Acute Kidney Injury

Real Cases, Real Thinking, Real Medicine

Amie and Ben discuss a case of 72-year-old male presenting with vomiting and  lethargy. 

What initially appears to be a straightforward  becomes a cautionary tale about cognitive bias. 

Can Amie figure out what is going on? 

As you listen, ask yourself: can you figure out the diagnosis? What would you have done in the situation?

Links & Resources

• RCPE Education: rcpe.ac.uk/education

Connect With Us

• Email: amie@homeofmedicine.com
• YouTube: Home of Medicine Channel

Disclaimer: All patient stories discussed in Home of Medicine are informed by real patient interactions. However, all identifying details have been removed or appropriately modified to protect patient confidentiality. 

This podcast is intended for education and professional development and should not replace independent clinical judgement or specialist consultation.

Transcript

 [Dr. Ben Lovell]: Hello everyone and welcome to an exciting new episode of the Home of Medicine Podcast. My name is Ben Lovell; I'm an acute physician working in London in the UK, and I'm joined by my ever-faithful and very intelligent co-.

 [Dr. Amie Burbridge]: I am laughing because I've never been described as very intelligent before! Thank you very much, Ben. I'm Dr. Amie Burbridge, and I'm an acute physician as well.

 [Dr. Ben Lovell]: It is time for me to present a case to you. Once more, we are on the medical take, our favorite place to be. This is a case that has been clarked, and you are going to see the patient on the post-take ward round.

The patient is a 72-year-old male who has been referred from the emergency department with an AKI (Acute Kidney Injury). It is a very simple story: a few days of lethargy, reduced oral intake, and a bit of vomiting, which is unusual for him, culminating in a hospital admission where he was found to have an AKI. He has been referred to medics for ongoing management. So far, so easy. What are your initial thoughts while walking to the bed space, and what questions do you ask next?

 [Dr. Amie Burbridge]: For a 72-year-old gentleman with an AKI, I immediately want to know the severity of the renal impairment. What are his exact urea, creatinine, and potassium levels? Given the lethargy and vomiting, I am wondering if he has had an acute gastroenteritis, or if he has been exposed to a specific high-risk medication.

When analysing renal impairment, my immediate framework is separating the causes into three distinct axes:

• Pre-renal: Driven by systemic hypovolemia, dehydration, or renal hypoperfusion.
• Renal (Intrinsic): Driven by direct structural damage to the kidney parenchyma, glomerulus, or tubules.
• Post-renal: Driven by acute mechanical obstruction within the urinary tract system.

Given his vomiting, a pre-renal cause is statistically the most probable. Is he taking maintenance diuretics while feeling unwell? Is his lethargy a direct metabolic consequence of the acute kidney injury, or was it pre-existing? I also need to check his blood pressure to see if he is hypotensive, and monitor his exact urine output.

 [Dr. Ben Lovell]: In acute medicine, the overwhelming majority of cases we see are pre-renal in nature. When a patient presents with a brief history of vomiting, diarrhea, or decreased oral intake alongside an elevated creatinine, it is easy to assume that a bit of intravenous fluid resuscitation will clear the problem quickly. However, we must always maintain our focus on intrinsic renal and post-renal obstructive causes as well.

Let's meet our patient. He confirms that he is usually fit and well, but has spent the last few days feeling generally under the weather with malaise. He has no diarrhea, but has vomited once or twice, lost his appetite completely, and developed a vague abdominal ache. He came to the emergency department expecting a quick discharge, but his baseline bloods revealed an unexpected serum creatinine of 220 µmol/L. We have no prior historical creatinine values to compare this against, but the working assumption is an acute kidney injury. Is there anything else you want to extract from his history?

 [Dr. Amie Burbridge]: Has he had a preceding viral or bacterial illness?

 [Dr. Ben Lovell]: He is unsure, but he denies any dysuria or urinary frequency that would point toward a urinary tract infection. He has no cough, cold, or sputum production indicating a respiratory tract infection. It is strictly an upset stomach, mild abdominal pain, poor oral intake, and isolated vomiting over a few days.

 [Dr. Amie Burbridge]: Any widespread myalgias or body aches?

 [Dr. Ben Lovell]: No, he denies any widespread body aches.

 [Dr. Amie Burbridge]: Is he visibly jaundiced?

 [Dr. Ben Lovell]: No, he is not clinically jaundiced at the bedside.

 [Dr. Amie Burbridge]: Has anyone else at home been unwell? If it were a typical infectious gastroenteritis, you frequently find that family members who share food or living spaces contract the same pathogen. I also typically ask if they have eaten any unusual food, dined at a new restaurant, or consumed undercooked poultry or questionable takeout. Has he experienced any acute dizziness or uremic pruritus? What is his past medical and drug history?

The "Triple Whammy" and Baseline Vitals

 [Dr. Ben Lovell]: His past medical history includes essential hypertension, for which he is prescribed Amlodipine and Losartan. He also has osteoarthritis, managing his joint aches with intermittent, over-the-counter Ibuprofen.

 [Dr. Amie Burbridge]: The combination of an Angiotensin Receptor Blocker (ARB) and a non-steroidal anti-inflammatory drug (NSAID) is highly significant. This is a major trigger for Acute Tubular Necrosis (ATN) and intrinsic renal injury.

The Intracranial Mechanics of Renal Perfusion:

• NSAIDs: Inhibit prostaglandins, leading to profound constriction of the afferent arterioles delivering blood into the glomerulus.
• ARBs / ACE Inhibitors: Prevent angiotensin II action, leading to profound dilation of the efferent arterioles exiting the glomerulus.

When a patient takes both concurrently—especially while dehydrated—the combined afferent constriction and efferent dilation drop the intraglomerular filtration pressure entirely, which can precipitate severe acute tubular necrosis. When screening for an AKI, auditing for these nephrotoxic medications is vital. The Ibuprofen must be stopped immediately, and the Losartan should be held while his kidneys recover. I would also be highly cautious with his Amlodipine; if his AKI is pre-renal and he is intravascularly depleted, his blood pressure may drop, making ongoing antihypertensive therapy inappropriate.

 [Dr. Ben Lovell]: Let's look at his social history. He is a retired non-smoker who lives with his wife. When asked about his alcohol history, he notes that he drinks approximately four pints of lager every single night.

 [Dr. Amie Burbridge]: That tracks as 28 pints a week, which safely exceeds 50 units of alcohol per week. That is a remarkably high intake. Do you counsel your patients regarding their alcohol volumes during an acute post-take ward round?

 [Dr. Ben Lovell]: If a patient is critically unwell or moribund, I obviously focus strictly on immediate resuscitation. But if they are stable and conversational, I deploy a light-touch warning, reminding them to monitor their intake.

 [Dr. Amie Burbridge]: I tend to dig into it much deeper, particularly in a Same Day Emergency Care setting where I have more dedicated clinic time. I establish whether they are drinking spirits, mixing beverages, drinking throughout the day, or binge drinking. My ward rounds can occasionally take two hours per patient because of those conversations! What did his physical examination reveal?

 [Dr. Ben Lovell]: On examination, he was slim and appeared clinically dry.

His objective vital signs were:

• Heart Rate: 98 bpm (regular rhythm)
• Blood Pressure: 141/89 mmHg
• Oxygen Saturations: 97% on room air
• Temperature: 36.7°C (afebrile)
• Respiratory Rate: 18 breaths/min

His chest was clear on auscultation, his abdomen was soft without organomegaly, and there was no peripheral edema or signs of deep vein thrombosis in his lower limbs.

Clinical Realities of Fluid Assessment

 [Dr. Amie Burbridge]: Did you perform a structured volume status assessment?

 [Dr. Ben Lovell]: Volume status assessment has incredibly high inter-observer variability. Unless a patient is completely dry or clearly fluid overloaded, physicians struggle to judge volume accurately; one clinician calls a patient underfilled, the next calls them euvolemic, and a third notes they look overfilled.

As a clinician, I examine the warmth of their extremities, feel their central pulse volume, check skin turgor, and look at the moisture of their oral mucous membranes. I evaluate the jugular venous pressure (JVP) to check for overfilling, but I don't find it useful for diagnosing a low-volume state. I avoid routine ortatic lying and standing blood pressure checks because younger patients regulate their blood pressure well until they are on the verge of decompressing. Finally, I check for pitting edema at the ankles and across the sacrum to catch systemic overload. Do you approach it differently?

 [Dr. Amie Burbridge]: You can utilize point-of-care ultrasound to evaluate the internal dimensions of the Inferior Vena Cava (IVC).

 [Dr. Ben Lovell]: I am trained to look at the IVC, but the evidence is challenging. A normal IVC tracks between one and two centimeters in diameter; if it drops below a centimeter or shows complete collapse when the patient sniffs, that points toward a low-volume state. However, intensive care colleagues emphasize that this doesn't correlate perfectly with fluid responsiveness because it fails to account for baseline cardiac function. If a patient has underlying heart failure, it throws the entire ultrasound interpretation into question. What are his primary laboratory values?

 [Dr. Ben Lovell]: His capillary glucose and lactate were entirely within normal parameters. An arterial blood gas wasn't performed in ED because he appeared stable.

His primary laboratory results showed:

• Serum Creatinine: 220 µmol/L (calculated eGFR of 37)
• Serum Potassium: 4.0 mmol/L (normal)
• Serum Sodium: 132 mmol/L (mild hyponatremia)
• C-Reactive Protein (CRP): 31 mg/L
• Coagulation (INR): 1.1 (normal)
• Liver Function Tests (LFTs): Completely normal
• Full Blood Count: Hemoglobin is low at 101 g/L, with a normal MCV of 92 fL (normocytic anemia). His white cell count was $8.8 \times 10^9/L$, and neutrophils were $5.1 \times 10^9/L$.

We do not routinely process serum urea in my clinical trust unless there is an active gastrointestinal bleed, so that value was absent. A baseline bone and calcium profile was also omitted during the initial emergency workup.

 [Dr. Amie Burbridge]: Finding a normocytic anemia alongside a serum creatinine of 220 µmol/L is important. It raises the question of whether this is an anemia of chronic kidney disease (CKD) rather than an acute kidney injury.

Long-standing renal decline leads to a structural drop in erythropoietin production, resulting in a normocytic anemia. Chronic dysfunction also causes shifts in calcium and phosphate metabolism, causing serum phosphate to rise.

What caused his potential background CKD? Essential hypertension is the most probable driver given his history, alongside diabetes mellitus. I had a junior consultant who always insisted that CKD is a clinical syndrome, not a primary diagnosis. He would remind us that writing "history of CKD" is incomplete; you must specify the primary driver, such as CKD secondary to hypertensive nephrosclerosis.

To exclude post-renal obstructive causes, we can use point-of-care ultrasound to look for hydronephrosis, perform a bedside bladder scan to check for volume retention, or complete a digital rectal examination to screen for benign prostatic hyperplasia.

 [Dr. Ben Lovell]: I also palpate and percuss the abdomen to check for a distended bladder. It is incredibly useful in cases of acute delirium when a patient cannot communicate their discomfort, and you find a bladder extending up to the umbilicus.

However, I reviewed the literature on this recently and was surprised to find that bladder palpation is remarkably unreliable. It demonstrates very low sensitivity and specificity for identifying urinary retention volumes between 600 mL and a full liter, especially in patients with obesity, ascites, or postpartum women. My key takeaway is that failing to feel a distended bladder does not rule out urinary retention.

The Post-Take Plan and the STOP-AKI Framework

 [Dr. Ben Lovell]: What is your definitive post-take management strategy for this patient?

 [Dr. Amie Burbridge]: He is hemodynamically stable, though his heart rate is on the higher side at 98 bpm, and his blood pressure remains hypertensive at 141/89 mmHg. We have no baseline blood tests to confirm if his creatinine was previously normal. If his baseline creatinine was 60 µmol/L, a jump to 220 µmol/L represents a Stage 3 AKI, which is a medical emergency that requires inpatient admission for close monitoring. If his baseline was 180 µmol/L, this represents a minor fluctuation.

To isolate whether this is pre-renal, renal, or post-renal, I would order a urine dipstick to look for hematuria and proteinuria, and check a urine protein-creatinine ratio (PCR) to evaluate renal excretion. I would screen for systemic autoimmune processes or vasculitides, such as anti-GBM disease or granulomatosis with polyangiitis, and consider a renal ultrasound to assess the vasculature. He has no markers of cardiac overload or pulmonary edema, his potassium is stable, and he has no severe metabolic acidosis, so he has no immediate indication for renal replacement therapy. I need to gather these results before deciding on intravenous fluids.

 [Dr. Ben Lovell]: Your approach is far more extensive than mine was at the time. I saw a clear history of poor oral intake and vomiting over several days alongside an elevated creatinine, which pointed directly to a pre-renal injury.

My strategy took about five minutes: admit him to the ward, prescribe one to two liters of intravenous fluids, hold his nephrotoxic medications (the Ibuprofen and Losartan), continue his Amlodipine, and repeat his renal panel the following morning. I don't order an automatic ultrasound or run an autoimmune screen on every pre-renal AKI.

National guidelines previously mandated an ultrasound within 12 hours for all Stage 3 AKIs, but that has shifted; we now only order formal imaging if there is a genuine clinical suspicion of mechanical obstruction. I was confident in my diagnosis and moved quickly to the next patient.

 [Dr. Amie Burbridge]: I need to complete a ward round with you, Ben, to see your efficiency in action! I would have easily spent 30 minutes working through those differentials.

 [Dr. Ben Lovell]: Speed doesn't always equal clinical effectiveness; I am fast, but I am prone to making mistakes.

You mentioned the STOP-AKI framework earlier. It was a highly publicized national safety campaign designed to help clinicians quickly identify and manage the four most common reversible causes of acute kidney injury:

The STOP-AKI Safety Framework:

• S – Sepsis: Actively screen for and treat underlying systemic infections.
• T – Toxins: Complete a comprehensive drug audit and immediately stop all nephrotoxic agents.
• O – Obstruction: Evaluate for post-renal blocks via bladder scans, catheterization, or renal ultrasounds.
• P – Parenchymal: Perform a urine dipstick to look for blood and protein, screening for intrinsic glomerulonephritis.

I omitted the urine dipstick on my initial round. We frequently emphasize the need to "ditch the dip" when screening for urinary tract infections in patients over 65 due to high rates of asymptomatic bacteriuria. However, you must never "ditch the dip" when investigating an AKI, as it is our primary screening tool for intrinsic parenchymal inflammation.

The Diagnostic Turn and Evolving the Case

 [Dr. Ben Lovell]: The next morning, I reviewed his repeat blood tests after he had received two liters of intravenous fluids. His serum creatinine had only dropped from 220 µmol/L to 210 µmol/L. What do you make of that minimal improvement?

 [Dr. Amie Burbridge]: That minimal response is concerning. If the injury were purely pre-renal, you expect a significant improvement or normalization of his creatinine within 24 hours. What was his exact urine output? When kidneys recover from severe hypoperfusion, they can enter a polyuric phase as the acute tubular necrosis begins to resolve.

 [Dr. Ben Lovell]: We weren't actively tracking his hourly urine output because he appeared clinically stable.

That lack of biochemistry response made me realize my initial pre-renal assumption was wrong. I went back to the bedside to re-evaluate him. The patient looked at me and said, "Doctor, please can I have my Ibuprofen back? My back pain is completely unmanageable without it. I know it isn't good for my kidneys, but I've taken it for a very long time and I can't cope without it."

That single statement changed everything. A presentation of unexplained renal impairment, normocytic anemia, and progressive back pain points directly toward an underlying systemic malignancy until proven otherwise.

I realized I needed to check his baseline calcium levels immediately. We added a formal bone profile to his labs, and it revealed a significantly elevated serum calcium of 2.82 mmol/L.

This fits the classic CRAB diagnostic mnemonic used to identify system-wide plasma cell dyscrasias and hidden malignancies:

The CRAB Diagnostic Mnemonic:

• C – Calcium: Hypercalcemia (serum calcium > 2.60 mmol/L).
• R – Renal Failure: Unexplained acute or chronic kidney injury.
• A – Anemia: Characteristically a normocytic, normochromic anemia.
• B – Bone Pain: Persistent back or skeletal pain driven by active osteolytic lesions.

We ordered an urgent serum protein electrophoresis and a urinary Bence-Jones protein assay. The electrophoresis detected a distinct clonal paraprotein band, and he was formally diagnosed with an underlying malignant hematological disorder.

His severe back pain was driven by widespread osteolytic spinal lesions, and his abdominal pain and nausea were secondary symptoms of hypercalcemia, which I had mistakenly attributed to viral gastroenteritis. Intravenous fluid hydration remains the primary treatment for hypercalcemia, as it promotes renal calcium excretion, so our fluid plan was still appropriate.

Overcoming Cognitive Biases in Medicine

 [Dr. Ben Lovell]: The goal of sharing this case isn't to suggest we must run an electrophoresis screen on every patient presenting with an AKI. The key takeaway is recognizing that an AKI is a clinical syndrome, not a final diagnosis; we must always complete the sentence by identifying the underlying cause.

I fell into the trap of search satisficing. This is a cognitive bias where once you find a plausible piece of evidence that satisfies your immediate curiosity—such as a history of vomiting explaining a pre-renal AKI—your mind stops searching for alternative possibilities. I anchored to that explanation too early at the front door.

However, when new clinical data emerged—specifically his lack of fluid response and his severe back pain—I didn't suffer from diagnostic closure. I accepted the new information and evolved my diagnosis. Changing your differential diagnosis over time in response to new data is the hallmark of a reflective clinician. These conditions often present insidiously, and it takes time and observation for the true underlying cause to unfold.

 [Dr. Amie Burbridge]: It is fascinating to look at how our minds process these cases. During our discussion, I mistakenly assumed his calcium was normal because my mind wanted to avoid the extra cognitive processing required to unmask a complex condition. We often subconsciously fill in clinical gaps, and we rely on our multi-disciplinary safety nets and electronic lab flags to pull us back and correct those assumptions.

These systemic malignancies are true masters of disguise, often presenting primarily through an isolated AKI.

Returning to our earlier discussion on Hickam’s Dictum, a patient can have as many diseases as they please. How can we be certain he didn't have an independent acute tubular necrosis driven by his Ibuprofen and Losartan use alongside his underlying condition?

 [Dr. Ben Lovell]: To differentiate them clearly, an established ATN typically enters a profound polyuric phase during recovery, and you see distinct changes in his urinary biochemistry. I had to double-check my parameters, but in true acute tubular necrosis, the urinary sodium concentration rises significantly.

To help remember this for postgraduate examinations, look at the spelling: the letter N at the end of ATN stands for Sodium (Na). Thinking of it as Acute Tubular Sodium Elevation is an easy way to remember that urinary sodium runs exceptionally high in ATN, which separates it from the low urinary sodium profile seen in simple pre-renal dehydration.

 [Dr. Amie Burbridge]: That is a brilliant clinical memory shortcut! I will never forget that trick now. Thank you, Ben, for an excellent case.

 [Dr. Ben Lovell]: Thank you for working through it with me, Amie. To our community of listeners, thank you for tuning in to the Home of Medicine Podcast. Please continue to rate, review, and share the show on your favorite platforms to help us reach new clinicians. We look forward to welcoming you back for our next episode. Have a wonderful day, and goodbye!

 [Dr. Amie Burbridge]: Thank you, everyone. Goodbye!

Clinical Concepts & Pathologies

• Acute Kidney Injury (AKI): A sudden, rapid decline in renal excretory function marked by an acute rise in serum creatinine.
• Acute Tubular Necrosis (ATN): An intrinsic renal pathology characterized by structural damage and necrosis of the tubular epithelial cells, frequently triggered by ischemia or nephrotoxic agents.
• Hypercalcemia: An abnormal elevation of calcium levels in the blood, which can manifest as nausea, abdominal pain, and altered mental status.
• Normocytic Anemia: A descriptive classification of anemia where the red blood cells are of normal size (normal MCV) but reduced in total concentration.
• Search Satisficing: A cognitive bias in clinical reasoning where a physician terminates the diagnostic search as soon as an initial plausible explanation is found.
• The Triple Whammy: The dangerous concurrent administration of an ACE inhibitor/ARB, a diuretic, and an NSAID, which drastically reduces glomerular filtration pressure.

Diagnostic Frameworks & Laboratory Tests

• STOP-AKI Mnemonic: A safety-net framework used to systematically screen for the four common triggers of renal impairment: Sepsis, Toxins, Obstruction, and Parenchymal disease.
• CRAB Criteria: A diagnostic staging mnemonic used to screen for systemic plasma cell neoplasms, tracking Hypercalcemia, Renal failure, Anemia, and Bone lesions.
• Serum Protein Electrophoresis: A targeted laboratory assay used to identify abnormal clonal paraprotein bands in the blood.
• Urinary Sodium Concentration: A biochemical test utilized to differentiate a functional pre-renal state (low urinary sodium) from intrinsic acute tubular necrosis (high urinary sodium).

What clinical indicators suggest an acute kidney injury has an underlying intrinsic or systemic cause rather than a simple pre-renal origin? When an elevated serum creatinine level fails to drop significantly or normalize following targeted fluid volume resuscitation, an isolated pre-renal volume depletion is unlikely. Clinicians must expand their evaluation to look for concurrent abnormalities like a normocytic anemia, unexplained bone or back pain, and hypercalcemia, which collectively signal a systemic parenchymal process.

How does the "STOP-AKI" framework optimize initial emergency screening for renal impairment? The STOP-AKI mnemonic organizes the four most common reversible drivers of acute renal decline: Sepsis, Toxins (nephrotoxic agents), Obstruction (post-renal blocks), and Parenchymal kidney diseases. This structure prompts clinicians to screen for systemic infections, audit high-risk prescriptions, evaluate the bladder for urinary retention, and dip the urine for intrinsic glomerular markers simultaneously.

What is the physiological relationship between urinary sodium levels and acute tubular necrosis (ATN)? In the presence of established acute tubular necrosis, structural damage to the renal tubular cells directly compromises their ability to reabsorb filtered electrolytes. This structural dysfunction forces the urinary sodium concentration to rise significantly, creating a high urinary sodium profile that helps differentiate intrinsic parenchymal injury from a functional, pre-renal state.

psychology, exploring how to recognize "search satisficing" and pivot a treatment strategy when clinical data changes.