In this episode Drs. Young, Mortaji and Ambruso again invite Dr. Juan Carlos Velez, acclaimed nephrologist and self-proclaimed "piss-prophet" Dr. Juan Carlo Velez to discuss specific cases and how urinalysis and urinary sediment help the diagnosis. Dr. Juan Carlo Velez is the Department Chair at Oschner Medical Center in New Orleans, LA. You can find Dr. Velez's other podcast at "Channel Your Enthusiasm - The Burton Rose Book Club". Check out Dr. Velez at his Twitter handle @VelezNephHepato
Edited by: Parisa Mortaji, MD and Sophia Ambruso, DO
Sophia Ambruso DO @Sophia_Kidney, Sarah Young MD @kidneycritic, Judy Blaine MD, Parisa Mortaji, MD
Last podcast we discussed urine sediment, this podcast we are going to do some clinical cases and discuss how the urinary sediment helps
Well with that lets jump into a case 1
A 55 yo male is admitted to the hospital with 5 days of nausea and vomiting. His baseline creatinine is 0.8mg/dL but on arrival to the ER his creatinine is 1.3mg/dL. His BP is 90/45 HR 110 He is making some urine and is able to provide a sample. Urine microscopy reveals 6 granular casts on LPF and 5 RTEC on high power field. The ER resident asks why you bothered to look at the urine…the patient clearly is dry and needs fluid. How do you respond?
Juan carlos
- Urine sediment is helpful with diagnosis- the sediment shows he has ATN not just prerenal azotemia
- Urine sediment can also predict clinical end points, the more casts and RTEC the higher your likelihood of having a deterioration in kidney function and/or need dialysis
Sophie
I think urine is very helpful in this scenario b/c we now can anticipate his creatinine to continue to rise and/or UOP to decline. This is no longer just prerenal azotemia from volume depletion. Prerenal azotemia would have been characterized by a bland urine sediment with maybe some hyaline casts
Hylaine casts are composed of uromodulin and occur with sluggish urine flow but they do not indicate tubular injury or necrosis
Parisa: As a hospitalist this “window” into what is going on in the kidney will alter how I resuscitate him overnight. I know that he is at his risk of going from being volume depleted to wet quickly as his kidney function declines/and or UOP declines and can anticipate it.
Okay well on to case #2
A 35 yo woman with RA is admitted to the hospital with epigastric pain. She takes NSAIDS regularly to manage her arthritis alternating between ibuprofen and celebrex because she was told celebrex is safer. Her baseline creatinine is 1.1mg/dL but on admission is 3mg/dL. BP 140/80 HR 90. You examine the urine and see occasional wbc, rbc, RTEC. The resident (a future nephrologist) says she sent off eos and the eosinophiluria was <1% so she does not think this is AIN, plus she adds there were RTEC on the UA so this is probably ATN
Juan carlos
- The diagnosis of AIN really requires a kidney biopsy
- Anywhere from 20-80% of AIN will have observed WBC so even in their absence it still could be the cause
- Not uncommon to see rbc in AIN (50%)
- Eosinophiluria a time honored test for AIN has been debunked- it does not separate AIn from other causes of kidney disease
- Only a fraction of AIN will have wbc casts (<20%)
- Even more problematic AIN may also have other casts (RTEC,hyaline,granular)
Sophie
AIN is really challenging because it can look like anything. Patients rarely have the triad of rash, fever and eosinophilia. We find AIN on 13-27% of kidney biopsies for AKI, but we are probably missing alot because a lot of AKI is never biopsied…so if you are suspicious you should biopsy.
Parisa- we see so much hospital acquired Aki and they are exposed to so many drugs which could be the cause of AIN. The fact that the only clue to AIN may be the rise in creatinine is quite humbling.
Okay on to our last case #3
A 50 yo construction worker is referred to you for hematuria, proteinuria and a creatinine of 1.2mg/dL/ His pcp has noticed hematuria for the past 6 months.he has fever,fatigue,malaise He also has proteinuria. His urine shows dysmorphic rbc’s, wbc and rbc casts. His ANCA comes back + (MPO) and a kidney biopsy confirms a pauci immune GN.
Sophie; so this is the classic finding of urine for a patient with nephritic syndrome including dysmorphic rbc, rbc casts and proteinuria. The urine does not tell you the cause of his nephritic syndrome but the biopsy with the ANCA + gives you a diagnosis of microscopic polyangiitis
So there is a 2nd part to this case. You treat your patient with steroids, rituxan and ace.He has had an excellent response with resolution of his proteinuria and his creatinine improves to 0.7mg/dl after 6 months. You see him 1 year after his presentation and on evaluation of his urine you find: dysmorphic rbc… how does this help
Juan carlos
- This case illustrates the importance not just of urine microscopy at the time of diagnosis but how it can be used for disease surveillance
- The presence of persistent hematuria in a patient with AAV is associated with a higher risk of renal relapse
- In addition worsening hematuria predicts the development of a renal relapse in the subsequent 6-12months
Well i think that wraps this episode of Kidney essentials Thank you to Juan carlos for joining us and providing his expertise, parisa and sophie you want to take us out with our learning objectives
Learning objectives:
- Urine microscopy in ATN vs prerenal AKI
- Prerenal; “bland”, hyaline casts
- ATN: RTEC,RTEC casts, coarse granular casts, “muddybrown casts”
- Urine microscopy in AIN
- The entire kitchen sink
- Wbc,wbc casts,Rtec,rtec cars, rbc occ rbc casts
- Urine microscopy in nephritic syndrome
- Dysmorphic rbc, wbc,rbc casts, wbc casts