Ten Things Nephrologists Wished Hospitalists Knew?

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Redpancreas

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I found a really great article on generic principles on ID. As a former resident, these are really good knowledge bites that if I had known in intern year I would have been better off for. I was wondering if someone would be willing to do something similar for Nephrology.


1.) I.E - Early dialysis shows no mortality benefits: blah blah blah
2.) IV Sodium Bicarb fixes the BMP, but not the kidney: etc. etc.
3.) FeNa isn't always reliable, but has its indications:: drug compliance, hepatology pts. asdjkl

Anyone willing to add some pearls?

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That was a cool article from ID, thanks.

1. Watch IVFs. It's fine to give them for hypotension or true volume depletion in advanced CKD or ESRD patients, but a lot of patients get IVFs by default (sepsis protocol though normo- or hypertensive, DKA, just because), and then we take it off at dialysis the next day. Patients may often miss dialysis if they come into the ED on the wrong day so they are often volume up if anything.

2. I don't care about the FENa or FEurea. I have not calculated that since I was a resident. If the urine sodium is low, that can help suggest a prerenal cause. If it is not low, then it is not very helpful either way.

3. Don't be afraid of the potassium in LR. There's 4 mEq in 1 L. We give 40 mEq of oral potassium with the expectation that K 3.6 will go to 4 so by the same logic, K 5.1 will go to 5.14 though it will probably be lower if anything by providing some base from the lactate and just increasing fluid volume by 1 L (dilution).

4. With AKI, always think about postrenal. I don't care if they are making a little urine. There's so many cases where a rapid AKI during a hospitalization is not due to vancomycin or contrast but urinary retention in the 80 year old guy who is post op. I probably get 1-2 consults like that a week where they just need a foley.

5. Feel free to be more aggressive with diuretics. I'll get calls about someone they think will need dialysis within the next day or two because of volume overload not responding to diuretics, but the diuretic doses are so small. Volume overload is bad too. I'm pleased to see when people have tried at least Bumex 3 mg or Lasix 100 mg or more when I have been called.

6. Transplant patients don't necessarily need their immunosuppression held for an infection unless they are critically ill. Even then, it might be a toss up.

7. We do try to avoid PICCs/midlines in advanced CKD or dialysis patients. A non-tunneled central line like a Hickman is a better option if someone is going home with antibiotics.

8. Ask yourself if those ESRD patients really need a foley. Sometimes they make urine, and sometimes they do not.

9. Bear in mind that creatinine is proportional to muscle mass. A debilitated old lady with a creatinine 1.5 is quite a bit worse off as there is overestimation of GFR as opposed to that younger lady with a creatinine of 1.5.

10. At time of disposition, make sure their outpatient hemodialysis unit can take them back. If there is a prolonged stay, they may have lost their scheduled seat time. If they go to a SNF instead of home, outpatient dialysis will need to be coordinated with the SNF.

BONUS - Dialysis does not suck out your soul. Probably.
 
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The top 10 things nephrologists wish every primary care physician knew​

Neil M Paige et al. Mayo Clin Proc. 2009 Feb.
 
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How about this. Don't go into nephrology if you can't stand the possibility of working harder to make less than a hospitalist.
Just because we're not interested in Nephro doesn't mean we don't have to know it well.
 
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Just because we're not interested in Nephro doesn't mean we don't have to know it well.

This. I’m a Hospitalist who once upon a time wanted to be a cardiologist. I love cardiology. As a result, I’ve learned to love pulmonology, like infectious disease and endocrinology, tolerate Gastronterology and nephrology and remain admittedly flummoxed by rheumatology. Still have to know enough about each to avoid being Captain Pan-consult while also knowing when to ask for help.
 
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That was a cool article from ID, thanks.

1. Watch IVFs. It's fine to give them for hypotension or true volume depletion in advanced CKD or ESRD patients, but a lot of patients get IVFs by default (sepsis protocol though normo- or hypertensive, DKA, just because), and then we take it off at dialysis the next day. Patients may often miss dialysis if they come into the ED on the wrong day so they are often volume up if anything.

2. I don't care about the FENa or FEurea. I have not calculated that since I was a resident. If the urine sodium is low, that can help suggest a prerenal cause. If it is not low, then it is not very helpful either way.

3. Don't be afraid of the potassium in LR. There's 4 mEq in 1 L. We give 40 mEq of oral potassium with the expectation that K 3.6 will go to 4 so by the same logic, K 5.1 will go to 5.14 though it will probably be lower if anything by providing some base from the lactate and just increasing fluid volume by 1 L (dilution).

4. With AKI, always think about postrenal. I don't care if they are making a little urine. There's so many cases where a rapid AKI during a hospitalization is not due to vancomycin or contrast but urinary retention in the 80 year old guy who is post op. I probably get 1-2 consults like that a week where they just need a foley.

5. Feel free to be more aggressive with diuretics. I'll get calls about someone they think will need dialysis within the next day or two because of volume overload not responding to diuretics, but the diuretic doses are so small. Volume overload is bad too. I'm pleased to see when people have tried at least Bumex 3 mg or Lasix 100 mg or more when I have been called.

6. Transplant patients don't necessarily need their immunosuppression held for an infection unless they are critically ill. Even then, it might be a toss up.

7. We do try to avoid PICCs/midlines in advanced CKD or dialysis patients. A non-tunneled central line like a Hickman is a better option if someone is going home with antibiotics.

8. Ask yourself if those ESRD patients really need a foley. Sometimes they make urine, and sometimes they do not.

9. Bear in mind that creatinine is proportional to muscle mass. A debilitated old lady with a creatinine 1.5 is quite a bit worse off as there is overestimation of GFR as opposed to that younger lady with a creatinine of 1.5.

10. At time of disposition, make sure their outpatient hemodialysis unit can take them back. If there is a prolonged stay, they may have lost their scheduled seat time. If they go to a SNF instead of home, outpatient dialysis will need to be coordinated with the SNF.

BONUS - Dialysis does not suck out your soul. Probably.
I think you probably just mis-typed but a hickman is a tunneled central line. Is there really any evidence that PICC's cause more vascular stenosis than other lines? What about subclavian lines? My nephrologists sometimes want me to put a subclavian instead of a PICC in ESRD pts.
 
I think you probably just mis-typed but a hickman is a tunneled central line. Is there really any evidence that PICC's cause more vascular stenosis than other lines? What about subclavian lines? My nephrologists sometimes want me to put a subclavian instead of a PICC in ESRD pts.
Oops, yes, I mistyped. I meant "non-dialysis tunneled central line."


That's not a bad little study. I've seen other studies and articles that guessestimate it could be as high as 20% of patients may have some degree of central venous damage. It's a nightmare if there is central vein stenosis. You can see SVC syndrome symptoms. We then have to look at leg access. Some patients will just exhaust their access options and die.

I think a subclavian would be better as the more distal vessels will not be affected, but IJ is better just given the route into the SVC. IJ access does not have to make that little turn as much.

IJ access can still cause stenosis but at a lower rate.
 
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Oops, yes, I mistyped. I meant "non-dialysis tunneled central line."


That's not a bad little study. I've seen other studies and articles that guessestimate it could be as high as 20% of patients may have some degree of central venous damage. It's a nightmare if there is central vein stenosis. You can see SVC syndrome symptoms. We then have to look at leg access. Some patients will just exhaust their access options and die.

I think a subclavian would be better as the more distal vessels will not be affected, but IJ is better just given the route into the SVC. IJ access does not have to make that little turn as much.

IJ access can still cause stenosis but at a lower rate.
Thanks for posting that. Its one of those things i’ve just never bothered to look up myself.
 
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Oops, yes, I mistyped. I meant "non-dialysis tunneled central line."


That's not a bad little study. I've seen other studies and articles that guessestimate it could be as high as 20% of patients may have some degree of central venous damage. It's a nightmare if there is central vein stenosis. You can see SVC syndrome symptoms. We then have to look at leg access. Some patients will just exhaust their access options and die.

I think a subclavian would be better as the more distal vessels will not be affected, but IJ is better just given the route into the SVC. IJ access does not have to make that little turn as much.

IJ access can still cause stenosis but at a lower rate.
Is there a reason why they can’t switch to PD to in that scenario?
 
Is there a reason why they can’t switch to PD to in that scenario?
That is a very good thought, but in reality, it seems like most ESRD patients are going to do PD first if they are going to do it so someone in that scenario may have already been through PD and had eventual peritoneal failure. It would also not be unusual for someone who has lived long enough (and hard enough) to lose all easier access sites may have had abdominal surgery/complications along the way that would preclude them from being good PD candidates. PD can also be quite burdensome if one is anuric, but one could do CCPD at night (the cycler) and manual dwells during the day, but they may have fluid dwelling nearly 24/7. But yes, that would need to be at least considered.

I should back up to make sure I have not given the impression that it is fairly common for an ESRD patient to lose just all possible forms of access. These folks typically have far outlived their life expectancy to get to that point. Leg access is not completely out of the ordinary, and people can have perm caths there too, but of course we do not like folks having those lines long term given risk of infection. Protecting the veins is more about preserving AVF/AVG options in the upper extremities and to avoid long term catheters and their complications.
 
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That is a very good thought, but in reality, it seems like most ESRD patients are going to do PD first if they are going to do it so someone in that scenario may have already been through PD and had eventual peritoneal failure. It would also not be unusual for someone who has lived long enough (and hard enough) to lose all easier access sites may have had abdominal surgery/complications along the way that would preclude them from being good PD candidates. PD can also be quite burdensome if one is anuric, but one could do CCPD at night (the cycler) and manual dwells during the day, but they may have fluid dwelling nearly 24/7. But yes, that would need to be at least considered.

I should back up to make sure I have not given the impression that it is fairly common for an ESRD patient to lose just all possible forms of access. These folks typically have far outlived their life expectancy to get to that point. Leg access is not completely out of the ordinary, and people can have perm caths there too, but of course we do not like folks having those lines long term given risk of infection. Protecting the veins is more about preserving AVF/AVG options in the upper extremities and to avoid long term catheters and their complications.
Thanks for the info. I always roll my eyes when the PICC people refuse to put one in to someone in the ICU who clearly will never outlive their access (eg abdominal disaster now TPN dependent) to 'protect' the potential fistula sites.
 
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Once, my team presented to me a patient stating ESRD on HD, with access in the abdomen. So I said “you mean PD right?” They said, though unsure, “I think it’s HD.”

Sure enough, upon examining the patient, found the tunneled HD cath in the abdomen, going into the IVC. That was my first one of those as a young attending.
 
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Once, my team presented to me a patient stating ESRD on HD, with access in the abdomen. So I said “you mean PD right?” They said, though unsure, “I think it’s HD.”

Sure enough, upon examining the patient, found the tunneled HD cath in the abdomen, going into the IVC. That was my first one of those as a young attending.
Pretty unusual, but yeah, IR can get creative and make it happen. Other unusual access is a necklace graft.
 
Pretty unusual, but yeah, IR can get creative and make it happen. Other unusual access is a necklace graft.

One of my nephrology friends said “IVC? Haha, I’ve seen one in the right atrium!”

geez, oneupmanship.
 
3. Don't be afraid of the potassium in LR. There's 4 mEq in 1 L. We give 40 mEq of oral potassium with the expectation that K 3.6 will go to 4 so by the same logic, K 5.1 will go to 5.14 though it will probably be lower if anything by providing some base from the lactate and just increasing fluid volume by 1 L (dilution).

Anesthesiologist here. We've had many nephrologists that demanded IVFs without potassium which make no sense. We routinely swap out that NS bag from the floor and switch it to LR or plasmalyte for intraop.
 
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Anesthesiologist here. We've had many nephrologists that demanded IVFs without potassium which make no sense. We routinely swap out that NS bag from the floor and switch it to LR or plasmalyte for intraop.
The only explanation is optics with the jury . Every neph (should ) knows that LR has 4.0 mEq/L of K and not straight up adding 4mEq of KCl to the body . But I can imagine a jury falling for a prosecuting lawyers demagoguery and ignoring the oh let’s just say the stenoses AVF outflow tract leading to recirculation issues . Math isn’t American educations strong suit
 
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What about establishing IV access on the hand/arm with a dialysis fistula vs graft?
Is this a definitive No-No? What is the true risk of contributing to infection and clotting in the fistula?
I would continue to avoid it. The risk over the life of the fistula and patient is enough to find an alternative.
 
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So not a transplant nephrologist but the basics of immunosuppression are tested on the general renal boards. I will give my non-transplant nephrologist's summary on the literature for these agents here briefly. Any full time academic nephrologists on here can please feel free to correct this part-time private practice nephrologist's summary of the literature (though I was briefly on academic faculty. Now I am on private practice voluntary faculty with the fellowships at the hospital I am credentialed at) .

ATG - Rabbit or Horse - purified gamma globulin obtained by immunizing horses / rabbits with human lymphocytes. Cytotoxic antibodies to various CDs on T and B lymphocytes. Depletes peripheral lymhocytes via complement mediated lysis and clearance by the RES.

Alemtuzumab is depleting protein that is an anti CD52humanizied monoclonal antibody. CD52 is found on all B and T cells, macrophages, NK cells and some granulocytes. The alemtuzumab CD25 complex triggers antibody dependent lysis - the depletion of lymphocytes can persist for one year until the immune system is fully reconstituted

Basixilimab is a non-depleting protein that is a chimeric human/mouse monoclonal antibody that competitively inhibits the activation of lymphocytes by IL-2.

BPAR - Biopsy proven acute rejection
DGF - Delayed graft function

Brennan DC et al NEJM 2006 compared Basiliximab vs rATG in high risk recipients (more HLA mismatches) and showed that there are similar composite end point of BPAR , DGF , allograft / patient survival. Subanalysis showed significantly lower rates of BPAR associated with r-ATG
But there was significantly higher rates of myelosuppression and overall infections seen with r-ATG.

Hanaway MJ et al 2011 compared Alemtuzumab vs Basilixmab in low risk patients and Alemtuzumab vs rATG in high risk patients
Efficacy vs basixilimab showed lower rates of BPAR at 6,12, and 36 months with alemtuzumab with a composite endpoint of freedom from rejection, graft loss or death was significantby better at 3 years with alemtuzumab. But there were lower rates of serious infectious complications seen with basiliximab.
Efficacy vs rATG showed the composite endpoint of freedom from rejection, graft loss or death was similar between both agents. But there were overall more infectious disease seen with rATG but similar rates of serious infectious complications.

All three can be used for induction
Only basiximab can be used for maintenance immunosuppression
only Alemtuzumab and rATG/eATG can be use for treatment of rejection

This is a figure from Matas et al 2015 detailing current trends in antibody induction use in kidney transplantation.
1649797616770.png


The transplant nephrologists I rotated under as a fellow usually favored basiliximab for a patient with good 6/6 match and low KPI score.
They tended to use rATG otherwise for HLA mismatched kidneys and/or high KPI.
They also did not tend to prefer to use alemtuzumab due to perceived more serious side effects in their experience.
but hey im not a transplant neph and i dont order these things so im sure there are more nuances than that. I'm sure this is all center specific.
 
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