AKI Tips and Tricks from Joel Topf MD, Kashlak’s Chief of Nephrology
Get a grip on acute kidney injury (AKI) with Dr. Joel Topf (AKA @kidney_boy), Kashlak’s Chief of Nephrology! We’ve put together an AKI highlight reel – focusing on practical tips and tricks to help you identify, diagnose and manage AKI, plus how to recognize AIN and random myths and musings on vancomycin, NSAIDS, contrast nephropathy, and the risk of NSF from gadolinium.
Written (including CME questions) and Produced by: Cyrus Askin, MD
Infographic by: Cyrus Askin, MD
Cover Art: Kate Grant MBChb, MRCGP
Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP
Editor: Matthew Watto MD, FACP (written materials); Clair Morgan of nodderly.com
Guest: Joel Topf, MD
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The KDIGO definition of AKI is helpful for research… not so helpful from a clinical/practical standpoint
sCr is a somewhat flawed / lagging indicator of renal function, keep an eye out for electrolyte disturbances and oliguria / anuria
The majority of AKI can be fixed by “a bag of LR & a Foley Catheter”… tincture of time may be all that’s necessary in many other cases
History is king: ask about NSAIDs, cocaine for rhabdo, antibiotics for sepsis/AIN, PPI for AIN, diarrhea, vomiting, ACEi, hypotension, new diuretics.
Urine electrolytes and urine eosinophils are often unhelpful, may lead to more confusion than anything else
A good chart biopsy can be very helpful in AKI: identify nephrotoxins and avoid them
Acute interstitial nephritis (AIN) is a diagnosis of exclusion with biopsy generally reserved for cases where steroids are being considered
Don’t fear contrast in AKI! There is no signal in the literature suggesting that contrast causes AKI
Save the renal ultrasound for part two of your AKI work up – consider an in-and-out catheterization and bladder scan if obstruction is on the differential
Acute Kidney Injury (AKI) In-Depth Show Notes
According to Dr. Topf, the definition of AKI is a sudden drop in GFR. As of 2012, KDIGO (Kidney Disease: Improving Global Outcomes) has published their definition of AKI with specific serum creatinine (sCr) cut offs. Dr. Topf feels these are useful for studies but not terribly helpful clinically:
1.5–1.9 x baseline OR
≥0.3mg/dl increase OR
Urine output (UOP) <0.5 ml/kg/hr x 6-12 hrs
2.0-2.9 x baseline OR
UOP <0.5 ml/kg/hr for ≥ 12 hrs
3x baseline OR
increase in serum creatinine to ≥ 4.0mg/dl OR
initiation of (renal replacement therapy) RRT OR
in patients < 18 years old, eGFR < 35ml/min /1.73 m2 OR
UOP <0.3 ml/kg/hr for ≥ 12 hrs OR
anuria for ≥ 12 hrs
Dr. Topf underlines the importance of UOP – often overlooked in favor of sCr. He uses the example of a patient being aggressively resuscitated who does not have an appreciable elevation in sCr but does have anuria or oliguria. Resuscitation can “dilute” the sCr.
This is not seen in volume-overloaded heart failure patients suffering from cardiorenal syndrome – this condition is almost always associated with a rise in sCr.
Buckets of AKI
Dr. Topf encourages folks to think of AKI in terms of pre-renal, intra-renal and post-renal etiologies:
Pre-Renal: Inadequate renal perfusion due to volume deficiency (vomiting, diarrhea, decreased PO intake, bleeding, non-hemorrhagic shock) or heart-failure (volume overload with venous congestion resulting in poor renal perfusion)
Intra-Renal: Acute Tubular Necrosis – the most common, acute interstitial nephritis / drug toxicities (vancomycin, aminoglycosides, etc.), glomerulonephritis, vasculitis (Makras & Spanou, 2016)
See the Clinical Problem Solver’s schema and discussion of intrinsic renal failure here
Post-Renal: Malignancy (ex: cervical cancer in women, prostate cancer in men), BPH, a kidney stone in a solitary kidney or retroperitoneal fibrosis
Key Insight for managing AKI
Somewhere between 70 & 90% of AKI is pre-renal or post-renal in etiology, meaning that fluid resuscitation and removal of the obstruction (i.e. a Foley) will resolve 70-90% of AKI! (Dr. Topf & Kaufman et al, 1991)
For intrinsic AKI, which is generally ATN, Dr. Topf says the treatment is also straight forward:
Dr. Topf’s initial approach to a pathologic elevation in sCr – it doesn’t end with a high creatinine!
Is the patient non-oliguric, oliguric or anuric?
Was this patient hypotensive?
Does this patient have severe heart failure and possible cardiorenal syndrome?
Was this patient on NSAIDs? Vancomycin? Other potential culprits?
Does the patient have significant electrolyte derangements?
Do they have a significant acid-base derangement?
To FeNa or not to FeNa: Depends on what you are looking for, may lead to discordant information
Ex: AKI associated with rhabdomyolysis is a cause of intrarenal AKI presenting with a low FeNa while most other intrinsic renal diseases should present with an elevated FeNa. (Corwin et al., 1984)
If you suspect the patient’s AKI is unlikely due to intrinsic renal disease – it is much faster to give fluid / assess for obstruction than to get urine electrolytes and other studies that take time and could lead to confounding results
Dr Topf: Can be seen in dry patients (urinalysis with high specific gravity, acidic urine) but generally, you’ll have assessed the patient and determined they are dry before looking at their urine for casts
Step 1: talk to the patient – See if their history is consistent with rhabdomyolysis
The cornerstone of treating rhabdomyolysis is fluid resuscitation to increase renal perfusion – Dr. Topf recommends ~200cc/hr of LR
Urine dipstick will be POSITIVE for blood, microscopy shows NO BLOOD – this is due to release of heme containing myoglobin from muscle tissue and the dipstick detecting free heme
How do you know if you are done treating?
There isn’t much guidance on this.
Dr. Topf recommends looking for a downtrending sCr and CPK – if the patient is responsible, otherwise healthy, and able to continue oral hydration, this type of patient should be safe for discharge and outpatient follow up
“If they don’t develop AKI early, they won’t develop it late.” – Dr. Topf’s expert opinion
A patient with evidence of rhabdomyolysis without AKI, who is otherwise healthy/stable and able to reliably hydrate at home, can likely be safely discharged without need for observation or admission
Heat? Exercise? Poor PO-intake? Consider volume depletion and pre-renal azotemia.
Dr. Topf recommends that, in an otherwise healthy patient who we suspect has pre-renal azotemia, it’s reasonable to give them 3-4 liters of fluid and recheck a sCr
The sCr should show a true improvement, assuming the patient has appropriate urine output (i.e. the volume should not dilute their sCr but instead truly improve renal perfusion)
Volume status exam: One of the most challenging things in medicine, but important! (van der Mullen et al.)
Dr. Topf recommends we favor “over-resuscitation” as young patients are at low-risk of suffering from clinically significant volume-overload, but the likelihood that they respond well to volume is high
Particularly important to remember in cases of rhabdomyolysis, as discussed above
NSAIDs? Consider NSAID-associated AKI.
Talk to the patient!
NSAIDs block prostaglandins. During volume depletion, prostaglandins help ensure adequate renal blood flow. NSAIDs, thus, can reduce the ability of the kidneys to maintain adequate perfusion during times of volume depletion, resulting in AKI. (Faubel & Topf, 1999; Imig, 2002; Zhang, 2017)
Treatment: volume resuscitation, hold NSAIDs, hold other nephrotoxins
Younger patients? Obstruction is generally low on the differential.
Dr. Topf tells us that these patients do, occasionally need RRT, however, they generally have an excellent prognosis if they don’t have prior kidney disease and/or have few-or-no medical comorbidities
AKI In the Critically Ill:
In Dr. Topf’s experience, 9/10 of these patients are suffering from acute tubular necrosis (ATN)
These patients are almost always adequately resuscitated (unlikely to be pre-renal azotemia)
Obstruction is unlikely – almost all these patients have foley catheters
Bloody intubation? Think about ANCA vasculitis and pulmonary-renal syndrome
Did patient recent vancomycin? And pip-tazo?
Could this be AIN?
Vancomycin and Pip-tazo
Don’t make the patient sicker – some evidence suggests the common combination of piperacillin-tazobactam and vancomycin may lead to an increased incidence of AKI in critically ill patients, however, it is admittedly difficult to determine whether this is association or true causation (luther et al., 2018) (Hammond et al., 2017) (Avedissian et al., 2020) –see below for more
Dr. Topf explains that there is not a significant signal in the literature for piperacillin-tazobactam, itself, leading to AKI
Vancomycin, historically, was plagued by nephrotoxic impurities – this is no longer an issue, perhaps explaining why some studies show a 0% incidence of AKI in patients given vancomycin monotherapy (Filippone et al.)
Vigilant monitoring of vancomycin levels can also help reduce AKI, however, this is confounded as well (Filippone et al.)
Dr. Topf mentioned there are some cases where patients on vancomycin have had renal biopsies, showing evidence of vancomycin casts, acute interstitial nephritis and damage to proximal tubular cells
Doesn’t cause AKI, but historically, not given to patients with CKD due to risk of nephrogenic systemic fibrosis (NSF)
A 2019 JAMA review and meta-analysis of 4,931 patients found zero cases of NSF in patients with CKD 4 or 5, suggesting that the harms of withholding gadolinium-based contrast agents are likely greater than this minimal risk of NSF (Woolen et al.)
Who needs Renal Replacement Therapy?
Does it make sense to start RRT earlier in a patient’s course? Well, the AKIKI trial would suggest that there is no benefit to this strategy, and you may save resources by going with a delayed approach to RRT. (Gaudry et al.)
Based on this data, Dr. Topf does not recommend early dialysis – instead, he will look for dangerous electrolyte abnormalities or volume overload to prompt initiation of RRT
A 2010 JAMA study suggests that the cost of renal ultrasound, and prevalence of obstruction make routine use inadvisable (Licurse et al)
Dr. Topf: “A low yield test,” use the renal ultrasound as part of your “second line” work up and instead, take a good history, consider a bladder scan and/or an in-and-out catheterization as a more cost-conscious means to evaluate for obstruction
Dr. Topf’s Take-Home Points:
We all learn about “neat” little AKI buckets – in reality, often times patients suffer from a combination of causes leading to their AKI
Urine electrolytes are overused in AKI – they are unreliable in many cases
Does the patient have volume-responsive AKI? Give the patient volume, look for a response!
Respect AKI, but remember, most patients will get better with some LR and a Foley Catheter… those that don’t likely have ATN which will get better with time!
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Listeners will develop a rational approach to the diagnosis and management of the patient with acute kidney injury (AKI).
After listening to this episode listeners will…
… be facile with the definition of AKI
… have a framework for approaching AKI including an understanding of what features in a patient’s history may shed light on the diagnosis
… appreciate prerenal azotemia and the relationship with ATN
… develop an approach to rhabdomyolysis and AKI
… be able to discuss the various types of AKI likely to be seen in the critically ill patient
… recognize the paradigm shift related to the safety when using iodinated contrast and gadolinium with regards to renal function
… know common medications implicated in AKI
… appreciate common AKI-related issues in the outpatient setting and have a head-start on how best to deal with them
Dr. Topf has received honoraria from AstraZeneca and Cara Therapeutics. He is joint venture partner in Davita Dialysis centers receiving dividends. The Curbsiders report no relevant financial disclosures.
Topf J, Askin CA, Williams PN, Watto MF. “#226 Kidney Boy on Acute Kidney Injury: Myths & Musings”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list. Original Air Date: July 20th, 2020.
Excellent episode as always ladies and gents !👍👍👍👍 Practice changing point regarding CT contrast use in CKD or AKI And MRI gandollinium I work in many smaller rural hospital settings Rads departments in these systems still have hard stops on contrast studies in patients whose serum cr is 1.5 or above or GFR below 50
Great episode! Thank you both Curbsiders and Kidney Boy for all the provided knowledge. I have three questions I would like to ask to Dr. Joel: 1. I noticed that the role of sUrea / BUN is not mentioned, not even in the pre-renal azotemia part. Did you omit it on purpose? As far as I know, sU is not needed to evaluate renal function (sCr better). It is often used to evaluate renal hypoperfusion though, but its role is not entirely clear to me. Last time I try to investigate it, I found that it didnt't have a very good accuracy, but I admit that I didn't do an extensive research. In my mind, it makes more sense to evaluate the volume status (like you mentioned) then to rely on an unique lab. Do you have any thoughts on that? 2. In the rhabdo part you talk about CK and AKI, but I had the impression that Myoglobin (apart from dehydration) was the molecule responsible for AKI. Is that correct? 3. About TMP/SMX, I also listened the CC podcast and I really liked it. I just started wondering what is the role of the other drugs secreted by OAT in "sCr false elevations" (some of them regularly used in practice). Do you have any thoughts? Bernardo, Internal Medicine Resident (Lisbon, Portugal)
would appreciate references for some of your assertions otherwise great presentation