Today, I was asked by a #medicalstudent what are the most exciting developments in nephrology in the last few years, things that have affected the way I practice. Gave a 60 sec answer. But this is what I really wanted to say:

1/ APOL1: yes, we don’t have a treatment yet, but how much better way we understand hypertensive CKD in AA is remarkable. Now, I type “CKD due to APOL1-FGGS” in my notes and I can talk to my pts about it. All CKD trials should include APOL1 testing. Transplant? Big impact. A+++

2/ PLA2R, absolutely incredible contribution for diagnosis of membranous nephrop. No longer idiopathic MN, it’s PLA2R-MN. Now we can diagnose without biopsy (if bx risk high), we can wean off IS faster or titrate it, we can catch recurrences. And the story has not ended. A+++

3/ eculizumab. I don’t want to hear rants about its cost. Before this new C5 inhibitor, dialysis-dependant AKI from TMA due to aHUS meant ESRD. I saw it, many times. Now, this drug gets patients off dialysis. As simple as that. A++

4/ vasopressin V2 receptor antagonists (conivaptan, tolvaptan). Fluid restriction in SIADH never worked for me as nicely as the book claims. Watching the Na go up by attacking the mechanism of disease has been gratifying in many ways. A+

5/ cinacalcet. Not a mineral bone disease connoisseur but this medication works well reducing PTH, buffering hypercalcemia in tertiary HPTH and skipping surgery in many instances. While I’m waiting to see it reducing fracture risk, it has affected my practice. B+

6/ EGFR-TRPM6 connection. The arrival of cetuximab and other anti-EGFR drugs forced us to learn more about tub Mg handling. When you have to chase it with weekly IV Mg you know that this is an important mechanism. I’m sure it’ll open other doors for advancement. B

7/ tolvaptan in ADPKD. Not a cystic guy here. I was skeptical when TEMPO came out. After REPRISE and the recent CJASN follow up data, the story has become hard to argue. Without hard ESRD data, or can’t get an A, but getting a treatment for this genetic entity is a triumph. B

8/ angiotensin II as a pressor. First, I’m obsessed with angiotensin. Second, we have a new pressor that can work in those sick pts on 3 pressors. And, Post hoc analysis suggests renal recovery in AKI-D. im@just excited about it. B-

9/ SGLT2i. CREDENCE is not out yet and I’m still ? by the glycemia factor. But when I c a strong anti hyperfiltration signal, I can’t avoid getting fascinated by it. Even if it only reduces rate of decline of GFR by a small % beyond RAASi, a new Rx for diabetic CKD is just great

10/ DNAJB9. We now have a way to indisputably diagnose the most challenging of all glomerular diseases. I’m convinced that it’s the beginning of a new era that will take us to find a better (or any) way to treat patients with fibrillary glomerulonephritis. B-

That’s it. Tomatoes are welcome. (COI: tolvaptan speaker).