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Ridgeview and the Ridgeview Continuing Medical Education Program are proud to present the Ridgeview Podcast: CME Series. Quality, portable and on-demand continuing medical education, featuring a variety of our exceptional physicians, providers and other staff from Ridgeview and it's affiliates. Hosting the program are Fred Demeuse, PA-C and Jason Hicks, PA-C. Thanks for tuning-in, downloading and listening! 

 

DISCLOSURE ANNOUNCEMENT 

The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview & Ridgeview Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws. 

It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented.

Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event.

Oct 18, 2019

In this podcast, Dr. Carl Dean, a Nephrologist with Kidney Specialists of Minnesota, presented at Ridgeview Medical Center's Live Friday CME Series on September 27th, 2019. At this event, Dr. Dean provided information on acute kidney injury (AKI)- its frequency, management, and treatment modalities available for AKI.

Enjoy the podcast!

Objectives:  
  Upon completion of this podcast, participants should be able to:

  • Evaluate for the cause of acute kidney injury.
  • Describe when a referral to a nephrologist is warranted.
  • Identify treatment options available for acute kidney injury.

CME credit is only offered to Ridgeview Providers for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org.

To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation.

 CME Evaluation

(**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.) 

The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition.”

 

FACULTY DISCLOSURE ANNOUNCEMENT 

It is our intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented.

Planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event.

SHOW NOTES:

Nephrons are the functional unit of the kidneys. The nephrons have specialized capillary beds that have low partial pressures of oxygen which make kidneys susceptible to AKI.

The afferent/efferent capillary bed have a unique ability to constrict and dilate to maintain GFR during times of physiologic stress, this is called autoregulation.

The thickness of the renal cortex (or essentially where all the glomeruli are located) is important for detecting or estimating the chronicity of kidney disease. A thick cortex tells us that you have decreased renal function.

The proximal tubule is the workhorse of the nephron where the electrolytes, proteins and glucose are reabsorbed.

Podocytes are specialized epithelial cells that surround the capillary within the glomeruli assisting with the filtration system of the kidney. A strong electronegative charge. A classic disruption of this system leads to nephritic syndrome.

The kidney gets about 20% of blood flow from the heart.

Prostaglandins and Angiotensin 2 maintain GFR by driving constriction and dilation of the afferent and efferent capillary beds.

NSAIDS (diminish the ability to generate prostaglandins through arachidonic acid pathway), ARBs and ACE inhibitors inhibit -- Angiotensin 2 which generates constriction on the afferent and efferent cap beds (preferential on efferent).

Patients susceptible to AKI generally have preexisting chronic kidney disease.

We detect AKI through creatinine and urine output.

Factors that affect creatinine function include: age, gender, lean muscle mass, drugs (bacterium, cimetidine, tyrosine kinase inhibitors), ethnicity, diet.

NGAL, KIM-1 and IL-18 are true markers of structural injury to the kidney. They can be found in the serum as well as urine. NGAL and KIM-1 tend to go up rather fast with AKI in comparison to say creatinine.  NGAL (neutrophil gelatinase-associated lipocalin) is one of the earliest and most robustly induced proteins in the kidney after ischemic or nephrotoxic AKI in animal models and KIM-1 (kidney injury molecule-1) is a type 1 transmembrane protein, with immunoglobulin and mucin domain, whose expression is markedly up-regulated in the proximal tubule in the post-ischemic rat kidney.

Pre-renal causes of CHF, hypovolemia, V/D, MI, PE, antihypertensives, anaphylaxis, cirrhosis, sepsis, hemorrhage, etc. Essentially: "The kidneys are not getting enough blood flow".

Post-renal causes include: obstruction can occur anywhere from renal tubule to the urethra. Generally, bilateral etiology to cause AKI.

1st step in evaluation for AKI is comparing present creatinine with previous and how rapidly the creatinine is rising.

Next, how is the patient feeling? Med review, screen of oral intake, loss, infection, etc. Recent procedures.

Labs to consider: UA, CBC, US, protein/CR ratio, CBC for TTP and micro-angiopathy.  Additional testing include: Renal U/S, PTH, and anemia may give clues to the duration of decreased renal function/

Active Urine Sediment - concerning for acute glomerulonephritis, hematuria and proteinuria, hematuria, only <10% of hematuria is glomerular, >80% is bladder, prostate or urethra disease. Quantify the proteinuria, screening for glomerular disease and its severity. <1 g: significant glomerular disease unlikely, 1-3g: glomerular disease is likely. >3g: glomerular disease is present.

Hyaline casts (Tamm Horsfall) made in Loop of Henle tell us that there is low flow through the tubules. (Generally a pre-renal issue). Granular cast or muddy brown cast which is pathognomonic for ATN which is generally the diagnosis. RBC cast is generally concerning for acute glomerulonephritis may want to consider a nephron consult.

Renal U/S is generally recommended for every new AKI. This evaluate for size, hydronephrosis, 2 kidneys, cortical thickness.

Management of AKI is managing electrolytes and acidosis. Volume expansion. Trial of vasopressors, dialysis. No benefit to diuretics. Adjusting appropriate drug dosages for patient with AKI.

Furosemide stress test can be implemented as diagnostic test to determine the severity of the AKI in volume resus oliguria patient.

AKI in the hospital are likely something we did iatrogenic meds, CT contrast, hemodynamics, obstruction, sepsis, volume depletion.

Acute Interstitial Nephritis:  Triad of rash, AKI and peripheral eosinophilia very rare (<10%). Need a high clinical suspicion. Although any drug can potentially cause DI-AIN, antibiotics, NSAIDS, and PPOIs are the most frequent offenders. Timing can be weeks to months until AKI develops. Renal biopsy confirms the diagnosis. Removal of offending drug sometimes use steroids.

Sepsis in AKI not well understood but thought 2nd to...

Macrovascular and microvascular dysfunction: Damage from inflammatory cytokines and leukocyte infiltration. Micro thrombi and capillary plugging. Development of ROS and high rates of apoptosis. Impaired oxygen delivery.

Contrast Nephropathy: A lot of discrepancy if this really exist. Generally, reversible cause. Risk of dialysis about 1%. Occurs about 2-4 days after exposure. Concerning patient groups would DM, cirrhotics, age, vascular disease, CKD. Mechanism poorly understood. Probably afferent vasoconstriction or free radical oxidation.  Hold ace inhibitors prior to contrast. No evidence, but empirically tends to make sense. Bicarb and NAC for contrast - induced AKI is over, done, capute -- no benefit.