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.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

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

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