Question of the Week # 218

218 )  A 36 year old woman presents to the office for a routine follow up visit. Her past medical history is significant for recurrent urinary tract infections which are unrelated to sexual intercourse. She was initially managed on intermittent self-treatment with Trimethoprim-Sulfamethoxazole. However, in view of frequent episodes of UTI she was started on continuous Trimthoprim prophylaxis one week ago. She denies any fever or abdominal pain. She has not had dysuria or frequency or urgency over the last 5 days. Physical examination is normal. Laboratory investigations reveal a WBC count of 6.3k/µl with normal differential, Sodium 140meq/l, Potassium 4.0meq/l, Blood urea nitrogen 10mg% and Creatinine 1.4mg% . Her labs obtained 1 month ago show Blood urea nitrogen of 12mg% and creatinine of 0.7mg%. The most likely explanation for her increased creatinine?

A) Allergic Interstitial Nephritis

B) Acute Tubular Necrosis

C) Pyelonephritis

D) Decreased tubular secretion

E) Papillary necrosis

5 Responses

  1. is it D??? none of the other choices makes sense.. never heard of trimethoprim causing AIN or ATN. Patient has no symptoms of pyelonephritis…

  2. Acute interstitial nephritis (AIN) secondary to trimethoprim-sulfamethoxazole (TMP-SMX) is well documented as a cause of acute renal failure in native kidneys,but this clinical picture is not consistent with interstitial nephritis.
    TMP inhibits renal tubular creatinine secretion, which can result in a significant decrease in creatinine clearance. These changes appear to be completely reversible upon discontinuation of therapy.

  3. D= isolated creatinine elevation

  4. D:) Treatment with the chemotherapeutic combination of 160 mg. trimethoprim plus 800 mg. sulfamethoxazole twice daily increased the serum creatinine level by an average of 2 mg. per 1. in 21 patients. The effect was clearly reversible. The chemical analysis of creatinine was not affected by the addition of trimethoprim, sulfamethoxazole or their metabolites. In 2 subjects given the drug combination for 12 days renal excretion and 24-hour clearances of creatinine decreased but iothalamate 131I clearance was unchanged. Consequently, the rise in serum creatinine does not indicate any decrease in the glomerular filtration rate. The serum creatinine started to rise within 4 hours after oral administration of a single dose. The rise in serum creatinine could be produced with trimethoprim alone but not with sulfamethoxazole alone. When the plasma creatinine was raised to 100 mg. per l. in healthy subjects (by giving creatinine orally), trimethoprim increased the creatinine levels 10 times as much as at normal plasma levels. The effect was interpreted as a competitive inhibition of the mechanism for tubular secretion of creatinine through the base-secreting pathway

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