Aashi
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A 30-year-old woman with a past medical history of severe asthma since childhood presents to the emergency department complaining of dysuria. She was started on prednisone four months ago for her asthma and has been taking ibuprofen for lower back pain for four months. On physical examination, her blood pressure is 140/80 mm Hg, and the rest of her physical examination is normal, except for 3+ pitting edema bilaterally. Urinalysis shows: protein 4+, erythrocytes 2-3/hpf, occasional fat bodies, white cells 10-20/hpf. Serum albumin 2.4 g/dL; cholesterol 440 mg/dL; C3 normal; 24-hour urine protein 6 g/d; sodium 149 mEq/dL, potassium 4.1 mEq/L, bicarbonate 24 mEq/L, BUN 26 mg/dL, creatinine 1.4 mg/dL, glucose 90 mg/dL. She is sent for a renal biopsy, which, under electron microscopy, shows effacement of the epithelial foot processes. What is the most effective treatment for her renal disease?
(A) Stop the NSAIDs and observe
(B) Cyclophosphamide
(C) Cyclosporine
(D) Captopril
(E) Interferon
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| prathapdoctor
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to minimal change disease, cyclophosphamide is the drug of choice along with coritcosteriods,so i will go with cyclophosphamide
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| robin082006
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Yes this is minimal change disease,
But the patient never has it before, just has it recently after treatment of prednisone and ibuprofen.
I go with A.
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| Mahwish Mushtaq
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i will go with A as u first observe & then treat
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| prathapdoctor
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what is the role of NSAIDS in this case.
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| dr.wad
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( A ) stop NSAID and observe .
minimal change lesion may be caused by NSAID.
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| Aashi
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Answer:
(A) Stop the NSAIDs and observe
Explanation:
This patient has nephrotic syndrome. This diagnosis is based on the urine protein being greater than 3 grams per day, hypoalbuminemia, hyperlipidemia, and edema. The histopathologic pattern is consistent with minimal change disease. This could be caused by NSAID use, as in this case, or from lymphoma.
In adults, "refractory" minimal change disease is sometimes due to focal segmental glomerulosclerosis, which was missed by sampling error on the first biopsy; thus, many nephrologists might elect to rebiopsy these cases. Although the initial therapy of minimal change disease might consist of steroids, this patient has already been on prednisone for four months, and logic dictates that she has failed this therapy. However, the dose of steroids for asthma is unlikely to be at a high enough or sustained enough dose to see an improvement.
If the patient is adequately treated with steroids and the diagnosis is certain, cytotoxic agents, such as chlorambucil or cyclophosphamide, might be considered because they can give remission of the nephrotic syndrome. This case is unique, however, because NSAIDS, as a class, can cause an allergic interstitial nephritis with a nephrotic syndrome. Therefore, although light microscopy results are not given, assuming there was some interstitial infiltrate, the most reasonable response would be to stop the NSAID and observe. Cytotoxic agents would not be used unless there was no improvement after stopping the NSAIDs and steroids at a high dose failed.
Low-dose cyclosporine might be effective in reducing proteinuria, but the response is not sustained, and there is the risk of long-term nephrotoxicity. ACE inhibitors, although they are a nonspecific method of reducing proteinuria, are often used in conjunction with other therapies. One rationale is that angiotensin has been implicated in scar formation; thus, blocking its production would stop renal scarring and long-term renal impairment.
Patients with cryoglobulinemia and a membranoproliferative pattern of glomerulonephritis may have hepatitis B- or C-associated renal disease. These cases have hypocomplementemia as a characteristic finding. Hepatitis-related cryoglobulinemia is treated with interferon, which may reduce proteinuria and improve the glomerular filtration rate. This patient has normal complement levels, making this unlikely.
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