I recently treated the below patient and would like to ask your opinion:
61 year old caucasian male with long standing diabetes-2 on insulin with baseline creatinine of 1.2-1.5 presented with left lower extremity swelling and fever. No h/o diabetic retinopathy. PMH includes CAD s/p CABG, charcots foot with recurrent right lower extremity cellulitis leading to right BKA. Creatinine at the time of this admission was 3.4. Has MRSA bacteremia and left lower extremity osteomyelitis of foot. Treated with daptomycin initially and then changed to lenezolid. Initial evaluation revealed 0.6 grms of proteinuria. Over a period of few days creatinine improved to 1.6. But started to worsen again gradually over next 10 days with peak creatinine of 3.8 and BUN 116. Developed fluid retention leading to pulmonary edema. Has worsening leukocytosis. He was started on Hemodialysis via right IJ tunnelled catheter.
1) What would be the cause of his recurrent AKI?
2) Would you do biopsy?
3) Any other investigations?
61 year old caucasian male with long standing diabetes-2 on insulin with baseline creatinine of 1.2-1.5 presented with left lower extremity swelling and fever. No h/o diabetic retinopathy. PMH includes CAD s/p CABG, charcots foot with recurrent right lower extremity cellulitis leading to right BKA. Creatinine at the time of this admission was 3.4. Has MRSA bacteremia and left lower extremity osteomyelitis of foot. Treated with daptomycin initially and then changed to lenezolid. Initial evaluation revealed 0.6 grms of proteinuria. Over a period of few days creatinine improved to 1.6. But started to worsen again gradually over next 10 days with peak creatinine of 3.8 and BUN 116. Developed fluid retention leading to pulmonary edema. Has worsening leukocytosis. He was started on Hemodialysis via right IJ tunnelled catheter.
1) What would be the cause of his recurrent AKI?
2) Would you do biopsy?
3) Any other investigations?
Since you are asking I assume that Rhabdo from dapto leading to renal failure is not the cause.
ReplyDeleteLinezolid leads to inhibition of mitochondrial oxidative phosphorylation and can cause renal failure and lactic acidosis. Mitochondrial polymorphism might have made her more susceptible to this. But i guess she has renal failure of not so clear cause so probably needs biospy. (Fellow rambling..:))
Check out the link below.. interesting. In this renal failure was from linezolid and kidney biopsy didn't show much. this also has reference to 2 other cases.
http://cid.oxfordjournals.org/content/42/8/1111.full.pdf+html
Nice one about linezolid. I repeated UA and showed 3+ proteinuria and hematuria. Plenty of rbc. Now has 3.5 gms of proteinuria.
ReplyDeleteSince you are asking i decided to look for the uncommon things hence the article. :)
ReplyDeleteThe first two things that come to me are AIN and Immune complex mediated MPGN which can explain ARF, Hematuria, nephrotic range proteinuria.
Given his clinical presentation he can have AIN from either of the antibiotics (though both are not classically known to cause AIN, my guess is that they may) or infection itself lead to immune complex mediated MPGN. Guess should do serological w/u and urine eos but he needs biopsy to find diagnosis.
I'm thinking post-infectious glomerulonephritis now. Low complement levels would support this. Although classically seen with streptococcal pharyngitis, post-infectious (or immune complex) GN can be seen with any chronic infection, including staph.
ReplyDeleteSee this review article on post-infectious GN published in KI just this week. Would probably biopsy. What did you do?
Excellent KI review Sharon. I do think IRGN (infection related GN) . Ideally biopsy would be diagnostic. However I did not do the biopsy because of various reasons : I think management would not change since the patient has recurrent debridements for cellulitis, I and D for abscess and osteomyelitis. All his serologies were negative and complements normal. We had around five cases of Ig-A dominant post infectious GN during my fellowship and with variable complement levels. In this cjasn article http://cjasn.asnjournals.org/content/1/6/1179.full.pdf 5 out of 8 patients had normal complements.
ReplyDeleteAlternatively based on our previous experience patients with underlying diabetic nephropathy can present as RPGN when they develop superimposed ATN.
This patient is scheduled for left BKA hence another approach would be to biopsy the kidney once the infectious source is removed if he has no renal recovery.
Post infetious IgA GN, wasn't aware, good to know this entity. I believed that HIV, Hep B, schistosomiasis are the only infections known to cause secondary IgA. Staph a cause, will keep this as a differential next time.
ReplyDeleteThanks for this one.
I mean,i knew post infectious IgA but not Stap leading to it.
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ReplyDelete"Alternatively based on our previous experience patients with underlying diabetic nephropathy can present as RPGN when they develop superimposed ATN." - what do you mean by this, Kiran? This is new to me.
ReplyDeleteIf you recall I present a case few months back in our renal rounds where in everything seems like RPGN but biopsy showed diabetic nephropathy and ATN. Patients with diabetic nephropathy who has hematuria and proteinuria can mimic RPGN if they have superimposed ATN.
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