I’ve seen many foreigners doing it. Also would it be easier to get to do IM residency in the USA after nephrology fellowship is donde?

In a patient that has membranous nephropathy that is already on lasix and needs better BP control, is adding a combo ARB with HCTZ advisable? Or stick with just the ARB? I can't seem to find much information on this.

Can somebody help me with the new ADPKD KDIGO guideline in PDF? Apparently it got deleted from the KDIGO website. Thank you in advance!

Compare*

Starting 2 week long rotation in a few weeks. I’d like to show that I’m up to date on recent important evidence. Hoping I can get some recommendations on finding recent papers that have generated a lot of interest in the nephrology community.

Also one of the ways we’re graded is if we “educate the team” with interesting new papers/clinical trials.

Additionally, any other recommendations to do a really well on my rotation?

If the serum creatinine elevates on lisinopril, is it reversible upon discontinuing lisinopril or does the serum creatinine stay elevated? Like that does become the new baseline? Thanks in advance.

Same as title. A good comprehensive resource that doesn't put an internal medicine resident on call to sleep 🙏🏼

Good day doctors!

I am a general physician in my country. I recently have a patient with 3 years straight slight elevation (1.3mg/dL) of creatinine levels in his labs. However there are no other derranged findings. Is the elevation significant?

Thank you

I like nephrology but really like procedures and have fun with the interventional stuff. Any thoughts on interventional as a field? My understanding is that it’s a niche field, with the pay being about the same as general nephrology, but more liability. You also compete with interventional radiology and vascular surgery who might have an edge over you in some areas. Reimbursements are also trending down, so I’m worried what the future hold for this field.

Hi there, I am interesting in pursuing nephro fellowship currently and IM resident i wanted to ask those who are currently doing the fellowship about thoughts on nephro, im not too worried about the salary as much as me enjoying the actual job. I am worried about the physiology being too difficult and the dialysis machine being too difficult to learn ? Any thoughts advice as to how I should go on about making a final decision, tips, things to consider or read more about ? The reason im interested in it is that it focuses on more than one organ, the heart the kidney, physiology of the body. Diuresis, HTN, DM etc so its a wide array if interlinking stuff. Need some guidance, Thank you

Feel free to share your thoughts and questions as to the possible etiology, thanks!

I came upon this interesting article published in kidney international:

https://www.sciencedirect.com/science/article/pii/S2468024924018606#appsec1

The discussion online for this specialty has been trending negative. There appear to have re-occurring themes in these online discussions:

1. high workload and low salaries, motivating some to do hospitalist medicine

2. fellowship programs using fellows solely for cheap labor

3. Senior partners exploiting new grads and not sharing revenue evenly

4. training programs exploiting IMGs w/o residency for the same reasons as #2

Economic exploitation/destitution seems to be a re-occurring topic in these online discussions.

Hi! Nephro here. I'm looking for either part time nephro work in patient only (not a fan of clnic) or nephro hospitalist work 1 on 1 off or 2 on 4 off schedule. It seems like a niche position and am wondering if yall have seen something like this? 

I have a question pertaining to a case I had a while ago. Patient with CHF exacerbation and cardiogenic shock was on a dobutamine and furosemide infusion. Urine output was 30-50 mL/h despite the furosemide infusion. Hours later, the patient began dumping hundreds of mL of urine per hour. Lactic acid was steadily trending down, and S&S of cardiogenic shock had resolved hours prior to the furosemide infusion achieving desired effect.

My question: what would cause the furosemide infusion to work hours later?

Hello lads. I'm a new nephrologist and I'm looking to work in Europe. What is in your opinion the best country for a nephrologist, in terms of money ?

I know that there is 2 ways of transportation of water across a cell membrane. Osmosis (via concn gradient) Facilitated diffusion (via aquaporins)

Also, TAL of LoH contains NO aquaporins, so i understand that there is no movement of water in or out via facilitated diffusion.

But it contains a hypertonic urine, and doesn’t that cause osmosis to occur and pull water in the lumen of Loop of Henle?

Why would the books refer to the cell membrane as “impermeable” if so? Or is there a difference in constitution of cell membrane?

I know that there is 2 ways of transportation of water across a cell membrane. Osmosis (via concn gradient) Facilitated diffusion (via aquaporins)

Also, TAL of LoH contains NO aquaporins, so i understand that there is no movement of water in or out via facilitated diffusion.

But it contains a hypertonic urine, and doesn’t that cause osmosis to occur and pull water in the lumen of Loop of Henle?

Why would the books refer to the cell membrane as “impermeable” if so? Or is there a difference in constitution of cell membrane?

Hi all,

I hope you are doing well!

I will soon start my first year of medical school in Canada, with the main goal of becoming a nephrologist. During my bachelor's in biochemistry, I had the opportunity to do a lot of research on ADPKD (which I am still pursuing), and I developed a passion for this field of medicine.

I was wondering if you have any advice for someone interested in nephrology and if you have insight for the future of this medical field.

Thank you in advance!

For example if a patient has CHF exacerbation but also has CKD. My attending asked me this, saying they had different MOAs but I swear they’re both loops. Besides the difference in potency so you can use less Bumex idk why she’s asking me this in detail 🙂 maybe that’s it and I’m just overthinking it lol

Hi,

I’m a crit fellow who has heard a few different things about the use of bicarb and CRRT and I was just hoping for some clarification. I’m trying to separate fact from opinion.

My previous understand regarding use of bicarb in the acidotic patient had been that the patient received an immediate albeit likely not longstanding buffering effect regardless your ability to ventilate off the resultant pco2. I had felt this was usually helpful in peri-arrest situations even if ventilation was a problem. After a conversation with a very smart and kind nephrologist last night I am starting to wonder if I am wrong…. For what it’s worth I have a bachelors in biochemistry and always thought I understood this. The nephrologist was telling me that the only way I get a pH change is if I increase ventilation in addition to adding bicarb (patient had combined respiratory and metabolic acidosis).

Also when adjusting flow rates on CRRT, is this essentially, when it comes to acid base, only the equivalent of adding bicarb to solution? Do I get no clearance of protons? Is there anywhere I can read more about this?

Thanks all

What are the main things that you found interesting new guidelines?

I'm seeing sources providing reference ranges for protein consumption in both % of total calories and grams consumed per bodweight. Which is very odd. Here is a paper talkin about % of total calories

Human data have also shown hyperfiltration with high protein consumption.^(7) The largest short-term (<6 months) trial showed that a high-protein diet (protein comprising 25% of calories) increased eGFR by 3.8 ml/min per 1.73 m^(2) after 6 weeks compared with a lower protein diet (protein comprising 15% of calories).^(9)^(,)^(10) In the early stages, glomerular hyperfiltration occurs as a rise in GFR, in proteinuria, or both, but may result in a loss of kidney function over time, particularly in those with underlying CKD, risk factors for CKD, or both.^(11)

Same article, now discussing it as Xg/kg of bodyweight:

.... In general, people with one kidney should avoid excessively high dietary protein intake (>1.2 g/kg per day)...

Consider someone eating a 2K calorie diet weighing 75KG. If he eats a normal 1.2g/KG protein per day (i.e. 90grams) thats 360 calories or 18% of total calories. If that person wanted to lose weight and ate at a 500 calorie deficit (taking from fats or carbs), his protein now consists 24% of total calories, which supposedly places him at a higher risk of CKD even though his protein intake hasn't changed.

Conversely, if that person eats 1.6g/kg of protein (120g * 4= 480cals or 24% of total cals at 2K) and overeats 666cals worth of chocolate a day, he is slowly becoming overweight while reducing his protein % of total calories to 18%. Is he at a lower risk of CKD?

TL;DR: Why is potential CKD risk from high protein intake measured as % of total calories as opposed to absolute intake per KG/lb bodyweight?

Mid 30s male with unilateral primary (congenital) hydronephrosis. Nuclear study showed fluid failed to drain from left kidney for duration of the test. Right kidney appears to function normally. Elevated blood lipids and low vitamin D, but other values in normal ranges. Possible ascites. Can unilateral kidney disfunction be the cause of these symptoms when serum proteins, electrolytes, etc. are in normal ranges? Not much accessable literature on the progression of unilateral hydronephrosis in adults. If anyone can point me in the direction of related studies I'd love to take a look.

Good evening, I’m an ER nurse looking for some insight regarding a case just worked on. I had a patient earlier this week that had stopped taking multiple anticoagulant meds for more than a month and came in pretty profoundly ill. We started her on a heparin drip, and 2 hours after, I started to see a steady increase in her UO, averaging out to about 300ml/hr. There was nothing abnormal noted regarding her kidneys on an abdominal CT. The only other med she was on was diltiazem, and she’d received a half mg of dilaudid about an hour after arrival. She had been NPO for about 8 hours at that point, and had not received any additional fluid volume. Can anyone offer a suggestion as to why she would be putting out so much urine?

What to expect during interview, oral/written exam (any tips), pre fellowship and fellowship training? Pros and Cons for both public and private institution? Any institution na marecommend nyo? Thank you!

Quick question, I am an RN and I understand a lot of this but just want clarification. If someone who has uncontrolled HTN, gross hematuria, flank pain and intermittent swelling of face, fingers and ankles starts taking HCTZ on top of Spironolactone (a ton), Lisinopril and PRN Clonidine, looses 7 pounds within a couple days of starting the HCTZ, what does that tell you?

Recently had a patient come through ED with extremely high gfr(highest I’ve seen) looking back through visits it has consistently been 800 or above. I know this isn’t much to go on but are there common disease pathways that lead to higher gfr?