). "The standard peritoneal permeability analysis: a tool for the assessment of peritoneal permeability characteristics in CAPD patients.". Kidney Int 48 (3): 866–75. doi:10.1038/ki.1995.363. PMID 7474677.
2. Twardowski ZJ1, Prowant BF, Moore HL, Lou LC, White E, Farris K (2003). Short peritoneal equilibration test: impact of preceding dwell time. Adv Perit Dial. 19:53-58.
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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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I have a patient with active ankylosing spondylitis(AS) and second (2007;2012) kidney transplantation (due to chronic glomerulonephritis). Ankylosing spondylitis is active with BASDAI . 5,5 -  6,0 during last 3 years, CRO changes from 11 - 25 mg/l (normal value 0 - 5 mg/l), spine ligament calcification has found in 3 cervical and lumbar spine ligaments  on X- ray. Due to kidney transplantation the patient use MMF and prednisolone. 
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I am unaware of any published reports on the concomitant use of a TNF inhibitor and mycophenolate mofetil in AS. It would seem reasonable to try this combination while monitoring closely for any potential adverse events in your patient. Before attempting this treatment regimen, I advise consulting with your local renal transplant colleagues.
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lower and upper limit of BP for starting hemodialysis?
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Dear marano 
thanks alot
usually we have drop in BP but sometimes due to excess renin excretion we have increase in BP . 
But I want to know is there any cutoff in high BP that we have to use IV nitroglycerine or other antihypertensive drugs before starting hemodialysis ?
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Could the dialysis tubing concept in nanoparticle purification be used as in vitro dissolution tests for suppositories?
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yes you can use it .According to my exper. non membrane dissolution test for supp. was better correlated to the in vivo data.
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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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I need some guides or protocols  related to the topic ,  included some parameters such as ; mesangial matrix expansion, glomerulosclerosis, tuft-to-capsule adhesions, hyalionosis( glomerular or tubular) , dilatation of urinary space and thickening basement membrane of bowman's capsule (light microscopy assessment)
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It is important to realise, that in most mouse models of diabetic nephropathy their kidneys do not develop the same level of progressive diabetic nephropathy (DN) as observed in patients with DN. So, class 1 and clas 2 DN can develop in most mouse models. Class 3 DN wich includes the development of nodular glomerulosclerosis, is only described in BTBR ob/ob mice that lack both the gene coding for leptin and the leptin receptor.
The level of mesangial sclerosis and hyalinosis can be quantified by Image-J assisted digital image analysis determining the area percentage of mesangial extracellular matrix using PAS-stained paraffin sections.
The level of interstitial fibrosis can be quantified using Sirius red stained paraffin sections.
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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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I am specifically looking for the interarrival times used for patients/kidneys in KSIM, as well as the resulting probabilities of transplant, death on wait list, and average time spent waiting. I know the the data came from the Organ Procurement and Transplant Network, but this data can only be retrieved through a request process. Is there another place online or in another publication where this information is more easily accessible?
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Dr Menth, my apologies for misunderstanding your question: the specific data that you requested appears to be available only from the authors of the article.  A similar full text is available at this website but does not contain the full data requested:
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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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Some patients with flank pain showed hydronephrosis in sonograghy and IVP, which can be due to UPJO. But in their EC-renal scan they may show non obstructive pattern. Some physicians  choose follow up but  others perform pyeloplasty.
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I think it is better to show the images. I believe if a patient has loin pain and hydronephrosis on IVU and u/s, that should be evident using diuretic renogram. 
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Capillary hydrostatic pressure in intestinal villous capillaries is 15 mm of Hg while it is 55 in glomeruli capillaries.
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Glomerular capillary hydraulic pressure is a better term because the fluid in the capillaries is not static but flowing.  The value for glomerular capillary hydraulic pressure of about 55 mmHg comes from experiments in rats and squirrel monkeys that have glomeruli on the surface of the kidney in which capillaries were punctured and pressure directly measured.  It is assumed to be similar in other mammalian species like man.  There must be some drop in pressure moving down the capillary from the afferent to the efferent arteriole for blood to flow, but it is probably small.  In contrast, the plasma protein concentration and corresponding oncotic pressure inside the capillary rises significantly moving from the afferent to the efferent arteriole.  As a result the net ultrafiltration pressure, which is the difference between the hydraulic pressure (favoring filtration) and the plasma oncotic pressure (opposing filtration) drops from 10-15 mmHg near the afferent end of the capillary network to zero or close to zero (depending primarily on plasma flow rate) by the termination of the glomerular capillaries at the origin of the efferent arteriole. 
Another factor contributing to the high rate of fluid movement across the glomerular capillary wall is the hydraulic conductivity of the capillary, which is significantly greater than other capillaries as well.   
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I have a patient with dengue fever, with nephrotic range proteiuria, no hematuria or cast. How should such case be approached?
Should such patients with significant proteinuria and normal platelets be subjected to kidney biopsy?
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An excellent recent review of kidney disease in Dengue fever by Lizarraga and Nayer appeared in Journal of Nephropathology 3(2): 57-62 (2014) but did not elaborate on pathophysiology of proteinuria. Full text at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999585/pdf/jnp-3-57.pdf
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The result of clinical studies suggested that statins appear to decrease the rate of reduction of estimated glomerular filtration rate (eGFR) and slow the progression of pathologic proteinuria moderately.
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see:Pharmacol Res. 2014 Oct;88:62-73. doi: 10.1016/j.phrs.2014.06.011. Epub 2014 Jul 1.
Statins in chronic kidney disease and kidney transplantation.
Kassimatis TI1, Goldsmith DJ2.
no evidence of effects of statins on proteinuria and progression of CKD!!!!
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For the past two or three weeks, we've noted a number of cases of vascular access bleeding after dialysis. The dose of the anticoagulant used not changed.
What are the possible and common reasons for this?
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The two main reasons for access vascular bleeding at the end of dialysis session are either excessive anticoagulation of the session or a stenosis on the venous site of the fistula
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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.
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Hypernatremic dehydration in exclusively breastfed newborns is a problem. Is it exclusively because of inadequate lactation counselling? Do some mother/baby duos also run a risk of hypernatremia despite proper lactational care? Or can this be totally abolished by good lactational counselling?
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Hi we have had in our Maternity some cases of hypernatremic dehydration, and in the study through the root cause analysis, which we have seen is that most of them had been instrumented deliveries (suction cup, forceps with epidural anesthesia) as well as some other contributing factors including unmotivated breastfeeding health personnel. I think the most important is to reinforce good BFHI practices and good control at 48 hours after discharge.
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Usually the ACEI should be discontinued weeks befor performing LDL Apheresis.
Do somebody have information about the danger of anaphylaxy whit Immunoadsorbers when ACEI are used by the patient?
Thank you all.
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this arises from historical reaction between ACE-I and polyacrylonitrile ?
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Although the advent of direct acting antivirals in the management of HCV are evolving such that they do not use interferons, technically these are not indicated for patients with renal failure, due to lack of clearance of metabolites. What experience is there in using them to clear HCV in patients awaiting kidney transplantation? Are these metabolites cleared by hemodialysis? There is a pilot study of sofosbuvir and ribavirin in genotype 1 or 3 hepatitis C virus infected patients who have chronic renal insufficiency (http://clinicaltrials.gov/ct2/show/NCT01958281?term=sofosbuvir+kidney&rank=1).
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The COSMOS study used this combination in cirrhotics, presented at EASL in April, but nothing published or presented in post-liver transplant patients. I spoke with Norah Terrault at UCSF and it appears they have experience with this combination post-transplant.
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Dihydropiridine calcium channel blockers and proteinuria
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There´s another point of view no clashing with the hypothesis of Solanke above: dihydropiridines like nifedipine, nitrendipine,anlodipine, manidipine, clinidipine, lercanidipine and others cause vasodilation only in gromerular afferent artery whilst the non-dihydropiridines (diltiazem, verapamil) make the same in afferent and efferent artery improving glomerular function and diminishes proteinuria
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And how it would be prevented or managed if it happened? And is it usual that it happened each session? Attach references if available.
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Check appropriateness of your UFR by a blood volume monitor or measure haematocrit at the HD start and end. High increase would mean the blood gets to dense and will have higher tendency to clotting. Check also for presence of any air bubbles in the arterial head - they may block blood pasage through some fibres. Temporary turning of the dialyzer with the venous outflow up may help to get rid of the air bubbles in the blood path.
Franta Lopot, General University Hospital, Prague
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What are expected results of Hb , hematocrit and creatinine in patients with CKD and hemodialysis?
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The Hct and Hb of CKD patients is usually low due to the renal anaemia. If the Hb level is less than 10g/dL then according to KDOQI and European Guidelines the therapy with iron and ESA should be initiated (all information available at KDOQI and EDTSA websites).
Creatinine levels are usually high in CKD mirroring the decline in GFR.- full info available at KDOQI and ERA ADTA Guidelines sites. Best regards, Michaela
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What are the last KDOQI guidelines for dialysate bicarbonate concentration?
Are there any limits? Or is the only recommendation pre-dialysis serum concentration of bicarbonate > 22 mmol/L? Is there any recommendation for post-dialysis serum concentration?
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To Marques and Liborio: I know these studies, I´m just preparing an article related to “acid-base disorder in patients on HDF”, where I am trying to comment them. I paste the relevant paragraphs:
To Marques:
Marques et al. argued that reducing the dialysate chloride concentration (by modifying sodium dialysate in the same proportion) will influence MAC due to the decrease of UA (retained unmeasured acid anions). This decline was explained by an increase of intracellular buffering capacity during the interdialytic period due to the lower intracellular chloride concentration on the basis of the Gibbs-Donnan effect. As an alternative hypothesis Marques pointed out the potential effect of lower dialysate chloride concentration on a higher clearance of strong acid anions, again based on the Gibbs-Donnan equilibrium.
However, when we divided the patients (our group of 68 patients on post-dilution HDF) into two groups according to the postdialysis chloride concentration, we found that in the high-chloride group (Cl- > 100 mmol/L, n = 38) the mean concentration of UA- was 0.2 mmol/L, whereas in the low-chloride group (Cl- < 101 mmol/L, n = 30) it was 4.4 mmol/L after dialysis. Furthermore, there was an absence of a significant correlation between intradialytic change of SBE (ΔSBE) and intradialytic change of Cl- (ΔCl). In accordance with other studies ΔSBE correlated only with ΔUA-. Based on these results, it seems that chlorides are likely to be increased in order to maintain plasma electroneutrality. This hypothesis is supported by the result in the distribution of file according to postdialysis concentration of UA-. After dialysis in the low-UA group (UA- < 2.3 mmol/L, n = 35) was significantly higher chloride concentration (101.1 vs 99.1 mmol/L), as well as bicarbonate (29.4 vs 27.1 mmol/L) and SBE (5.3 vs 2.6 mmol/L).
To Liborio:
Liborio described a similar phenomenon in dialysis patients with ARF, when a group of patients with higher predialysis chloride concentration - compared with dialysate concentration - had higher increase of SBE compared with the low-chlorides group, using the same hemodialysis parameters. First, it is a mistake to suppose that the same concentration of plasma and dialysate corresponds to neutral gradient (as already mentioned above in the discussion). Dialysate chloride concentration 109,5 mEq/L, in the case of standard protein concentration, leads after taking into account the Donnan coefficient of 0.96 to the reduction of plasma water chloride concentrations into 105 mEq/L. And after the conversion of plasma water on the plasma concentration the final chloride concentration is 97.8 mEq/L. It is ilustrated by decrease of Cl- from 108 to 107 mEq/L although we were expecting the chloride increase. The decrease from 108 to 107 mEq/L is quite low probably due to the hypoproteinemia in patients with ARF. Further, given that predialysis SBE were comparable in both groups, it is clear, that in low-chloride group had to be higher concentration of UA- (unfortunately authors did not publish these parameters for each group).
One can hypothesize, that the reason why the high-chloride group had higher SBE is the combination of hyperchloremic acidosis and acidosis with higher AG, where, unlike the second group, correction runs parallel in two ways: by elimination of UA- and by substitution of missing bicarbonate, while SBE of low-chloride group depends especially on the quantity of eliminated UA-. Given that results we can conclude that combinated MAC is easier correctable by dialysis than simple MAC with increased AG. This theory is supported by our results: after splitting the file into two groups according to predialysis chloride concentration, low-chloride group (Cl <104, n = 39) and high-chloride group (Cl> 103, n = 29). In both groups were predialysis SBE comparable, but differed in UA-, which was higher in low-chloride group. Postdialysis SBE was significantly higher in high-chloride group, ie the group with predialysis lower concentration of UA-. In both groups was UA- decrease comparable.
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In nephrologists' clinical experience, the overactivation of the complement alternative pathway (AP) is acquiring more and more importance in kidney failure etiopathogenesis. Indeed AP is involved in membranoproliferative glomerulonephritis, in atypical hemolytic uremic syndrome, in post-infectious glomerulonephritis, and now we are debating about a role of AP complement overactivation in ANCA associated vasculitis, in MGUS related nephrophaties.....Often patients with an AP dysregulation simulate Lupus without Lupus antibodies (SLE without SLE) and we observed some patients that overlaps with hypocomplementemic cutaneous vasculitis and/or cryoglobulinemic vasculitis
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Yes it's true. But the question is about AP overactivation/dysregulation without any infectious or immunocomplexes trigger. This pathogenetic pathway was clearly showed in atypical haemolitic uremic syndrome, in dense deposit disease, in C3 glomerulonephritis. In ANCA associated vascultiis is described that ANCA primed neutrophils are able to activate the AP, and so on...
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A 65 year old woman with CKD (urate nephropathy) with severe chronic asymptomatic hyponatremia (S-Na 121 mmol/L), elevation of creatinin kinase (7 ukat/L), polyuria (3600ml/day), polydipsia. No episodes of seizures, no clinical signs of dehydration, no medications affecting diuresis or natriuresis.
Serum Na 121, K 4, Cl 82, P 1.31, Ca 2.5, urea 9.2 mmol/L, OSM 254 mmol/kg, creatinine 97 umol/L, CK 7 ukat/L.
Urine Na 36, K 9, Cl 26 , P 3.7, Ca 0.21, urea 59, creatinine 1.28 mmol/L, OSM 147 mmol/kg.
Fractional excretion of Na 2.25%, OSM 4.4%, water 7.6%, urea 48.6%.
pH 7.41, pCO2 5.9 kPa, HCO3 28 mmol/L. Creatinine clearance 0.56 ml/s.
After 4 hours of fluid restriction diuresis was 400ml, increased urine osmolality from 147 to 265 mmol/L, increased urine sodium from 36 to 57 mmol/l, slightly decreased serum osmolality from 254 to 252 mmol/kg, serum sodium remained unchanged.
What is the diagnosis?
Is it water diuresis? Serum osmolality is higher than urinary, but fractional excretion of osmolal substances is high.
Could be primary polydipsia - urine osmolality increased after water restriction, so probably it is not diabetes insipidus, ADH should be present, at least partially.
Why did serum sodium not increase after fluid restriction? Could it be the combination of primary polydipsia and decreased tubular reabsorption of sodium (urate nephropathy)? Why is CK elevated without episodes of seizures?
Thank you for your opinions.
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In this patient the primary problem is polyuria . Is the polyuria due to water diuresis or solute diuresis . Chronic Interstitial nephritis can produces both nephrogenic diabetes insipidus as well as salt losing nephropathy . The evidence for nephrogenic DI is low urinary Osm , which is partial , as there is improvement with water restriction . The increase in urinary sodium is probably due to correction of hypovolemia , due to salt wasting nephropathy . The hypontremia is probably due to excess water consumption , with restricted salt intake causing hypovolemic hyponatremia . I would treat this patient with salt & water or IV 0.9% Nacl of about 2.5 - 3 litres / day . Francois Brivet used to state that decreased renal function is a sign of volume depletion , even if there are no clinical signs . Whether , this is CKD or AKI or AKI on CKD would be determined by recovery of renal function after correction with saline .
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Why is the dexamethazone is not used widely as anti inflammatory agent compared to the prednizolone or methyleprednizolone inspite of being more potent than them and even not for short time use ( like the methylprednizolone use in the rapidly progressive glomerulonephritis for 5 days as pulse therapy)
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Sir the difference may be due to rapidity of action, of prednisolone rather than dexamethasone.
titering of the drug may be difficult in case of long acting potent steroid.
In case of any underlying infection steroid may be an inhibiting factor and dexamethasone may be a ditterent.
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It is very important to have a surveillance system for early diagnosis of HCV infection in dialysis centers and for control of it we should attend to some strategies, such as:
1. Less transfusion, more use of erytropoithin.
2. More education for the nurses in dialysis centers.
3. Treatment of HCV infected patients.
Do you agree with dedication of HCV infected from non-infected patients in dialysis centers?
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I strongly agree with this statement, but let me underscore that HCV infected patients are to be considered only those with HCV-RNA detectable. Indeed a lot of my patients have HCV antibody with undetectable RNA and I think no isolation is required
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I am interested in developing a trial model implementing intraperitoneal (IP) administration of heparin in GI cancer surgery (with special interest in cytoreductive surgery and hyperthermic intraperitoneal chemotherapy -HIPEC), combining intra-operative and post-operative administrations. I would appreciate if somebody can share his/her relevant experience regarding any aspects of IP use of heparin (subtypes, doses, complications, effect on peritoneal membrane, anti-cancerous/immuno-regulating properties, etc). Thank you in advance.
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Dr Strazdins,
Many thanks for your valuable feedback. The information provided is very useful.
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Renal stone is a prevalent disease with loud symptoms, and osteoporosis a prevalent and silent disease. I read about their relation and the role of IL6, but I would like to hear details about your clinical experience. As a GP or specialist, do you ask for a bone mineral density (BMD) for renal stone patients or at least for some of them? Or even think about the probability of low BMD in them? Do you have any experience of pathological fracture and patients with renal stone?
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Dear Jose
Your opinion is absolutely correct.
I have a new project: Preventive Medicine/Osteoporosis). I will measure the following parameters regarding calcium metabolism: Calcium in serum and in urine, PTH and Calcitonin and Vitamin-D in serum.
Thanks and with kind regards
Eva
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It's to know the differential kidney function.
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Differential blood sampling from each kidney is technically feasible using a selective renal vein sampling approach similar to the the selective adrenal vein sampling approach using to functionally localise hyperaldosteronism. In many instances services such as this may be provided by Interventional Radiology services.
With regard to differential renal function measurement, nuclear medicine studies such as MAG3 scanning are able to help delineate this relatively non-invasively.
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I recently used a serum creatinine assay kit from abcam (link below) and obtained some unexpected results. I was wondering if anyone here could share their experience with measurement of serum creatinine that could possibly shed light on what's going wrong:
Serum samples taken from 2010 to 2011 from elderly patients with prostate cancer were stored at -80 degrees Celsius, previously aliquoted, hence at the time of assay at most two or three freeze thaw cycles would've been performed.
This assay is based on conversion of creatinine to sarcosine, which is then oxidised and reacts with a probe to produce red colour measured with a spectrophotometer set at 570nm. The reaction is performed using a reaction mix containing all supplied enzymes and then again without creatininase in the reaction mix to account for background. The concentration is determined from the difference between the sample reading and its background.
I ended up with measurements of serum creatinine around 10pg/microlitre whereas the normal range is 45 to 110pg/microlitre. I tested serum samples from three subjects, and all of them had around 10pg/uL. If I don't subtract background, the serum creatinine concentration would calculate to be at the lower end of the normal range, however the absorbance reading of the background is high enough that it can't be ignored. The serum samples had varying amounts of haemolysis, but the background reading should account for this. If anything, haemolysis should overestimate the concentration, not underestimate it. The concentration of 10pg/uL appears to be way below the lower limit of the normal range.
I did not dilute the serum samples.
The standard curve was linear and covered 0 to 200pg/uL, with absorbances from 0.0052 (water + reaction mix in the well) to 1.778, which suggests I didn't dilute the standards incorrectly either (given that our spectrophotometer measures from 0.000 to 4.000).
So far I can only think of three explanations, the first that the serum samples were diluted (I have confirmed that this is not the case), secondly that the 2 or 3 freeze-thaw cycles have caused significant degradation of creatinine (unlikely), and thirdly that perhaps there's something in the serum that is inhibiting the enzymes (unlikely, given that this assay is optimised for serum samples). What could possibly explain these unexpected results, and how may I be able to fix this problem?
If anyone could help, it would be much appreciated.
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Hi,
I can only think that there was a high concentration of proteins in the samples that interfered with the assay. The protocol suggests filtering through a 10kDa MW cut-off filter. Also make sure that all reagents are at the right temperature. Also the protocol does not say whether to use flat or V shaped plates. I would recommend flat or try both and that the plate is recommended for your type of application.
Good luck and let me know!
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I usually use 2 photon microscope to visualize the entire body organs of the Zebrafish.
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try these if it works. Oil Red O – demonstrates lipid in CRYOSECTIONS and
Sudan IV or Sudan Black – demonstrates lipid