ClinicoPathologic Conference A Case of Polyneuropathy and Proteinuria


Introductory Remarks Gerald B. Appel, MD: Welcome to the ASN 2006 CPC. The CPC is always a major challenge. The CPC is not to see if the clinician gets the answer right. It’s his thought process that counts—to see if his thought process matches your thought process. We have the right people here today. We have two colleagues who will be doing this CPC today. First, Dr. Steve Korbet from Rush University Medical Center in Chicago, our clinician, who we will put to the test to see his clinical smarts and thought process. Working hand in hand with him, we have Dr. Steve Bonsib from Indiana University. So let’s get started with the Midwestern group of presenters we have here. Steve Korbet: It’s a pleasure to be a part of this CPC. Dr. Bonsib and I have a little history. I have been involved in doing CPC-like vignettes with him at previous ASNs and at his institution as a visiting professor in Indianapolis. My diagnostic success rate has not been too good, one for seven I believe, and I’m sure today will be no different. Dr. Bonsib will no doubt prove again that the gift of the renal biopsy given to us some 50 yr ago by Iversen and Brun in Denmark and Kark and Muehrcke here in the United States is still as precious and valuable in managing patients and guiding therapy as it was 50 yr ago (1–3). I think that one thing we can count on, whether I get the case right or not, is that the clinical value of the renal biopsy remains immeasurable. I was asked to do the CPC by Dr. Paul Kimmel some months ago. On August 15, 2006, I received an e-mail with the case which read, “Please call or write if you have any questions. Good luck,” and I thought, since this is coming from Washington, DC, it was possible Dr. Kimmel might not be able to express in writing everything he wanted, and maybe something was encrypted. So I had our chief research technician take the e-mail back to the lab to evaluate it further, and sure enough, an additional message was found: “Good luck. Because we’re not going to answer any questions you have.” So, to get on to the case: The patient is a 66-yr-old Hispanic female, born and raised in the United States. The chief complaint is she’s dizzy, became lightheaded, and nearly fainted when getting out of her car. She has since restricted her activity as a result of this. She has had no recent routine medical care, although she has been treated in the past for urinary tract infections. She states that her health has overall been good. She specifically denied systemic symptoms, such as fever and chills, nausea, and vomiting but mentioned occasional bouts of diarrhea over the past few months. She has noted numbness and tingling in her upper and lower extremities and decreased sensation in her lower extremities as well. She has denied lower urinary tract symptoms, such as frequency, urgency, or pain on urination, and did not notice blood in her urine. She has not traveled outside of the United States and has no ill pets or recent insect bites. She is on no medications whatsoever, we’re told. Her family history is important in that there is no known family history of renal disease. The patient’s father had congestive heart failure and was disabled. He was wheelchair-bound, because of an undiagnosed type of neuropathy. He died suddenly at age 58. There was no autopsy performed. Review of symptoms was negative, except for what was noted. “On physical exam, her BP was 160/95. We’re not told if she’s orthostatic or not. Her heart rate is 72, her weight is 155 lb. HEENT exam is unremarkable, lungs were clear to percussion and auscultation. Heart exam was regular with no murmurs, rubs, but she did have an S3. Abdominal exam was nontender, and there was no organomegaly. On musculoskeletal exam, she had mild right costophrenic angle tenderness, no joint swelling. On extremity exam, she had trace bilateral lower extremity edema, no rashes, clubbing, or cyanosis. The neurologic exam was remarkable for bilateral decreased distal sensation to touch and vibration.” We were given a host of laboratory data. Her sodium was 140, potassium 5.1, chloride was 107, and bicarb was low at 21. The anion gap was 12. We’re not given a blood gas pH, or a Pco2, but I’m going to just assume that maybe she has a metabolic acidosis, nonanion gap in nature. The BUN was 48 and creatinine was 3.6 mg/dl. If you estimate her GFR using the MDRD formula, assuming this represents chronic kidney disease (CKD), and I don’t know that for a fact, you get an estimated GFR of about 14 ml/min, which would put her in category 5 CKD. Her fasting glucose was 115 mg/dl, and we were only given one result for this. We were not given any hemoglobin A1C values. The calcium (9.4 mg/dl), albumin (4.4 g/dl), AST, and ALT were normal, but her alkaline phosphatase was elevated. The CBC demonstrated an anemia with a hemoglobin of 10.6 mg/dl, hematocrit of 31.4%, and the white count was 6.3 10/mm with a normal differential and the platelet count was Published online ahead of print. Publication date available at

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@inproceedings{Korbet2008ClinicoPathologicCA, title={ClinicoPathologic Conference A Case of Polyneuropathy and Proteinuria}, author={Stephen M. Korbet and Stephen M. Bonsib}, year={2008} }