Nephrology
Clinical discussions on kidney disease management, dialysis, transplantation, and electrolyte disorders.
Recent Discussions
How do you approach chronic T cell mediated rejection when patient is intolerant to steroids?
I would really want to know in what way the patient is intolerant to steroids. Depending on the degree of activity, I would also consider thymoglobulin and maximize the mycophenolate. CNI dosing would depend on the degree of chronicity, but in general, I would aim for a tacrolimus level of 6-8 ng/ml...
Would you recommend the use of an ACE inhibitor to patients with Type 1 diabetes mellitus who are normotensive but have persistent moderate proteinuria?
My answer would be “yes”. ADA Standards of Care 2025 notes “ACE inhibitors and ARBs remain a mainstay of management for people with CKD with albuminuria”. Specifically, Figure 11.2 shows first-line drug therapy to be RAS inhibitor at maximum tolerated dose for treatment of albuminuria or HTN. RAS bl...
Should CT coronary calcium score be avoided in dialysis patients in light of presumed high prevalence of CAC in this population?
The incidence of coronary calcifications in patients on dialysis exceeds 80% and is between 50-80% in patients with CKD. In addition, dialysis and ESRD cause two types of vascular calcification - in the medial and intimal layers, the latter being the one that correlates best with atherosclerotic pla...
Do you make adjustments to the immunosuppressive regimen for kidney transplant recipients on tacrolimus who develop posterior reversible encephalopathy syndrome (PRES)?
Agree, fortunately it is a rare occurrence. There is some association with low cholesterol and the development of PRES. When I have seen it, I typically change the calcineurin inhibitor from tacrolimus to cyclosporine, though this can also be seen with cyclosporine. In some cases I have converted fr...
What are your top takeaways from ASN 2024?
APOL1 Bi- and Monoallelic Variant and CKD in West Africans (Gbadegesin et al., PMID 39465900) - NEJM This is an important study that examined the genetic risk of CKD associated with APOL1 in West Africa. In addition to finding higher risks for CKD and FSGS in high-risk APOL1 carriers (which was kn...
Would you avoid starting potassium citrate in a patient with recurrent calcium oxalate nephrolithiasis and hypocitraturia if they have metabolic alkalosis?
If the metabolic alkalosis was from hypokalemia and/or thiazide, as is common in stone formers, I would not hesitate, as the potassium would be beneficial in reducing the excess renal ammonia excretion. If from other causes, everything would depend on the cause.
How often do you recommend eye examinations in your patients with primary hyperoxaluria?
I think the risk of oxalosis and associated eye findings is low unless the patient develops CKD, since plasma oxalate remains fairly normal until CKD stage 3B or so. I would suggest that yearly eye exams are reasonable if the eGFR is < 45, and certainly if eGFR is < 30 or the patient is on renal rep...
Would you avoid using cephalosporins in a patient with a history of cephalosporin neurotoxicity in the setting of CKD?
In elderly patients with underlying CNS disease, renal dysfunction and prior history of cephalosporin neurotoxicity, I would avoid the use of Cephalosporin therapy if possible. If there are not other alternatives, I would strive to give the lowest possible therapeutic dose of the antibiotic to dimin...
How do you advise a patient with CKD who wants to take an herbal medication that is not known to be nephrotoxic, given that herbal medications are not regulated?
Dr. @Dr. First Last' answer is spot on. We just don't know what these drugs do in CKD. We have been fooled many times in the past, thinking it was safe, and they were not. But not all supplements are the same, and you have to look at the bottle; many are just homeopathic nonsense and can be taken.
How would you approach a patient with class III and V lupus nephritis, already on HCQ, MMF, voclosporin and losartan, but has continued proteinuria not yet attaining complete renal response?
Few things are more complicated than lupus nephritis, and this question is not answered easily. It depends on hematuria, Cr, proteinuria, C3, C4, dsDNA, and systemic symptoms. So, it depends on what I think is causing the incomplete clinical response. If I believe it is the class V lesion, I would g...