farxiga

[Cbailey]

Hello, I was wondering if any of you had went on farxiga with a low GFR and what was your experience? My GFR is at a 31 and my doc has discussed the possibility of putting me on it.

[Bassetmommer NKF Ambassador]

My husband went on it and it works great for him. His GFR was in the low 30's and actually came up. They have a patient assistance program that will pay for it.

[renegade70 in reply to Bassetmommer]

thats really good to know.

[Cbailey in reply to Bassetmommer]

That’s wonderful news for your husband!

[Gauvian]

Hello, my nephrologist put me on Farxiga last June as my gfr had dropped from 40 to 34. My last labs in january my gfr was 34 so no change but at least it hasnt dropped any further (apart from the initial drop when you first start taking it, it then normalises after about a month). At this stage i had no protein in the urine, from what i understand most of the studies have shown it works for people who have protein in the urine. Please let us know how it works for you and all the best

[purifire7777]

Good morning, I never heard of it but I am going to check it out. I want to be at a 90's.

[jodaer]

I take Jardiance, I believe it's the same family of drugs at Farxiga. My proteinuria has gone way down, although still high, since I started taking it in Jan 2023.

[nonna70]

I also take Farxiga; the thing I have noticed is 500mg of sugar in my urine!

[TylerPeyton]

my GFR was stable at 30-32. My Dr put me on it. My GFR dropped to 15! He d/c it. But said he at some point would like me on it. He said it’s easy to become dehydrated on it

It did increase my urine output tremendously

[GoldenBailey]

My Nephrologist put me on Farxiga a couple of months ago. My last eGFR was 17 (stage 4). I also have extremely high protein (around 3,000). My next appointment is scheduled for six months out so I'm patiently waiting to learn if Farxiga works for me. I'll keep checking this post for other's experience. I'm in the US. Hopeful.

[Blackknight1989]

Farxiga is a SGLT2 Inhibitor that was developed as a co-treatment for those with T2D AND proteinuria which is defined signal from your body that nephrons are being damaged actively….The lab test used for this is UCAR…UCAR measures kidney damage while eGFR measure current kidney function, or how well they are functioning at the time of the lab…AFTER a confirmation of CKD UCAR is used to track how treatment is working and if your kidneys are responding well or if the underlying cause of CKD (T2D/HBP etc) is being treated effectively. This class of drugs has been throughly studied (at least here in the US) and they have tremendous renoprotective properties especially for those of us suffering from severe CKD like stage 4. The name of the study specific to Farxia is the EMPA-Kidney study of 4400 stage 1-4 CKD patients with and w/o T2D…sorry for the length but here is the SCIENCE behind these new potentially life change for some of us class of drugs…unfortunately I can’t find a nephrologist who is willing to read a medical study or two in order to prescribe them to me in my current rural setting of Northeast Arkansas USA…my current neph actually said at my last appointment “why are you asking about a T2D treatment I didn’t think you had diabetes, do you…continuing he said “Besides the lisinopril will do a better job and as far as I know there is no benefit for you to change your diet or lower your protein intake, we want you “protein loaded” for the start of dialysis in the next couple of years…”. I of course argued abd asked if he’d even heard of the ASN and KIDGO guidelines for “shared-decision making” as the newest thinking in treatment of chronic disease like CKD and of course he hadn’t, then proceeded to tell me of all his wonderful academic and residence training, how long he had to be in training to become a specialist…where he went to med-school (Ivy-league of course yet here he is in BFE USA treating “problems” like me) and of course I was impressed with all his proper learning…so much so that I managed to get tired as his patient because he became so upset with me (I had to relate my puny 4 years at the US Military Academy and how that didn’t completely make me into a tremendous combat leader, that came after by experience and listening to both my subordinates AND my colleagues…he stormed out of the examination room sent his nurse in about 10 minutes later to tell me I was “Dr. W thinks you’d be better served by another specialist…” of course he does…but as a Veteran’s Association primary patient and due to the “rural” setting he was stuck with me…sure enough next visit I had a new diagnosis T2D despite a 5.6 A1C…it’s hard to get a diagnosis REMOVED from your records, that’s been my issue the past 12 months it’s so but I digress…here is the link as promised, an initial eGFR drop is the norm but several studies all agree that’s not an issue(much like my experience with the joint replacement surgeries when eGFR went as low as 10 immediately post-op but recovered in 24 hours to my “normal” sometimes you gotta educate your doc…lol:

“The sodium-glucose cotransporter 2 (SGLT2) inhibitors have become an integral part of clinical practice guidelines to slow the progression of CKD in patients with and without diabetes mellitus. Although initially developed as antihyperglycemic drugs, their effect on the kidney is multifactorial resulting from profuse glycosuria and natriuresis consequent to their primary site of action. Hemodynamic and metabolic changes ensue that mediate kidney-protective effects, including ( 1 ) decreased workload of proximal tubular cells and prevention of aberrant increases in glycolysis, contributing to a decreased risk of AKI; ( 2 ) lowering of intraglomerular pressure by activating tubular glomerular feedback and reductions in BP and tissue sodium content; ( 3 ) initiation of nutrient-sensing pathways reminiscent of starvation activating ketogenesis, increased autophagy, and restoration of carbon flow through the mitochondria without production of reactive oxygen species; ( 4 ) body weight loss without a reduction in basal metabolic rate due to increases in nonshivering thermogenesis; and ( 5 ) favorable changes in quantity and characteristics of perirenal fat leading to decreased release of adipokines, which adversely affect the glomerular capillary and signal increased sympathetic outflow. Additionally, these drugs stimulate phosphate and magnesium reabsorption and increase uric acid excretion. Familiarity with kidney-specific mechanisms of action, potential changes in kidney function, and/or alterations in electrolytes and volume status, which are induced by these widely prescribed drugs, will facilitate usage in the patients for whom they are indicated.”

LINK: pubmed.ncbi.nlm.nih.gov/362...