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Quiz page answers August 2003
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QUIZ PAGE ANSWERS AUGUST 2003
A 55-year-old African-American man presented with a 6-day history of swelling in his hands and feet. An outside physician noted an increased serum creatinine, and the patient was treated with furosemide. He had a history of diarrhea for the week prior to admission. Serum creatinine was 4.9 mg/dL (433 mol/L), white blood count was normal, hemoglobin was normal, and on urinalysis there were 1 to 3 white blood cells and 7 to 10 red blood cells per high-power field with trace proteinuria. He had no dysuria and had not noted any decreased urine output. He had a history of hypertension and peptic ulcer disease and was taking aspirin and a diuretic on admission. He had also taken nonsteroidal antiinflammatory drugs (NSAIDs) for back pain. On admission, blood pressure was 193/110 mm Hg, and there was trace lower and upper extremity edema. The rest of the physical examination was unremarkable. Screening laboratory and serological tests were normal. A renal biopsy was done.
What is your clinical differential diagnosis? The clinical differential diagnosis included acute tubular necrosis caused by dehydration with NSAIDs-induced toxicity, malignant hypertensive damage, and hemolytic uremic syndrome.
Figure 19A.
What do you see by light microscopy?
There is acute tubular necrosis, with flattened, regenerating-type tubular epithelium (hematoxylin and eosin, original magnification ⫻200).
Figures 19B and C.
What additional lesion do you see?
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QUIZ PAGE ANSWERS (continued)
The glomeruli appear unremarkable, but there is a tubulointerstitial inflammatory infiltrate with edema. The infiltrate is composed primarily of lymphocytes, with scattered eosinophils (Fig 19B, Jones’ silver stain, original magnification ⫻100; Fig 19C, periodic acid–Schiff, original magnification ⫻400). These findings are indicative of an acute interstitial nephritis, with eosinophils suggesting a possible hypersensitivity component.
Figure 19D.
What do you see by electron microscopy?
Electron microscopy shows no deposits, but there is complete effacement of foot processes (transmission electron microscopy, original magnification ⫻8,000).
How do you correlate the electron microscopy findings with the clinical setting? The patient did not have significant proteinuria by dipstick. However, the complete foot process effacement by electron microscopy strongly suggests a minimal change disease–type lesion, which, when associated with acute interstitial nephritis, strongly points to NSAIDs as the underlying etiology. Proteinuria may not manifest when glomerular filtration rate is very low, as in this patient. Indeed, as the patient received supportive treatment and recovered his glomerular filtration rate over the ensuing 10 days, he had marked increase in urine proteinuria to 6 g/24 h. On subsequent follow-up, he had normal renal function and no proteinuria.
Final diagnosis: Acute interstitial nephritis and minimal change disease lesion, caused by NSAID injury Case provided by Agnes B. Fogo, MD, Department of Pathology, Vanderbilt University Medical Center, Nashville, TN.
If you have an interesting case you would like to submit for consideration, please contact the AJKD Editorial Office.
QUIZ PAGE ANSWERS AUGUST 2003
A 55-year-old African-American man presented with a 6-day history of swelling in his hands and feet. An outside physician noted an increased serum creatinine, and the patient was treated with furosemide. He had a history of diarrhea for the week prior to admission. Serum creatinine was 4.9 mg/dL (433 mol/L), white blood count was normal, hemoglobin was normal, and on urinalysis there were 1 to 3 white blood cells and 7 to 10 red blood cells per high-power field with trace proteinuria. He had no dysuria and had not noted any decreased urine output. He had a history of hypertension and peptic ulcer disease and was taking aspirin and a diuretic on admission. He had also taken nonsteroidal antiinflammatory drugs (NSAIDs) for back pain. On admission, blood pressure was 193/110 mm Hg, and there was trace lower and upper extremity edema. The rest of the physical examination was unremarkable. Screening laboratory and serological tests were normal. A renal biopsy was done.
What is your clinical differential diagnosis? The clinical differential diagnosis included acute tubular necrosis caused by dehydration with NSAIDs-induced toxicity, malignant hypertensive damage, and hemolytic uremic syndrome.
Figure 19A.
What do you see by light microscopy?
There is acute tubular necrosis, with flattened, regenerating-type tubular epithelium (hematoxylin and eosin, original magnification ⫻200).
Figures 19B and C.
What additional lesion do you see?
AJKD
QUIZ PAGE ANSWERS (continued)
The glomeruli appear unremarkable, but there is a tubulointerstitial inflammatory infiltrate with edema. The infiltrate is composed primarily of lymphocytes, with scattered eosinophils (Fig 19B, Jones’ silver stain, original magnification ⫻100; Fig 19C, periodic acid–Schiff, original magnification ⫻400). These findings are indicative of an acute interstitial nephritis, with eosinophils suggesting a possible hypersensitivity component.
Figure 19D.
What do you see by electron microscopy?
Electron microscopy shows no deposits, but there is complete effacement of foot processes (transmission electron microscopy, original magnification ⫻8,000).
How do you correlate the electron microscopy findings with the clinical setting? The patient did not have significant proteinuria by dipstick. However, the complete foot process effacement by electron microscopy strongly suggests a minimal change disease–type lesion, which, when associated with acute interstitial nephritis, strongly points to NSAIDs as the underlying etiology. Proteinuria may not manifest when glomerular filtration rate is very low, as in this patient. Indeed, as the patient received supportive treatment and recovered his glomerular filtration rate over the ensuing 10 days, he had marked increase in urine proteinuria to 6 g/24 h. On subsequent follow-up, he had normal renal function and no proteinuria.
Final diagnosis: Acute interstitial nephritis and minimal change disease lesion, caused by NSAID injury Case provided by Agnes B. Fogo, MD, Department of Pathology, Vanderbilt University Medical Center, Nashville, TN.
If you have an interesting case you would like to submit for consideration, please contact the AJKD Editorial Office.