Kidney-related adverse reactions?

[fattymckee]

I came across something saying Reta shouldn't be used by people who have chronic kidney disease, yet I can't locate much detail on this. Has anyone else seen anything like that?

I've been on 15mg of tirz for a while and now I have to switch things up since I'm not losing weight, so I'm looking into what else is out there. Thanks!

 

[Chili777]

Wow. I happened to be reading through the Phase 2 trial data at that exact moment, and nothing in it points to kidney harm - if anything, Reta looks better on this front than Tirz:

On the renal side, the phase 2 data showed UACR falling sharply with retatrutide, in diabetic and non-diabetic participants alike. The unexpected part: among the non-diabetics, eGFR and Cystatin-C based GFR rose by 8-10ml/min - an INCREASE rather than the decline you would expect. Once dosing stopped, that gain disappeared. That is why studies are now under way looking into renal outcomes in people with overweight/obesity and chronic kidney disease, with results anticipated in late 2025 or early 2026. No approved drug so far has produced a GFR climb of that size. If Lilly can confirm the gain is genuine, it would be a groundbreaking discovery, and frankly unprecedented in modern medicine.

In plain terms, eGFR estimates the volume of blood your kidneys clear each minute. In most medical situations:

• Better filtration goes with a higher eGFR
  
• Worse filtration goes with a lower eGFR

Taken at face value, a rise sounds great - but context decides. It might equally reflect kidneys overworked by diabetes, a high protein diet, certain medications, or plain stress. That effect reversed once dosing stopped in Phase 2, which argues against kidney damage, and no currently approved drug has produced an eGFR climb that big. The rise came bundled with better weight, inflammation, lipids and UACR (a kidney-stress marker), so nothing in the presented trial data pointed to hyperfiltration injury, and because both creatinine-based and cystatin-C-based GFR moved up, a statistical artifact becomes a harder explanation to defend.

Full disclosure: I am not a doctor (nowhere close to one). I just happened to be reading the trial data with Gemini helping me make sense of it, and your question arrived at a good moment. If kidney disease is part of your life, or that of someone you care about, take these findings to that person's doctor and ask whether the interpretation holds.

 

[fattymckee]

Chili777 said:

Wow. I happened to be reading through the Phase 2 trial data at that exact moment, and nothing in it points to kidney harm - if anything, Reta looks better on this front than Tirz:

On the renal side, the phase 2 data showed UACR falling sharply with retatrutide, in diabetic and non-diabetic participants alike. The unexpected part: among the non-diabetics, eGFR and Cystatin-C based GFR rose by 8-10ml/min - an INCREASE rather than the decline you would expect. Once dosing stopped, that gain disappeared. That is why studies are now under way looking into renal outcomes in people with overweight/obesity and chronic kidney disease, with results anticipated in late 2025 or early 2026. No approved drug so far has produced a GFR climb of that size. If Lilly can confirm the gain is genuine, it would be a groundbreaking discovery, and frankly unprecedented in modern medicine.

In plain terms, eGFR estimates the volume of blood your kidneys clear each minute. In most medical situations:

• Better filtration goes with a higher eGFR
  
• Worse filtration goes with a lower eGFR

Taken at face value, a rise sounds great - but context decides. It might equally reflect kidneys overworked by diabetes, a high protein diet, certain medications, or plain stress. That effect reversed once dosing stopped in Phase 2, which argues against kidney damage, and no currently approved drug has produced an eGFR climb that big. The rise came bundled with better weight, inflammation, lipids and UACR (a kidney-stress marker), so nothing in the presented trial data pointed to hyperfiltration injury, and because both creatinine-based and cystatin-C-based GFR moved up, a statistical artifact becomes a harder explanation to defend.

Full disclosure: I am not a doctor (nowhere close to one). I just happened to be reading the trial data with Gemini helping me make sense of it, and your question arrived at a good moment. If kidney disease is part of your life, or that of someone you care about, take these findings to that person's doctor and ask whether the interpretation holds.

I appreciate it! That matches what I came across not long ago, or at least something close. Still, I could have sworn I saw the reverse at some point earlier lol. That's why I wanted to check whether anyone here had additional insight

 

[lessthanhalf]

For chronic kidney disease, Semaglutide and Tirzepatide rank as key therapies — they have been shown to delay renal failure progression, trailing only SLGTi treatment and blood pressure management. Since Reta hasn't received approval, no formal recommendation exists for it at this point, and I suspect the large trials needed to demonstrate this benefit for Reta haven't been completed, though the early signs look encouraging.

 

[Chili777]

lessthanhalf said:

For chronic kidney disease, Semaglutide and Tirzepatide rank as key therapies — they have been shown to delay renal failure progression, trailing only SLGTi treatment and blood pressure management. Since Reta hasn't received approval, no formal recommendation exists for it at this point, and I suspect the large trials needed to demonstrate this benefit for Reta haven't been completed, though the early signs look encouraging.

Yeah, Reta isn't something they're able to prescribe, plus what we have is only Phase 2 trial data. Considering how it impacts eGRF, I wouldn't be shocked if a separate trial zeroed in on that. As for where the OP got their info, I have no idea, but if my kidneys were already chronically impaired, I wouldn't choose to begin using it on my own without a doctor's guidance tailored to my situation.

 

[lessthanhalf]

Many individuals whose kidney disease is at an early stage, or even at a middle stage, have no idea that anything is wrong. Kidney problems brought on by obesity—along with obesity-related hyperfiltration and proteinuria—show up very frequently. Close to 30 years back I myself had a considerable amount of proteinuria, and I worried it would become a serious long-term issue, yet fortunately it improved whenever I shed weight and appears not to have left much lasting damage. That outcome is not guaranteed, and these days obesity ranks among the more frequent causes of renal failure. The trouble is that if you carry excess weight and have never had your urine protein measured, you simply will not know a problem exists. A Chatgpt estimate puts the figure at 10-30% among people with a BMI of 40 or above.

When renal function is genuinely impaired, that is unquestionably a situation for seeking solid specialist guidance, and doing so is probably also wise if what you have is only hyperfiltration and proteinuria.

For older people who have been obese for a long time, I would add a urine protein check to the list alongside lipids, blood sugars and blood pressure. Even a tiny amount of proteinuria on its own justifies statin and aspirin therapy, regardless of lipid levels, since it strongly predicts cardiovascular risk. GLP's will likely head off a great many future cases of renal failure.

My view is that at stage 1 or 2, reta is probably safe enough provided you make sure to have renal function and protein rechecked a few months after beginning it, confirming nothing is worsening. For anything beyond that, leaning on better-established treatments and professional advice would be the more sensible path.