Acute Kidney Injury

FeNa is a valuable diagnostic tool to help differentiate prerenal AKI from intrinsic renal failure (especially acute tubular necrosis, ATN): FeNa <1% → suggests prerenal AKI (kidneys conserving sodium), FeNa >2% → suggests intrinsic AKI (tubular damage impairs sodium reabsorption). CT abdomen is more helpful in postrenal (obstructive) causes. ECG detects electrolyte abnormalities, not the type of renal failure. Platelet count is unrelated to renal failure classification.

The earliest clinical sign of acute kidney injury (AKI) is often oliguria, defined as urine output <400 mL/day. This reflects a sudden drop in kidney function and filtration capacity. Edema and hyperkalemia may appear later. Anemia is usually a feature of chronic kidney disease, not acute.

In rhabdomyolysis, massive muscle breakdown leads to the release of myoglobin into the bloodstream. Myoglobin is toxic to renal tubules, especially in the setting of volume depletion or aciduria, and can cause acute tubular necrosis (ATN), leading to acute kidney injury (AKI). Calcium levels may decrease in early rhabdomyolysis. Creatinine kinase is a diagnostic marker of muscle injury but does not directly cause AKI. Hemoglobin can be nephrotoxic but is associated with hemolysis, not rhabdomyolysis.

BPH is a very common cause of postrenal AKI in older men. It leads to lower urinary tract obstruction, which impedes urine flow and causes back pressure on the kidneys, eventually reducing GFR. Nephrotic syndrome and ATN are causes of intrinsic renal failure. Interstitial nephritis is also intrinsic and typically drug-induced. Only BPH is a mechanical obstruction, making it a true postrenal cause.

Acute tubular necrosis (ATN), the most common cause of intrinsic AKI, typically progresses through three phases: Initiation phase – injury occurs, Oliguric phase – reduced urine output, Diuretic phase – high urine output as tubules begin to recover and Recovery phase – gradual normalization of renal function. Fluids alone are not always sufficient; management depends on the cause and severity. ATN does not always lead to ESRD; it is often reversible with supportive care. ATN requires close monitoring of fluids, electrolytes, and renal function.

Prerenal AKI results from acute reductions in renal perfusion. Common causes include: Hemorrhage → volume loss, Diarrhea → dehydration and Heart failure → decreased effective arterial blood volume. Chronic renal artery stenosis, while it can contribute to chronic kidney disease, is less likely to cause an acute prerenal AKI unless there's superimposed acute ischemia or bilateral involvement.

Daily weight monitoring is the most accurate and practical bedside method to assess changes in fluid status in patients with acute kidney injury (AKI). Even small changes in weight can indicate fluid retention or loss. Serum creatinine monitors kidney function, not fluid balance. Blood pressure alone can be influenced by many factors and may not reflect subtle fluid changes. Hematocrit may change with hemoconcentration or dilution but is less specific for fluid status.

Acute tubular necrosis (ATN) is most commonly caused by: Ischemia (e.g., from hypotension or sepsis), Nephrotoxins such as: Aminoglycosides, Radiographic contrast agents and Heavy metals and myoglobin. Benign prostatic hyperplasia (BPH) causes postrenal obstruction, not intrinsic tubular injury. Although BPH can lead to postrenal AKI, it is not a direct cause of ATN.

Oliguria (urine output <400 mL/day) is the most common clinical symptom of acute kidney injury (AKI), particularly in the early phase. It reflects a sudden drop in glomerular filtration and is often the earliest detectable sign. Polyuria may occur in the recovery phase of AKI but is not typical at onset. Pruritus is more associated with chronic kidney disease (CKD) and uremia. Orthopnea is a symptom of heart failure, not specific to AKI.

A Fractional Excretion of Sodium (FeNa) <1% suggests that the kidneys are functionally intact and actively reabsorbing sodium — a classic finding in prerenal azotemia, where low perfusion (e.g., dehydration, heart failure) prompts sodium conservation. Key FeNa interpretations: <1% → ✅ Prerenal AKI, >2% → Intrinsic renal failure, like acute tubular necrosis (ATN), Variable FeNa in postrenal and AIN (interstitial nephritis) may also have variable FeNa, but not typically <1%.

In acute kidney failure (AKI), the kidneys lose the ability to excrete potassium efficiently, leading to hyperkalemia, which can be life-threatening due to its effects on cardiac conduction. Hypokalemia is typically associated with diuretic use or gastrointestinal loss, not AKI. Hypophosphatemia is more common in refeeding syndrome. Hypercalcemia is not typical in AKI; in fact, hypocalcemia is more common due to phosphate retention and vitamin D disturbances.

Uremia refers to the clinical syndrome caused by the accumulation of nitrogenous waste products, especially blood urea nitrogen (BUN) and creatinine, due to reduced kidney function. Elevated BUN is a key lab finding in uremia. Hypokalemia is unlikely; hyperkalemia is more typical. Hypercalcemia is uncommon; uremia often causes hypocalcemia. Low phosphate is also not expected; phosphate usually accumulates, causing hyperphosphatemia.

Severe hyperkalemia (typically serum K⁺ >6.5 mmol/L or with ECG changes) is a life-threatening emergency and a clear indication for urgent dialysis in the setting of acute kidney injury (AKI). Other classic indications for urgent dialysis in AKI include: Refractory fluid overload, Severe acidosis unresponsive to treatment, Uremic symptoms (e.g., encephalopathy, pericarditis) and Mild acidosis can often be managed medically. Creatinine >2 is not itself an indication unless accompanied by life-threatening complications. Elevated BUN alone is not an absolute indication without clinical signs of uremia.

While urine color may suggest dehydration, hematuria, or other abnormalities, it is highly nonspecific and not a reliable measure of renal function. In contrast: Serum creatinine reflects glomerular filtration rate (GFR) (though with a time lag). Urine output is a direct, practical indicator of renal perfusion and function. BUN can be influenced by multiple factors but still gives important information in AKI. Therefore, urine color is the least reliable among the options listed.

A key diagnostic marker of acute kidney injury (AKI) is a rapid rise in serum creatinine, which reflects a decline in glomerular filtration rate (GFR). Hypokalemia is not typical; in fact, hyperkalemia is more common due to impaired renal excretion. Hypercalcemia is not characteristic of AKI. Blood urea nitrogen (BUN) is usually elevated, not low.

Hyperkalemia, commonly seen in acute kidney injury (AKI) due to impaired potassium excretion, can lead to life-threatening ventricular arrhythmias. This occurs because high serum potassium levels disrupt normal cardiac conduction and repolarization. ECG changes in hyperkalemia include peaked T waves, widened QRS, and sine wave patterns before progressing to ventricular fibrillation or asystole. Bradycardia may occur but is less immediately dangerous than ventricular arrhythmias. Atrial flutter and complete heart block are less commonly caused by hyperkalemia.

In prerenal AKI, the kidneys conserve sodium due to decreased perfusion. Therefore, urinary sodium is typically low (<20 mEq/L) as the body attempts to retain fluid. Hypotension, Volume depletion, and High BUN/Creatinine ratio (>20:1) are classic features of prerenal AKI. High urinary sodium suggests an intrinsic cause like acute tubular necrosis (ATN), where the tubules cannot reabsorb sodium effectively.

Prerenal AKI is caused by decreased renal perfusion, often due to hypovolemia, dehydration, or low effective circulating volume (e.g., in heart failure). The cornerstone of treatment is to restore perfusion with appropriate fluid resuscitation, typically using IV isotonic fluids. Diuretics are contraindicated in volume-depleted states. Dialysis is reserved for complications like refractory hyperkalemia or volume overload. Corticosteroids are used in some intrinsic renal conditions (e.g., interstitial nephritis), not prerenal AKI.

Uremia is a clinical syndrome due to the accumulation of nitrogenous waste products in advanced renal failure. Common manifestations include: Pericarditis (uremic pericarditis), Anorexia (due to toxin buildup), and Encephalopathy (confusion, lethargy, seizures). However: Hypercalcemia is not typical in uremia. In fact, hypocalcemia is more common due to phosphate retention and impaired vitamin D activation.

Radiocontrast agents used in imaging studies (e.g., CT scans with contrast) are a major cause of hospital-acquired acute kidney injury (AKI). This condition, known as contrast-induced nephropathy (CIN), typically occurs within 24–72 hours after contrast exposure and is preventable with adequate hydration and risk stratification. Hypothyroidism, depression, and anemia are not typical direct causes of AKI in hospitalized patients.

Red blood cell (RBC) casts in the urine are a hallmark of acute glomerulonephritis, indicating that red blood cells have passed through a damaged glomerular basement membrane and become trapped in proteinaceous casts within the renal tubules. Waxy casts are more typical of chronic kidney disease. Eosinophils suggest acute interstitial nephritis, not glomerulonephritis. Hyaline casts can be seen in normal individuals, especially after exercise or dehydration.

In prerenal AKI, decreased renal perfusion leads to increased reabsorption of urea (BUN) in the proximal tubules due to slower tubular flow. Creatinine, however, is not reabsorbed, so its concentration doesn't increase as much. This causes a disproportionate rise in BUN relative to creatinine, yielding a BUN: Creatinine ratio >20:1, which is characteristic of prerenal azotemia. Ratios <10:1 or 10–15:1 are more consistent with intrinsic renal damage (e.g., acute tubular necrosis). The ratio is indeed altered in prerenal AKI.

Acute interstitial nephritis (AIN) is often drug-induced and associated with allergic-type inflammation in the renal interstitium. A key clue on urinalysis is the presence of urinary eosinophils, especially when confirmed with special stains like Hansel's stain. Fatty casts are seen in nephrotic syndrome. RBC casts are characteristic of glomerulonephritis. Uric acid crystals may be seen in tumor lysis syndrome or gout, not AIN.

While many cases of intrinsic acute kidney injury (AKI) can be diagnosed clinically, the most definitive test to identify the exact underlying pathology (e.g., glomerulonephritis, vasculitis, interstitial nephritis) is a renal biopsy. It allows direct histological examination of kidney tissue. CT scan may be useful for detecting obstruction but does not diagnose intrinsic causes. Urine sodium and creatinine clearance help differentiate AKI types, but they are not definitive for intrinsic renal disease.

Crush injuries result in extensive muscle breakdown (rhabdomyolysis), releasing myoglobin into the bloodstream. Myoglobin is nephrotoxic, especially in the setting of hypovolemia and aciduria, and can lead to acute tubular necrosis (ATN) and acute kidney injury (AKI). Hemorrhage and sepsis may contribute to AKI, but in crush injuries, myoglobinuria is the primary cause. Ureteral rupture is rare and would cause postrenal AKI, not typical of crush trauma.

The most reliable lab distinction between acute tubular necrosis (ATN) and prerenal AKI is based on urinary sodium concentration and fractional excretion of sodium (FeNa): In prerenal AKI, the kidneys conserve sodium: Urinary Na⁺ < 20 mEq/L and FeNa < 1%. In ATN, damaged tubules cannot reabsorb sodium: Urinary Na⁺ > 40 mEq/L and FeNa > 2%. Serum creatinine, Hematuria, and BUN level may be elevated in both conditions and are less specific for differentiation.

The most life-threatening complication of acute kidney injury (AKI) is hyperkalemia-induced arrhythmia. As the kidneys fail to excrete potassium, serum levels rise, potentially leading to: Peaked T waves, Widened QRS, and Ventricular arrhythmias
Cardiac arrest. This requires immediate recognition and management. Anemia and proteinuria are typically chronic complications. Volume depletion may contribute to prerenal AKI but is not as acutely fatal as hyperkalemia.

In chronic or prolonged AKI, the kidneys lose the ability to convert inactive vitamin D (calcidiol) into its active form (calcitriol). This results in: Vitamin D deficiency, Impaired calcium absorption, Secondary hyperparathyroidism and Renal bone disease (renal osteodystrophy). Vitamin C may be lost in dialysis but is not characteristically deficient in AKI. Vitamin B12 deficiency is more common in malabsorption or after gastric surgery. Vitamin K deficiency may occur in liver disease or with malabsorption, not typically due to AKI.

Acute interstitial nephritis (AIN) is an immune-mediated hypersensitivity reaction that causes inflammation of the renal interstitium. It is commonly triggered by medications, with NSAIDs being one of the most frequent culprits, especially after prolonged use. Metformin is more associated with lactic acidosis in renal impairment, not AIN. Simvastatin is linked to rhabdomyolysis, not AIN. Aspirin, although an NSAID, at typical analgesic doses is less commonly linked to AIN compared to other NSAIDs like ibuprofen or naproxen.

Acute tubular necrosis (ATN) is a common cause of intrinsic acute kidney injury and is classically associated with “muddy brown” granular casts on urinalysis. These are formed from sloughed-off tubular epithelial cells and debris, indicating tubular damage. RBC casts are typical of glomerulonephritis. WBCs suggest infection or interstitial nephritis. Fatty casts are seen in nephrotic syndrome.

Contrast-induced nephropathy (CIN) is a form of acute tubular injury that can occur after administration of iodinated contrast media. It is often preventable and reversible with: Adequate pre- and post-procedure hydration, Avoiding contrast in high-risk patients, Using low- or iso-osmolar contrast agents. Glomerulonephritis typically requires immunosuppressive treatment and is not resolved with hydration alone. BPH causes postrenal AKI and often needs catheterization or surgery. Polycystic kidney disease is chronic and genetic, not reversible with fluids

In acute kidney injury (AKI), serum creatinine alone can lag behind actual changes in kidney function. The most accurate bedside method for estimating glomerular filtration rate (GFR) in AKI is measured creatinine clearance, typically using a 24-hour urine collection or short-interval urine sampling. Serum creatinine can be misleading due to delayed elevation in AKI. Cystatin C is an emerging marker but not as widely available or validated in AKI. Urine dipstick gives qualitative data and is not used to measure GFR.

In prerenal acute kidney injury (AKI), the kidneys retain sodium to conserve volume due to reduced perfusion. As a result, the fractional excretion of sodium (FeNa) is <1%, indicating effective tubular sodium reabsorption. 1–2% can be seen in early or resolving AKI. >2% is typical of intrinsic AKI like acute tubular necrosis (ATN), where the tubules are damaged and cannot reabsorb sodium efficiently. >4% is rarely used as a diagnostic cutoff.

Acute tubular necrosis (ATN) progresses through several phases: Initiation phase – Initial insult leading to tubular injury, Oliguric phase – Low urine output and rising creatinine, Diuretic phase – Increasing urine output, but impaired concentrating ability and Recovery phase – Gradual improvement in glomerular filtration rate (GFR) and normalization of kidney function. Oliguric and maintenance phases are associated with impaired function, not recovery.

In bilateral renal artery stenosis, both kidneys receive reduced blood flow. The renin-angiotensin system compensates by constricting the efferent arterioles to maintain glomerular filtration pressure. ACE inhibitors (and ARBs) block this mechanism, leading to a drop in glomerular pressure and worsening of renal function, potentially triggering acute kidney injury (AKI). Beta-blockers, calcium channel blockers, and diuretics may affect renal perfusion mildly, but they do not directly impair autoregulation like ACE inhibitors do in this context.

Renal ultrasound is the first-line imaging modality for evaluating postrenal causes of acute kidney injury (AKI), such as urinary tract obstruction. It is non-invasive, quick, and does not require contrast, making it ideal in patients with compromised renal function. MRI is not typically used for initial AKI assessment. CT with contrast can be nephrotoxic and is avoided in AKI unless absolutely necessary. Bone scan is unrelated to kidney evaluation.

The hallmark histologic feature of ATN is necrosis and sloughing of tubular epithelial cells, particularly in the proximal tubule and thick ascending limb of Henle’s loop. This leads to obstruction of tubules and impaired filtration. Glomerular sclerosis is characteristic of chronic glomerular diseases, such as diabetic nephropathy. Crescent formation is seen in rapidly progressive glomerulonephritis (RPGN). Interstitial fibrosis is typical of chronic interstitial nephritis, not acute ATN.

Anuria is defined as urine output <100 mL/day and indicates severe renal dysfunction, often requiring urgent evaluation and potentially dialysis. Oliguria = 100–400 mL/day, Normal urine output ≈ 800–2000 mL/day (depending on fluid intake), Polyuria = >3 L/day. So, 100 mL/day meets the threshold for anuria.

Acute glomerulonephritis is characterized by signs of glomerular inflammation and damage, including: RBC casts (pathognomonic), Hematuria (often with dysmorphic red cells) and Proteinuria (usually mild to moderate). Eosinophils in urine are not typical of glomerulonephritis. They are more commonly seen in acute interstitial nephritis (AIN), usually due to drug hypersensitivity.

Uremic encephalopathy is a serious neurological complication of advanced kidney failure and is a clear indication for urgent dialysis. It manifests as confusion, asterixis, seizures, or coma due to accumulation of uremic toxins. Other classic indications for dialysis in AKI include: Refractory hyperkalemia, Severe metabolic acidosis and Volume overload not responsive to diuretics. Serum creatinine >2.0 is not an absolute indication on its own. Anemia and Hypertension are managed medically and do not usually require dialysis acutely.

Serum creatinine is the most widely used and reliable lab marker to assess recent changes in renal function. It is a byproduct of muscle metabolism and is primarily excreted by the kidneys. A rising creatinine level indicates a reduction in glomerular filtration rate (GFR). BUN can be influenced by factors like hydration, protein intake, and GI bleeding, so it's less specific. Hemoglobin and albumin are not acute indicators of renal function and typically reflect chronic conditions.

Prerenal causes of acute kidney injury (AKI) are related to decreased renal perfusion without intrinsic kidney damage. Common prerenal causes include: Hypovolemia (e.g., from hemorrhage or dehydration), Sepsis (due to systemic vasodilation and hypotension) and Heart failure (due to reduced cardiac output). Ureteral obstruction is a postrenal cause, not prerenal, as it involves blockage of urine flow after it has left the kidneys.

Acute interstitial nephritis (AIN) is typically due to a hypersensitivity reaction, often drug-induced (e.g., NSAIDs, antibiotics). Key urinalysis findings include: Eosinophils (especially with Hansel’s stain), White blood cell (WBC) casts, and Sterile pyuria (WBCs without infection) Fatty casts → Nephrotic syndrome, RBC casts → Glomerulonephritis and Calcium oxalate crystals → Ethylene glycol poisoning or stone disease

Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in hospitalized patients. It often results from ischemia (e.g., due to prolonged hypotension or sepsis) or nephrotoxic insults (e.g., drugs like aminoglycosides or contrast agents). Glomerulonephritis is a less common cause and usually presents with hematuria and proteinuria. Post-renal obstruction can cause AKI but is less frequent in the inpatient setting. Polycystic kidney disease is a chronic condition, not an acute cause.

Uremic pericarditis is a classic manifestation of severe uremia, typically seen in advanced kidney failure. It results from the accumulation of nitrogenous waste products and requires urgent dialysis. Diarrhea is not a hallmark of uremia. Hematemesis suggests GI bleeding, not uremia. Hypotension can occur in many settings but is not specific to uremia.

Fractional excretion of sodium (FeNa) measures the percentage of filtered sodium that is excreted in the urine. A FeNa >2% typically indicates intrinsic renal injury, such as acute tubular necrosis (ATN), where damaged tubules cannot reabsorb sodium efficiently. A FeNa <1% is more consistent with prerenal AKI, where the kidneys conserve sodium. Postrenal AKI can have variable FeNa values depending on the phase. Normal kidney function is not characterized by such a high FeNa.

NSAIDs are a common cause of acute interstitial nephritis (AIN), an immune-mediated kidney injury. It often presents with: Acute kidney injury (AKI), History of recent drug exposure (especially NSAIDs, antibiotics, PPIs), Urinalysis showing eosinophils or WBCs and May have rash, fever, or eosinophilia. ATN can also occur with NSAIDs but is less common than AIN in this setting. Postrenal obstruction is not associated with NSAIDs. Diabetic nephropathy is a chronic condition, not an acute process.

Trimethoprim, an antibiotic often combined with sulfamethoxazole, inhibits tubular secretion of creatinine. This leads to a rise in serum creatinine without an actual decrease in glomerular filtration rate (GFR). Thus, kidney function is preserved, but the lab value appears elevated — mimicking AKI. Sepsis can cause true AKI through hypoperfusion. Hyperkalemia is a result, not a cause, of renal dysfunction. Hypertension contributes to chronic kidney disease, not false elevations of creatinine.

Postrenal AKI occurs due to obstruction of urine flow anywhere from the renal pelvis to the urethra. BPH is a common cause of lower urinary tract obstruction in older men, leading to postrenal AKI if severe enough. Sepsis is a prerenal cause due to hypotension and poor perfusion. Myoglobinuria is an intrinsic cause, typically from rhabdomyolysis damaging the renal tubules. Lupus nephritis is an intrinsic renal cause due to autoimmune glomerular inflammation.

Pulmonary edema in the setting of acute kidney injury (AKI) signifies fluid overload, often unresponsive to diuretics. In such cases, urgent dialysis is indicated to: Remove excess fluid, Correct electrolyte imbalances and Prevent respiratory failure. Corticosteroids are used in some intrinsic kidney diseases but not for volume overload. High protein diet is not advised in AKI due to risk of worsening uremia. NSAIDs can worsen renal perfusion and are contraindicated in AKI.