Episode 201: AKI Roadmap.
Future Dr. Ayyagari describes the different types of acute kidney injury and shares some elements of management for each category. Dr. Arreaza shares some input about statistics and the importance of drinking water during summer.
Written by Tejasvi Ayyagari, MSIV, Ross University School of Medicine. Edits and comments by Hector Arreaza, MD.
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INTRODUCTION:
Dr. Arreaza: Hello everyone, and welcome back to Rio Bravo qWeek — your weekly dose of knowledge. I’m Dr. Arreaza, I am a faculty member and associate program director of the Rio Bravo FM residency program. In Episode 126, we briefly introduced the topic of Acute Kidney Injury (AKI), but today, we’re taking a deep dive into the matter. I have here alongside my cohost, future Dr. Ayyagari, AKA TJ. Please, TJ, introduce yourself.
TJ: Hey everyone, good to be back on the podcast. My name is TJ Ayyagari, and I am currently finishing my last rotation of medical school with Rio Bravo CSV outpatient. I hope everyone is doing well and staying safe.
Dr. Arreaza: So, TJ prepared this discussion about acute kidney injury, also known as AKI. This is a critical topic for our Kern community, especially during the summer months when the risk of AKI increases. You will face many patients with AKI on the wards, in the clinic, and especially on your future board exam. Hopefully, by the end of this episode, you all will have more information on AKI, but also the three different types: prerenal, intrinsic, and postrenal.
TJ: Without further ado, let’s get started, Dr. Arreaza.
SECTION 1 – What is AKI?
Dr Arreaza: Let’s start with the definition. Let’s explain what AKI is.
TJ: Absolutely. So, an AKI is not just a bump in the patient’s creatinine. According to the Kidney Disease Improving Global Outcomes (KDIGO) definition, an AKI embodies any of the following criteria:
- Increase in serum creatinine by ≥0.3 mg/dL within 48 hours, OR
- Increase in serum creatinine to ≥1.5 times baseline within the prior 7 days, OR
- Urine volume <0.5 mL/kg/h for 6 hours
Dr. Arreaza: The numbers show that AKI is increasing in our hospitals. According to the CDC, the incidence rate of newly diagnosed AKI has increased from 80 per 1,000 patient-years in 2007 to 242 per 1,000 patient-years in 2022. We must be vigilant and diagnose AKI appropriately because time is gold. We need to correct it and prevent further kidney damage, if possible. A critical step in the treatment is determining why the AKI is happening. Let’s start by discussing prerenal AKI.
SECTION 2 – Prerenal AKI
Dr. Arreaza: Let’s remember our Latin language, “pre” means before, and “renal” means kidney. So, when you say pre-renal, it sounds like you’re referring to an event that happens before the kidneys.
TJ: You’re right.A prerenal AKI is the most common type, and it refers to a problem that occurs before the kidney. The keyword here is perfusion — the kidneys are fine structurally, but they’re not getting enough blood flow.
Common causes:
- Hypovolemia: vomiting, diarrhea, bleeding, and overdiuresis (surreptitious diuretic use).
- Low cardiac output: heart failure, MI (if the heart cannot pump blood effectively across the body, the kidneys suffer)
- Systemic vasodilation: sepsis, cirrhosis (with widespread vasodilation and increased capillary permeability, resulting in more fluids shifting across the vasculature to tissues, which means less is available for the kidneys).
Dr. Arreaza: So, less perfusion means less oxygen, less nutrients and more damage to the kidney.
TJ: However, the good news is that it’s often reversible if you fix the underlying cause quickly.
Dr. Arreaza: What would we expect to see on lab values?
TJ: As a result of low kidney perfusion, the kidneys do their best to conserve sodium and water, and urea reabsorption is increased in the proximal tubule. Subsequently, BUN rises disproportionately compared to creatinine (BUN: Cr ratio > 20:1). There is also a lab value called the Fractional excretion of sodium, otherwise known as FeNa, which will appear as <1% suggesting a prerenal AKI because the kidneys are holding onto sodium to preserve volume.
Dr. Arreaza: Let’s talk about correction of prerenal AKI. If there is no perfusion, let’s improve renal perfusion!
TJ: Of course! The treatment is to restore volume — fluids if hypovolemic, improve cardiac output if heart-related, and treat infection if septic. But remember, in CHF or cirrhosis, fluids can be tricky.
SECTION 3 – Intrinsic AKI
Dr. Arreaza: Excellent explanation, TJ. So, let’s talk about the second type of AKI: intrinsic. Intrinsic AKI means the problem is inside the kidney itself. If you’re comparing it to simple terms, the plumbing and water pressure are fine (perfusion is normal), the drains are fine (no obstructions), but the kidney’s filter is damaged.
TJ: Major categories:
- Acute tubular necrosis (ATN): Most common intrinsic cause. Usually from ischemia or toxins (like aminoglycosides, IV contrast, ethylene glycol).
- Acute interstitial nephritis (AIN): Often an allergic reaction to drugs. Here’s a quick little mnemonic with the 6Ps to help remember the most common causes.
Pee — diuretics like furosemide or thiazides.
Pain-free — NSAIDs.
Penicillin — and other beta-lactam antibiotics.
Proton pump inhibitors — like omeprazole.
rifamPin — and other rifamycin antibiotics.
Cimetidine — yes, the old-school H₂ blocker still shows up on exams.
- Glomerulonephritis: Autoimmune, post-infectious, or vasculitis. You’ll see proteinuria, hematuria, and RBC casts.
Dr. Arreaza: A common cause of AKI is diabetes. Diabetes causes prerenal AKI (dehydration caused by uncontrolled diabetes) and intrinsic from renal parenchymal damage and tubular necrosis. So clinically, what would we expect?
TJ: With Intrinsic AKI, as a result of tubular damage, there is impaired urea reabsorption. Subsequently, BUN and creatinine both rise more proportionally (BUN: Cr ratio closer to 10 –15:1).
- With ATN, muddy brown casts can be appreciated in UA
- With AIN, look for fever, rash, and especially eosinophilia, as well as a UA displaying eosinophils or WBC casts.
- With Glomerulonephritis, look for RBC casts and proteinuria on UA, and you may even see edema on physical exam with hypertension.
Dr. Arreaza: Treating intrinsic AKI will depend on etiology. Hydration would not fix the problem in most cases. Let’s mention some treatment options for intrinsic AKI.
TJ: Intrinsic AKI is a bit like fixing a flooded house — you don’t just start bailing water; you find the source of the leak, stop it, and protect what’s left. Whether it’s ATN, AIN, or GN, the playbook is: remove the injury, give the kidney a rest, and treat the underlying cause.
Dr. Arreaza: Sure. We start with supportive care, especially treating hyper or hypotension, maintaining normovolemia, correcting electrolyte imbalances, and using antibiotics in case of infection.
-We must identify and remove reversible causes, such as discontinuing nephrotoxic agents such as NSAIDs, aminoglycosides, and iodine contrast. -Also, other reversible factors must be corrected such as hypovolemia (IV fluids), hypotension (vasopressors) to prevent further kidney damage.
TJ: -Hemodialysis or renal replacement therapy (RRT) is reserved for severe cases of refractory hyperkalemia, metabolic acidosis, volume overload unresponsive to diuretics, and uremic symptoms (encephalopathy, pericarditis, pleuritis).
Dr. Arreaza: Immunosuppression is required for specific types of glomerulonephritis. For instance, rapidly progressive crescentic glomerulonephritis warrants high-dose glucocorticoids and cyclophosphamide. In ANCA-associated vasculitis, glucocorticoids plus cyclophosphamide or rituximab, and sometimes plasma exchange, are standard.
SECTION 4 – Postrenal AKI
Dr. Arreaza: We spent enough time in intrinsic AKI. Why don’t we move on to our last topic of AKI, postrenal.
TJ: So, withpostrenal AKI, imagine that urine leaving the kidney encounters a roadblock. Urine can’t get out, so pressure builds up, damaging the kidney.
Common causes:
- For men, benign prostatic hyperplasia (BPH) is a significant factor (as the prostate grows bigger, it can compress the urethra, leading to urine backflow, which can not only cause AKI, but can also lead to possible UTIs in the process).
- Kidney stones, tumors, strictures, and neurogenic bladder
When doing my urology and nephrology rotations at Kern Medical, I encountered many kidney stones and urethral strictures, and unfortunately, a fair number of patients suffering from RCC that caused not only the AKI but also extreme discomfort.
Dr. Arreaza: It seems like we need some imaging to diagnose postrenal AKI.
TJ: Yes.If you’re concerned about obstruction, a renal U/S can quickly help diagnose an underlying obstruction, or a CT scan for more details.
Lab patterns?
- In the early phase (before tubular injury):
- BUN: Cr ratio >20:1 — looks like prerenal.
- FeNa <1%.
- Urine osmolality >500 mOsm/kg.
- In the later phase (after prolonged obstruction → tubular injury):
- BUN: Cr ratio ~10–15:1 — now looks intrinsic.
- FeNa >2%.
- Urine osmolality ~300 mOsm/kg.
Dr. Arreaza: BUN:Cr ratio and FeNa are not reliable to diagnose postrenal AKI, so we must rely more in imaging and clinical presentation. Let´s talk about the management of postrenal AKI.
TJ: Absolutely! The main way to treat a post-renal AKI is to relieve the obstruction causing it in the first place, whether it be through surgery, TURP, lithotripsy, etc.
Dr. Arreaza: I think the favorite treatment done by urology to relieve obstruction is a ureteral stent, which, remember, needs to be removed later. Typically, 1-2 weeks is sufficient to treat kidney stones. The risk of encrustation and infection increases significantly after 4–6 weeks, and stents should ideally be exchanged within 3 months to minimize complications.
SECTION 5 – Closing
Dr. Arreaza: I know you’ve spent a decent amount of time explaining the details of the AKI types with us, TJ, but could you give us a summary?
TJ: Viewers, if there’s anything to take away from this, remember:
- Prerenal: Poor perfusion, fix the flow.
- Intrinsic: Structural damage inside the kidney — think ATN, AIN, GN.
- Postrenal: Obstruction — relieve the blockage.
When you see AKI, think: Before the kidney, in the kidney, or after the kidney? That simple framework can help you move fast and help your patient recover kidney function.
Dr. Arreaza, any advice you want to give to the viewers?
Dr. Arreaza: Yes,weare in the middle of summer, and we treat a large amount of farm workers, construction workers and people who spend time outdoors, in general, remind your patients to drink water. Water is life, especially for the kidneys, there is no substitute. That’s it for today’s episode of Rio Bravo qWeek. If you enjoyed this review, share it with a colleague or medical student who could use a quick AKI refresher. And remember — the kidneys may be small, but they’re mighty… and they hold grudges when you ignore them. I’m Dr. Arreaza, signing off.
TJ: Thank you for tuning in, everyone. Have a nice day!
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week!
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References:
- Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements. 2012;2:1–13. https://kdigo.org/guidelines/acute-kidney-injury/.
- Kaur A, Sharma GS, Kumbala DR. Acute kidney injury in diabetic patients: A narrative review. Medicine (Baltimore). 2023 May 26;102(21):e33888. doi: 10.1097/MD.0000000000033888. PMID: 37233407; PMCID: PMC10219694. https://pmc.ncbi.nlm.nih.gov/articles/PMC10219694/
- Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
