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I didn't send the rest of the UA to you from yesterday on my case study patient.
It was:
RBCs          0-2          (0-2)
WBCs          6-10        (0-5)
squamous epi 20-100    (0-20)
bacteria          neg.        (0)
cast          6-10       (0-2)
coarse granular cast present  (0)
amorphous crystal    present
mucus          many

The patient died today.  First he started having respiratory distress and was intubated.  Then he went to ICU and coded.  His gases showed metabolic acidosis yet initially the CO2 was low, but then got high and looked more like an acidosis, ARDS type picture.  They talked about rhabdomyolysis, but his potassium stayed normal and CK went from 611 to 785 to 1750, which I am told isn't all that high for rhabdo.  Blood cultures, which came too late for him, grew staph aureus with 0.5 susceptible to oxacillin and 1.0 to vancomycin.  A repeat UA had no bacteria in urine. He was given steroids by the ER doctor who saw him 3 days before this admit, a dose IV and a Medrol dosepak.

So, my questions to you are, did he have glomerulonephritis in the first place?  Can glomerulonephritis cause sepsis?  Did he also have a urinary tract infection?  I thought not.  Urine cultures were negative.  Do you think he had rhabdo?  He also had some suspicious nodules in both lungs that they are speculating were septic emboli.  I read that most people recover from glomerulonephritis with supportive care, but could renal failure have killed him that quickly or was that from the sepsis?  If so, should he have been given steroids by the previous ER doc?  At that ER visit WBC was 12.5, bands 87.  He was also a pack a day smoker.  Could that have caused the WBC and band elevation?  I really want to understand what happened here and any help you can give would be appreciated.  He's suddenly become an extremely complicated  case study and I've been researching the internet forever.  Please let me know if you didn't get my question from yesterday.  The original question was whether or not there was underlying infection or was it purely glomerulonephritis.  I can resend the first page of the UA.

Thank you,

Hi Nancy,

Thanks for asking my help on Allexperts.

Clinically, most patients with acute glomerulonephritis (AGN) would have a sudden history of drop in urine output, edema and hypertension. Physical examination would confirm peripheral edema and hypertension. UA would show moderate to severe proteinuria and microscopic hematuria. Serum creatinine would be elevated according to the severity of the disease. What was your patient's creatinine?

Based on lab results that you have provided, it seems less likely that your patient was suffering from AGN. As you know, AGN is an inflammatory response. It does not cause sepsis, but sepsis can cause AGN. You are right about the assumption that renal failure could not have killed him so quickly.

A history of drug abuse, leucocystosis, bandemia and blood that grew staphylococci points to a diagnosis of sepsis. Sepsis can kill people pretty fast.


Dr. Shah


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Dr. Shamik Shah, MD, DNB (Nephrology), ISN Fellow


I can answer all questions related to kidney diseases, hypertension, plasmapheresis and kidney transplantation. I am an Indian-Board certified Nephrologist. I was a post-Doctoral Scholar at the Division of Nephrology & Hypertension,Department of Medicine, University of California, San Diego. My area of interest is Critical care Nephrology and Acute Kidney Injury.

Please mention the units in which your lab results were reported and the normal reference range for your laboratory.

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Ten years as a Critical Care & Transplant Nephrologist

International Society of Nephrology
Indian Society of Nephrology
Indian Medical Association
European Renal Association

- Shah SH, Cerda J. Acute Tubular Necrosis; Lerma, Edgar V., Rosner, Mitchell eds. Clinical Decisions in Nephrology, Hypertension and Kidney Transplantation. Springer ISBN 978-1-4614-4453-4, pp. 191-198
- Shah SH, Cerda J. Management of Acute Kidney Injury; Lerma, Edgar V., Rosner, Mitchell eds. Clinical Decisions in Nephrology, Hypertension and Kidney Transplantation. Springer ISBN 978-1-4614-4453-4
- Cerda J, Tolwani A, Shah SH, Ronco C. Continuous Renal Replacement Therapies in Modeling and Control of Dialysis Systems edited by Azar AT, Springer-Verlag, Heidelberg, Germany (In Press)
- Shah SH, Cerda J, Kellum JA. Acute Kidney Injury in Special Circumstances. John Kellum, Jorge Cerda, eds. Renal and Metabolic Disorders, Oxford University Press (In press)
- Shah SH, Mehta RL. “Anticoagulation in CRRT: Is Citrate better?”; Vineet Nayyar Ed. Critical Care Update 2009, Jaypee Brothers (In press)
- Shah SH, Mehta RL. “Non-dialytic management of acute kidney disease”; Evidence based Nephrology, BMJ, (In press)
- Shah SH, Mehta RL. “Epidemiology of Community-acquired AKI”; Ronco C, Bellomo R, Kellum J Eds. Critical Care Nephrology, Saunders. ISBN 1-4160-4252-0
- Abdeen O, Shah SH, Mehta RL; “Dialysis therapies in the surgical intensive care unit”; William Wilson, Christopher Grande, David Hoyt Eds. Trauma: Resuscitation, Anesthesia, and Critical Care, Informa Healthcare, NY 2007. ISBN 0-8247-2920-X
- Shah SH, Mehta RL. Acute kidney injury in critical care: time for a paradigm shift? Curr Opin Nephrol Hypertens. 2006 Nov;15(6):561-5.
- Shah, SH, Soroko S, Lischer E, Mehta RL. Delivered vs. Prescribed dose of Dialysis in Hospitalized Patients: Results of an Audit. J Am Soc Nephrol 17(Abstracts Issue): 2006, 107A.
- Shah SH et al “Biochemical Nutritional Parameters in Non-vegetarian and Vegetarian CAPD patients” Perit Dial Int 2001; 21 Suppl 2: S1-182

MBBS, MD (Internal Medicine), Diplomate of National board (Nephrology), ISN Fellow

Awards and Honors
Educational Ambassador of the International Society of Nephrology 2010
Fellowship of the International Society of Nephrology 2005.
Young Investigator Award by the International Society of Peritoneal Dialysis 2001

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