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Looks like I'm going to have to go in long term prednisone therapy. (FSGS disease I'm spilling a tremendous amount of protein into my urine) wondering how to counteract prednisones catabolic effects? A bodybuilding friend told me I was going to lose muscle mass on the drug and would be tired often. Would a mild dose of test help? Var? Or could aas worsen the condition?
Eat meticulous, train ridiculous for best results.
Prednisone is powerful stuff and can wreak havoc over the long term. I have ulcerative colitis and just finished up an 8 week run of prednisone starting at 40mg and tapering by 5mg every week.
I am on trt and upped my dose of test by 200 mg/ week and threw in 30 mg of var for the last 4 weeks. I still put on some belly fat but my diet was off. Prednisone makes some very hungry-me included. What dose will you be on and when you say long term what do you mean?
I should mention when I was down to my 10mg week and 5 mg week I had several days where I felt like I could not wake up fully or even get out of bed because I felt so tired/drained. Other days I was totally fine. This is caused by adrenal fatigue. My body temperature on those days was always under 98 degrees and typically in the 96.xx degree range too. You may want to Look up prednisone and adrenal fatigue.
The doctors initial prognosis said 6 months + of an "aggressive dose". No clue what that mean but he just got labs back and called me today and said it looks like my FSGS is secondary instead of primary. When u did research on that if my high blood pressure was the cause then we gave that under control and might only need treatment of the FSGS with ACE inhibitors or ARB's. I meet with the doctors face to face late next week. Just when he suggested prednisone and I did some research the results were less than pleasing.
Eat meticulous, train ridiculous for best results.
What's your doctors specialty?
This may be one of those times where health is more important than muscles. Worse case scenario, kidney failure and dialysis. Who would care about muscles when that happens? I suggest you go off aas completely and follow your doctor's orders strictly (I am assuming he is a nephrologist). You can always rely on muscle memory once you get everything under control. Good luck.
I would be using Golden seal and liver function support such as liv52 and N-Acetyl L-Cysteine (NAC)
I love prednisone for short term use when I have sciatic nerve issue that wont go away.
When you said Golden Seal I got a good nostalgic laugh. I remember back in the day the weed smokers used a product called Golden Seal to pass urinalysis in the Military lol.
Prednisone is not to be trifled with. It is the most dangerous drug if misused on the planet in my opinion. In a nutshell it shuts down your immune system to allow a drug that would normally be destroyed by the immune system to exist. If your Doctor is not a pro at treating your specific ailment and got his treatment advice from reference material (online) get a new doc before going down that path. There is no way on the face of the earth I would put anything in my body that the consulting physician was unaware of. I would not even eat meat or seafood when I was on it.
Stay off the protein powder excess will add to the issue.
Thanks everybody. He is the leading nephrologist in the area. He told me to do some research before we meet again next week so I'll have some understanding of what's going on and quite frankly the prednisone therapy has me worried. Hopefully we can figure out another treatment.
Eat meticulous, train ridiculous for best results.
in your research, have you read this page yet?
Medscape: Medscape Access
Medical Care
Treatment of FSGS can be divided into the following:
Nonspecific; nutritional management
Nonimmunosuppressive therapy - Diuretics for edema, angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) for reduction of proteinuria, other antihypertensive agents for hypertension, and lipid-lowering drugs for hyperlipidemia
Nonspecific treatment
Nonspecific treatment goals in NS include maintenance of adequate nutrition, minimization or elimination of proteinuria, and prevention of complications resulting from edema. Control of hypertension is one of the most important aspects of overall management. Lowering of lipid levels is necessary to reduce cardiovascular risk and to possibly delay the progression of renal disease.
The mainstay of treatment is reduction in daily salt intake to 2 g of sodium (6 g of salt) and the use of diuretics in varying doses and combinations. A high level of protein intake may further aggravate proteinuria, adversely affecting renal function. Current recommendations call for an intake of 1-1.3 g of high biologic value protein per kilogram of body weight and a reduction of fat intake.
In most patients, loop diuretics (eg, furosemide) are needed to promote diuresis. Patients with massive edema with impaired oral absorption may require intravenous administration. In patients with refractory conditions, addition of other diuretics (eg, metolazone) and potassium-sparing agents (eg, spironolactone, triamterene) facilitates diuresis and prevents hypokalemia. Rarely, some patients (especially children) with intractable edema may need intravenous albumin and mannitol in a hospital setting to initiate diuresis. Protracted use of intravenous albumin should be discouraged; the regimen is expensive and ineffective, because most of the infused albumin is lost in the urine.
Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are nonspecific agents that reduce proteinuria because of their antihypertensive and intrarenal hemodynamic effects of reducing glomerular capillary pressure and resistance. ACEIs and ARBs are effective in reducing protein loss even in normotensive patients. These agents do not eliminate proteinuria completely or reverse the primary glomerular disease process.
Since most patients with idiopathic FSGS develop hypertension, which further contributes to renal functional deterioration, meticulous attention must be paid to maintain BP in the reference range. All classes of antihypertensive agents, which effectively lower BP, have a beneficial effect in reducing proteinuria. In many patients, combination antihypertensive therapy may be needed to maintain normal blood pressure. Another nonspecific therapy uses lipid-lowering agents to control hyperlipidemia. The statin class of drugs is better tolerated than some of the older agents.
Specific treatment
Idiopathic FSGS is a difficult disease to treat because of its highly variable clinical course. The specific treatment approach is still empirical, and no consensus has evolved because of a lack of prospective controlled trials. Spontaneous remissions are very rare, probably occurring in less than 5% of patients. In those with non-nephritic proteinuria, many physicians use only the nonspecific measures outlined above, and the general consensus is that aggressive approaches should be used in persistently nephritic patients. Ultimately, prognosis in nephritic FSGS patients is determined by their response to prednisone and other immunosuppressive agents.
Current evidence, mostly derived from retrospective analyses, favors prolonged corticosteroid therapy (6 mo or longer) to induce remission in patients with idiopathic FSGS.
Since long-term steroid therapy may lead to serious toxicity, patient counseling and close monitoring for adverse effects are essential before embarking on such a protracted regimen. The current approach calls for initiating therapy with prednisone in a dose of 1 mg/kg (60-80 mg/d) for 2-6 months or longer, depending on patient response as assessed by presence or absence of edema, 24-hour urine protein excretions, CrCl, SCr, serum albumin, and lipid levels.
Studies indicate that 30-60% of patients may undergo complete or partial remission to such a regimen, and relapses are frequent when steroids are discontinued. Complete remission is protein excretion of less than 200-300 mg/d, and partial response is excretion of 200-3500 mg/d, or a greater than 50% reduction in baseline proteinuria. In children, results from several studies show a remission of proteinuria in 11% of patients, persistence of NS with preservation of renal function in 31%, decline in the glomerular filtration rate in 23%, and development of ESRD in 21%. In adults, 10-year renal survival in nephrotic patients ranges from 25-55%, compared with 85-90% in patients with mild proteinuria.
In general, patients with tip lesions on histology are more responsive to corticosteroids, with excellent renal preservation compared with those with other forms of FSGS. Blacks and patients with collapsing FSGS are generally refractory to treatment and progress to renal failure. In responding patients, the goal is to titrate prednisone to the lowest dose to stop or reduce proteinuria and to prevent relapses. Use of steroids on alternate days can also reduce toxicity. Some have used a combination of prednisone and a cytotoxic agent such as cyclophosphamide as initial therapy to reduce the dose and duration of corticosteroids. The optimal treatment duration is uncertain; some authorities recommend the use of steroids indefinitely. In patients who are refractory to 2-3 months of prednisone therapy, the recommendation is to reduce the steroid dose and to add cyclophosphamide (2.5 mg/kg [150-200 mg/d]).
Monitor patients for bone marrow suppression, and encourage them to drink adequate fluids to prevent hemorrhagic cystitis.
Prolonged use of cyclophosphamide may lead to gonadal toxicity; therefore, persisting with cyclophosphamide beyond 3 months in patients who do not respond is unwise.
Randomized controlled trials and uncontrolled studies indicate that cyclosporine (CsA) in a dose of 5-10 mg/kg/d may be beneficial in patients unresponsive to prednisone and cyclophosphamide. Few limited studies have employed tacrolimus. Since both of these calcineurin inhibitors can cause nephrotoxicity, the recommendation is to avoid them in patients with renal insufficiency.
Because of favorable results in other glomerular diseases, mycophenolate mofetil (MMF) has also been evaluated in FSGS. Although the experience is limited, the suggested dose is 750-1000 mg twice daily in patients who are refractory to corticosteroids and in whom calcineurin inhibitors may not be appropriate. To assess whether treatment with MMF and oral pulses of dexamethasone (DEXA) was more effective than treatment with CsA alone for steroid-resistant FSGS, a National Institutes of Health–sponsored multicenter randomized controlled trial, the largest study to date, was conducted in 138 patients aged 2-40 years. At the end of the 52-week treatment period, the incidence of complete and partial remissions was 33% in the MMF and DEXA group compared with 46% in the CsA group and was not significantly different. A critical analysis of this study highlights the limitations of current practices in the treatment of the individual patient with FSGS.[32]
Isolated reports have suggested that in patients who are refractory to steroids and cyclophosphamide, treatment with other immunosuppressive agents, such as tacrolimus (Prograf) and sirolimus (Rapamune), may be beneficial in inducing remissions. However, studies using these agents were uncontrolled investigations that were limited to a few patients.
Recent reviews highlight most of the prospective and retrospective studies and outline current treatment approaches and guidelines.[33, 34]
Despite all attempts, some patients continue to deteriorate and progress to ESRD. Counsel patients and their families early regarding treatment choices for ESRD. A well-informed patient can choose among maintenance hemodialysis, continuous ambulatory peritoneal dialysis, or cadaver or living donor transplantation. FSGS may recur in the transplanted kidney, but most renal physicians do not consider this a contraindication for renal transplantation.
Management of secondary FSGS is directed toward the etiology or associated disorder.
it sounds like the game-changer might be whether its primary or secondary. find out what he means exactly when he said you're secondary.
AD that article rocked. HUGE thank you for posting. I agree needing to know where I am as far as primary or secondary. This waiting game sucks bigtime and doctors not wanting to get hopes up is not good for my blood pressure. I just completed the collection of my urine for 24 hours to test how much protein is spilling over. Should have those results early next week and dr consult shortly thereafter.Quote:
Originally Posted by AD
Thanks again for the info. This site rocks.
Eat meticulous, train ridiculous for best results.
glad you found it useful. they don't call me the google ninja for nothing :)Quote:
Originally Posted by evander87
one thing that i would like to say again is, don't be afraid of pred. it can definitely be harmful if taken unnecessarily, or at unnecessary doses, or for unnecessarily long duration. but this potential harm needs to be weighed against the disease it is treating, the benefits of pred treatment, and the potential consequences if left untreated, or if treated with a less effective medicine.
granted my knowledge on this subject is limited, i still believe that pred may be your best option.
good luck! and get well soon :)
I've taken craploads of prednisone in the past for my Crohn's, I don't remember how much for how long but it was upper limit, at the end there wasn't an inch of my upper body that didn't have some sort of acne or rash and my face was swollen like if I had gone a couple of rounds in the ring with Mike Tyson! That shit will stress your liver! Talk to your doctor about it, certain anabolic steroids will only make things worst and some may diminish the effect of the prednisone wich is precisely what you don't want. My advice is to just ride the wave, til you feel better rest and recover. I know it ****ing sucks but you probably won't even feel like going to the gym anyways. But don't worry, you can bouce right back when you're good again, take it from me, I've tried almost every single med on the planet for crohn, had 6 surgeries over the years for it, got my whole colon taken out, with a J-pouch since I'm 21. But at 25 I did a strongman competition, benched 540lbs raw and many other things. Some say there there is no such thing as muscle memory, I say bullshit! I don't know how many times I lost everything and bounced right back up. You need an iron will, mental toughness but you'll go through it. Good Luck!
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Thanks for all the great info you guys are awesome. I do have a update. And it's GREAT news. My FSGS is secondary and no further treatment is needed at this time. Just need to manage my blood pressure. It's. HUGE relief. That prednisone therapy scared the shit out of me. I'm a couple months away from moving back to LA to further my acting career and that would have royaly screwed that.
Thank again guys.
Eat meticulous, train ridiculous for best results.
Congrats :)Quote:
Originally Posted by evander87
good to hear. Thanks for the update.Quote:
Originally Posted by evander87