They say I have acute tubular necrosis-they say its known as sleeping kidney. i looked it up i know what it is but id like to know if any of you know of anyone who has recovered from it and what should i expect . wondering how long it will take- been passing urine but not nearly enough. please tell me what you know
I’m sorry to hear about the ATN, Rickysyfee. Unfortunately, having that problem tends to mean the kidney won’t work as well or last as long even if/when it does kick in. Are you taking cyclosporin? I was able to find a couple of studies that found a benefit from reducing the dose:
1Transpl Int. 2000;13 Suppl 1:S82-3. Links
Withdrawal of cyclosporine in renal transplant recipients with acute tubular necrosis improves renal function.
Kahn D, Botha JF, Pascoe MD, Pontin AR, Halkett J, Tandon V.
Department of Surgery, University of Cape Town and Groote Schuur Hospital, South Africa. email@example.com
In this study, patients with acute tubular necrosis (ATN) after renal transplantation were prospectively randomized to either conventional immunosuppression or withdrawal of cyclosporine and replacement with anti-thymocyte globulin (ATG). The patients treated with cyclosporine withdrawal and ATG had a significantly shorter duration of ATN (8.9 +/- 1.5 vs 10.8 +/- 1.4 days; P < 0.05) and better renal function (mean serum creatinine on day 5 postoperatively: 740 +/- 49 vs 918 +/- 73 micromol/l; P < 0.05). The incidence of acute rejection was lower in the patients with cyclosporine withdrawal and ATG. In conclusion, cyclosporine is toxic to the renal allograft with ATN, and withdrawal of cyclosporine shortens the duration of ATN and improves renal function.
Transplantation. 2002 Dec 15;74(11):1560-7. Links
Improved renal function in sirolimus-treated renal transplant patients after early cyclosporine elimination.
Gonwa TA, Hricik DE, Brinker K, Grinyo JM, Schena FP; Sirolimus Renal Function Study Group. Baylor University Medical Center, Dallas, TX, USA. firstname.lastname@example.org.
BACKGROUND: Sirolimus (Rapamune; SRL) in combination with cyclosporine (CsA) reduces the incidence of acute rejection episodes in renal allograft recipients. This study evaluated whether renal function could be improved by elimination of CsA from an SRL-based regimen. METHODS: This phase 2, open-label, controlled, randomized study was conducted at 17 centers in the United States and Europe. Two hundred forty-six first cadaveric renal allograft recipients were enrolled, and 197 were randomized to full-dose CsA (microemulsion) plus fixed-dose SRL (2 mg/day; group A, n=97) or reduced-dose CsA plus concentration-controlled SRL (troughs 10-20 ng/mL; group B, n=100). Most patients with acute tubular necrosis-delayed graft function that resolved later than posttransplantation day 7 were not randomized but were assigned to a third group (nonrandomized, n=49) and received up to 5 mg per day of SRL as part of their individualized treatment regimen. All patients received standard doses of corticosteroids. At the end of posttransplantation month 2, eligible patients (those not treated for rejection within 3 weeks) in group B had CsA tapered and eliminated over the subsequent 4 to 6 weeks. RESULTS: At 12 months after transplantation, renal function was significantly better in the CsA-elimination arm. In patients who were on therapy and who had not experienced an acute rejection episode before month 6, serum creatinine level was significantly lower (1.38 mg/dL vs. 1.82 mg/dL, P < 0.001) and calculated glomerular filtration rate (Nankivell method) was significantly higher (73.5 mL/min vs. 57.1 mL/min, P < 0.001) in group B than in group A. In the intention-to-treat population, rates of biopsy-confirmed acute rejection at 12 months were similar between groups A and B (18.6% vs. 22.0%, respectively; P = 0.598). In addition, graft survival (92.8% and 95.0%) and patient survival (96.9% and 96.0%) rates at 12 months were not significantly different between groups A and B, respectively. Furthermore, there were no significant differences between black and nonblack recipients within treatment groups in terms of rejection rates and graft survival at 12 months. Black recipients in group B had better serum creatinine levels at 12 months compared with black recipients in group A (1.55 mg/dL vs. 2.69 mg/dL, respectively, P = 0.011), as did nonblack recipients in group B compared with nonblack recipients in group A (1.53 mg/dL vs. 1.75 mg/dL, respectively, P = 0.055). Black patients in group A had higher mean serum creatinine levels (2.69 mg/dL) than nonblack patients in group A (1.75 mg/dL, P = 0.028). Hypertension, edema, hypomagnesemia, and dyspnea were reported significantly less frequently in patients randomly assigned to undergo CsA elimination compared with patients in group A (P < 0.05); group B patients had a significantly greater (P < 0.05) incidence of abnormal liver function tests, diarrhea, hypokalemia, and thrombocytopenia. CONCLUSION: Concentration-controlled SRL with early elimination of CsA is safe and results in improved renal function. Reduced exposure to CsA does not result in a clinically significant increase in the incidence of acute rejection episodes. This is true for both black and nonblack recipients. SRL may be used to reduce the exposure of renal allograft recipients to the nephrotoxic effects of CsA.
ATN can be caused by the time the kidney was stored before it was placed in your body, anti-rejection drugs, or the quality of the kidney itself. ATN is not uncommon in kidney transplants, especially when the kidney comes from a deceased donor. It sometimes takes a few days or weeks for the kidney to start working, but if ATN is the problem is probably will start working. Meanwhile, you can do dialysis and let the kidney “rest.” Here’s a patient education guide that describes ATN:
Has your doctor suggested (or done) a kidney biopsy to tell whether it’s ATN or acute rejection. If the kidney isn’t functioning because of acute rejection, it may never work or never work very well or very long.
I have known people who had transplants that never worked or worked for a few days or months and not very well then. Although they were very disappointed that their kidney transplant didn’t work, most did dialysis until another kidney became available if they didn’t have a living donor.
no , i am not on cyclosporin-(prograf,cellcept,predisone) still doing nhd and have 2 ultrasounds to check blood flow inside the kidney, which they say is good and a biopsy which was also good. They say they will repeat in 7- 10 days meanwhile i am at home. I am getting used to all the meds and dont have much appetite been drinking low carb meal replacement shakes (low carb due to the blood sugar spikes they are made with splenda) and drinking water to keep it hydrated. dont know anything else I can do. thanks
Believe it or not, my Neph told me to talk to my kidney. So as I sat at the University of Michigan I named my kidney, “Annie” - a knick name I use for my wife who donated her kidney to me. I was there for three weeks talking to the darn thing. I’m sure some of the visitors thought they reached the pysche ward when they saw me. Whe n I went to the bathroom I prayed for more urine.
But alas it wasn’t to be. It turned out I didn’t have ATN rather FSGS.
So I think you should take solace in the fact that you have good labs, some urine and keep the faith! I will keep you in my prayers.
Just, if you start talking to it, you may want to use your inner monologue. Erich
did you ever have any urine at all?
I did have some urine. I would go to the bathroom anf pray for 200 cc’s but often only got 50 cc’s.
But there is still hope for your kidney. If you are religious pray for it to kick in. If your not, send the kidney positive vibes. And of course don’t give up hope. I kept positive because I so very much wanted it to work for the life that I thought I would return to. Despite the outcome, it wasn’t a waste of time. Because at that point that was my job to follow the doctors orders and to stay positive and keep hope alive.
Of course the post script to my story, is that I’m living an incredibly active life of short term daily dialysis. If I could have a working kidney I would switch in a New York minute, but thankfully I have found a system that has given me the best 18 months since I was diagnosed with end stage renal disease seven years ago.
Good luck - I mean it! Erich
it started working a little last friday but i am up to 800 ml yesterday and going during the night.
My husband had ATN with his transplant in 99. He remained on limited dialysis for 5 months! We thought the kidney would never work & had just about given up, but it worked for nearly 6 yrs and he was able to get off dialysis. A biopsy showed he actually had an allergic reaction and the kidney tubules were very inflamed. My husband is allergic to sulfa and he was not taking that but loop diuretics such as lasix, demedex, and nearly all diuretics on the market today, have a molecule in them that is very similar to a sulfa molecule. Some people who are allergic to sulfa, also react to diuretics. His neph took him off lasix and demedex, and put him on Edecrin - an old diuretic and the only one that does not have that sulfa-like molecule. His kidney immediately began to improve and he got off dialysis.
Gancyclovir is also hard on the kidney, but usually given to prevent CMV infection. With your doc, go over all your meds to see if anything may be irritating the kidney.
Don’t give up!
Blessings to you,