I received the results of my biopsy and I have moderate nephritis. Has anyone been diagnosed with this and is it a permernant condition? My dr's appt. is not until the 14th? I'm really scared.. what does this mean?? Is this curable and will I have to have dialysis???
I'm so sorry about your diagnosis! I haven't had nephritis, but I know many who have, and have recovered. If your doctor is waiting until the 14th to see you, s/he must not be too worried, or you'd be hospitalized by now.
Have faith, follow your doctors orders between now and the 14th (meds? water? rest?) and stay out of the sun.
Sending hugs and keeping you in my thoughts...
Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE). SLE causes harm to the skin, joints, kidneys, and brain. Lupus nephritis may cause weight gain, high blood pressure, dark urine, or swelling around the eyes, legs, ankles, or fingers. Diagnosis may require urine and blood tests and x rays of the kidneys as well as a kidney biopsy. Treatment depends on the symptoms. Medicines can decrease swelling, lower blood pressure, and decrease inflammation by suppressing the immune system. Patients may need to limit protein, sodium, and potassium intake in their diet. Lupus nephritis is a glomerular disease. Glomerular diseases include many conditions with a variety of genetic and environmental causes, but they fall into two major categories:
1) Glomerulonephritis (gloh-MAIR-yoo-loh-neh-FRY-tis) describes the inflammation of the membrane tissue in the kidney that serves as a filter, separating wastes and extra fluid from the blood.
2) Glomerulosclerosis (gloh-MAIR-yoo-loh-skleh-ROH-sis) describes the scarring or hardening of the tiny blood vessels within the kidney
Glomerular diseases damage the glomeruli, letting protein and sometimes red blood cells leak into the urine. Sometimes a glomerular disease also interferes with the clearance of waste products by the kidney, so they begin to build up in the blood. Furthermore, loss of blood proteins like albumin in the urine can result in a fall in their level in the bloodstream. In normal blood, albumin acts like a sponge, drawing extra fluid from the body into the bloodstream, where it remains until the kidneys remove it. But when albumin leaks into the urine, the blood loses its capacity to absorb extra fluid from the body. Fluid can accumulate outside the circulatory system in the face, hands, feet, or ankles and cause swelling.
Systemic lupus erythematosus affects women more than men, some researchers believe that a sex-linked genetic factor may play a part in making a person susceptible, although viral infection has also been implicated as a triggering factor. Lupus nephritis occurs when autoantibodies form or are deposited in the glomeruli, causing inflammation. Ultimately, the inflammation may create scars that keep the kidneys from functioning properly.
Treatment methods have recently found that adding cyclophosphamide or azathioprine to steroids has better results than steroids alone. This combination of drugs improves the functioning of the kidneys.
Treatment of lupus nephritis requires an understanding of the immunopathogenesis, risk stratification by WHO classification and NIH indices, appropriateness of renal biopsy and finally; familiarity with the specific therapeutic modalities. It is useful to discuss the various agents which have merit in the therapy of this condition and then discuss them in the context of the specific WHO class of lupus renal disease.
Glucocorticoids, usually as prednisone or methylprednisolone, remain the most effective and rapidly acting immunomodulator therapy of both the initial episode or the recurrence of active renal disease. Prednisone, or equivalent, at a dose of 1 mg per kg. per day for from four to twelve weeks is the typical initial treatment. Alternatively, two to four mg per kg. administered every other day has been recommended. However, the suggestion this is of equal efficacy yet associated with a lower incidence of toxicity has not been established or generally accepted.
The major problem with steroid treatment is the toxicity associated with chronic use and observation in the NIH cohort that, in the long term, therapy limited to prednisone alone is more associated with increasing chronicity score on renal biopsy, deterioration of renal function and end stage renal disease than the addition of cytotoxic therapy to low dose oral prednisone for recurrent active lupus renal disease. The toxicities of chronic steroids include accelerated development of cataracts, glaucoma, hypertension, osteoporosis, atherosclerosis, diabetes, avascular necrosis, striae, capillary fragility with ecchymoses, Cushinoid appearance, insomnia, agitation, anxiety disorder, and risk of infection.
An additional approach to the use of glucocorticoids in the management of lupus nephritis relies on pulses of intravenous methylprednisolone (13,14). One gram doses of methylprednisolone administered for one to three days and then monthly from three to twelve months has been associated with efficacy. This may be especially the case with rapidly progressive disease of recent duration (13). There may be a delay from three to four months in the benefit of cytotoxics in the management of active nephritis and it is during this period that steroids may prove beneficial. Risks of methylprednisolone pulses include those generally associated with steroids as well as malignant hypertension, seizures, cardiac arrhythmias, acute electrolyte disturbances and rare case reports of sudden death.
Cyclophosphamide is considered the most effective cytotoxic in the management of lupus renal disease. As mentioned, steroids are more rapidly acting but over time can be associated with a greater degree of renal scarring than is observed in patients receiving cyclophosphamide. The role for cyclophosphamide in the treatment of lupus nephritis was first established in two prospective, controlled studies performed at the NIH (15-17). In the first study, Austin et al. enrolled 111 patients between 1969 and 1981 in a randomized protocol comparing prednisone to cytotoxic treatment. Ten of the 28 patients receiving prednisone alone progressed to ESRD compared with only one of the 20 receiving cyclophosphamide (15). In a second study, Boumpas et al. reported on 45 patients who were enrolled between 1981 and 1986 and randomly assigned to receive short course cyclophosphamide, long course cyclophosphamide, or pulse methylprednisolone. Long course cyclophosphamide was superior to pulse methylprednisolone as two compared with six patients progressed to ESRD and superior to short course cyclophosphamide as there were fewer exacerbations (17). In support of the NIH studies are uncontrolled studies of adults in the USA (18,19) and Europe (20), as well as in children (21,22). The major toxicities of cyclophosphamide are alopecia, temporary secondary amenorrhea, permanent ovarian failure with infertility, risk of infection, bone marrow suppression with peripheral cytopenias, theoretic risk of malignancy, and risk of hemorrhagic cystitis. Studies suggest that either the oral or parenteral route of cyclophosphamide administration is effective in the treatment of lupus nephritis. However, the risk for hemorrhagic cystitis and permanent gonadal failure with infertility is greater in patients treated with oral cyclophosphamide.
Azathioprine also has proven effective in the therapy of lupus and lupus nephritis. For non-renal lupus disease manifestations azathioprine is useful as a steroid sparing agent. Candidates for azathioprine include patients who do not tolerate or experience a significant toxicity with cyclophosphamide. Some clinicians believe that after induction of a response in patients with lupus nephritis with either steroid or cyclophosphamide, azathioprine is a more prudent maintenance immunosuppressive therapy because of its more favorably toxicity profile. Additionally, meta-analysis both in the 1980s and most recently in 1996, combining the major double blind controlled clinical trials of lupus nephritis, suggest a benefit of azathioprine addition to prednisone compared to prednisone alone (23,24). The major toxicities of azathioprine include nausea, vomiting, transaminitis, and cytopenias.
Cyclosporin has been evaluated in small trials of patients with lupus and lupus nephritis (25,26). Cyclosporin has been associated with reduced clinical disease activity over time and, in uncontrolled trials, proven effective especially for patients with pure lupus membranous nephritis (27). Cyclosporin is associated with dose dependent nephrotoxicity, hypertension, hyperuricemia, headache, tremor, hypertrichosis, increased risk of infection and theoretic risk of malignancy. Additionally, in patients with mixed proliferative and membranous lupus nephritis, as compared to patients with pure membranous, cyclosporin may be disadvantageous and associated with renal deterioration.
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Peace and Blessings
I have Lupus Nephritis - Type 4 - the severest, and have been under treatment since 12/2003. I was able to avoid Cytoxan even at my most unhealthy moments, and have been on a cocktail of Prdnisone and Cellcept, along with vitamins and minerals and blood pressure meds. Usually when your kidneys are off, your blood pressure is affected. I am doing very well now, and have been able to go from not being able to work, to working part-time.
Hope this helps!
:?: one eyed bishop? what is that?
I saw your post about a naturopath, Missy, and may find one in my area, that's such a good idea!
My doctor suspect that I do have Lupus Nephritis but she said I need to undergo more tests before they can perform kidney biopsy. Its scaring me, thanks for all the informations..
There is nothing we can do to make God love us more and there's absolutely nothing we've done to make Him love us less... God loves us without conditions for just the way we are!
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