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
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.
international journal of urology and nephrology
Please share experience with Archives of Nephrology and Urology journal. Is it authentic or fake/predatory.
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
Kindly. Looking for s medical journal indexed Scopus, with Nephrology and Biochemistry subspeciality. Any suggestions?
Need Expert opinion, how nephrology is running their HD machines on covid-19 patients even on heparin without getting clogged!
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.
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.
Which dose of vitamin C is the risk of forming oxalic stones? above 3 gm?
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


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
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
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.
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.
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...
I am a paediatrician b with special interest in nephrology.
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.
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?
Estimated glomerular filtration rate ( eGFR ) is the basis for the classification of chronic kidney disease (CKD)?How.
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.
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.
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)?
creatinine increased up to 4 milligrams in 5 days after IV contrast and starting hydration and antioxidant treatmnet
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.
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??
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.
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?
Hyponatremia is a frequent finding in the critically ill; most of these patients are euvolemic.
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?
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?
Should we worry and what is our strategy
Antidiabetic drugs limitations according to GFR, a presentation from French society of Nephrology conference 2015

We give pirfenidone at dose of 100 mg/kg/d in three devided doses, by oral gavage
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.
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.
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?
The impact of dystrophic calcification in pressure injury management for client with a spinal cord injury
what is the role of 99mTc-DTPA exercise renogram in the evaluation of renal disorders ?
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.
The boy has received treatment with steroids, cyclophosphamide and cyclosporine A, without a good response.
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.
Sepsis, Nephrology, Internal Medicine.
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
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.
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!
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).
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.
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?
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?
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?
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.
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?
Oncology ; Nephrology ; Intensive Care ; Hematology
What is the best way to measure urine bicarbonate (HCO3-)?
patients with tx glomerulopathy have been seen commonly recently. management of tx glomerulopathy is diffucult.
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.
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.
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
Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. is the same efect in patients with familial glucosuria?
All I can find in the literature is intravenous injection followed be several timepoints of blood sampling.
Thanks
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?
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?
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.
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?
Seeking information on IPD intermittent peritoneal dialysis.
dialyzer size - pump speed - dialysate speed - max Ultrafiltration and the relation with sex - age - BMI and cardiac health
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?
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?
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?
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.
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.
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.
What is the role of anp on renoprotective and what is mechanism behind it?
Renal transplantation and JC & BK polyoma virus induced nephropathy
How effective are these therapies?
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?