Acute Kidney Injury: Pearls and Pitfalls

Authors: Subhanir Sunil Chitnis, MD (EM Resident Physician, Rutgers NJMS; @ChitnisMD) and Karma Warren, MD (EM Attending Physician, Rutgers NJMS) // Editor: Alex Koyfman, MD (@EMHighAK) and Manpreet Singh, MD (@MPrizzleER)

KidneyIntroduction:

Acute kidney injury (AKI) is a sudden, potentially reversible, kidney dysfunction with partial or complete loss of glomerular filtration resulting in electrolyte and fluid abnormalities as well as retention of nitrogenous waste products [1]. In contrast, Chronic Kidney Disease (CKD) describes loss of kidney function for at least three months [2]. While a decrease in Glomerular Filtration Rate (GFR) is used to categorize CKD, an increase in serum creatinine or decrease in urine output is used to characterize AKI. The most recent definition of AKI is provided by the Kidney Disease: Improving Global Outcomes (KDIGO) group which reconciled the 2004 RIFLE criteria and the follow-up AKIN update. [2,3]

Accordingly, acute kidney injury is defined by any of the following:

  • Increase in serum creatinine by ≥0.3 mg/dL within 48 hours; or
  • Increase in serum creatinine by ≥1.5 times baseline within seven days; or
  • Urine volume <0.5 mL/kg/h for six hours

Classification

Acute kidney injury is classified into three categories (Prerenal, Intrinsic, or Postrenal) based on the physiologic mechanism that prevents production or excretion of urine. The excretion of urine requires (1: Prerenal) adequate volume of blood flow with adequate hydrostatic pressure, (2: Prerenal/Intrinsic) ultrafiltration by the glomeruli which is dependent on glomerular structure, hydrostatic capillary pressure and oncotic pressure, (3: Intrinsic) tubular reabsorption and secretion of various solutes and reabsorption of most of the free water, and (4: Postrenal) drainage of the resultant urine via the genitourinary tract extending from the renal pelvis to the urethral meatus (4, 5). A patient may have more than one cause of acute kidney injury simultaneously due to derangements of any of the above four processes. Additionally, most patients with previously normal kidneys may not have an elevation in serum markers in the event of an acute injury to one kidney.

Prerenal

  1. Hypovolemia: commonly due to decreased intake, increased losses, diuretic use, blood loss, third spacing, salt-wasting nephropathy, hypoaldosteronism
  2. Hypotension: shock state, heart failure, antihypertensive use, Addison’s disease
  3. Renal artery vascular diseases: renal artery stenosis or fibrosis, thromboembolic events, aortic dissection, aortic aneurysm, NSAID/ARB/ACE inhibitor use, pre-eclampsia, HUS, DIC, traumatic devascularization
  4. Other: hepatorenal disease, aortic cross-clamping, renal vein thrombosis

Intrinsic

  1. Interstitial diseases: Infection (pyelonephritis, infected stone, abscesses, emphysematous pyelitis), infiltration (amyloid, myeloma, sarcoid, lymphoma), autoimmune (SLE), drug-induced interstitial nephritis, loss of parenchyma due to polycystic disease
  2. Glomerular diseases: post-infectious glomerulonephritis, HSP, SLE, Wegener’s, Goodpasture’s, membranoproliferative.
  3. Nephrotoxins: may result in interstitial and glomerular injury. Medications (classically NSAIDS, aminoglycosides, radiocontrast (good evidence mounting against this – topic of upcoming emdocs.net write-up), amphotericin, sulfonamides), heme moieties from hemolysis or rhabdomyolysis, uric acid, calcium oxalate, amyloid deposits

Postrenal acute kidney injury

  1. Intraluminal obstruction: calculi, obstructed catheters, urethral strictures, posterior urethral valves, vesicoureteral reflux, failed ureteral stents
  2. Extrinsic compression: BPH, GU/GYN/GI cancers, pregnancy, ascites, expanding hematoma, penile fractures
  3. Other: traumatic disruption, neurogenic bladder, spinal cord injury (cauda equina syndrome), anticholinergic and alpha-adrenergic antagonist toxicity, surgical injury

Clues for acute renal injury

  1. By etiology: Patients with Prerenal Acute Kidney Injury may present with hypotension, tachycardia, shock, peripheral edema, vomiting, diarrhea, acute blood loss, flank or back pain, oliguria or anuria. Intrinsic Acute Renal Injury may present with flank and back pain, hematuria, proteinuria, urinary casts and sediments, infectious prodrome, and history or presentation of systemic diseases causing microangiopathy and hemolysis like HUS, TTP, scleroderma, and DIC. Postrenal Acute Kidney Injury patients present with obstruction to urine flow associated with a history of renal calculi, urinary urge, failure to void, incontinence, mechanical failure of indwelling catheter, pelvic and flank pain, palpable large urinary bladder, CVA tenderness, and hydronephrosis or hydroureter on imaging studies.
  2. By consequence: Acute kidney injury may present with a variety signs and symptoms consistent with uremia, electrolyte disturbances, and fluid status. These may include third spacing with shortness of breath, pleural and pericardial effusions, interstitial edema, and ascites. Hyperkalemia may present with acutely life-threatening arrhythmias and requires emergent diagnosis and management. Uremia may present with uremic pericarditis, effusion and life-threatening pericardial tamponade requiring emergent diagnosis and management. Acute hypertension with hypertensive emergency also requires emergent management.

ED-Focused Work-Up

  1. Labs – Serum chemistry, CK, BUN/Cr ratio, FeNa, Specific gravity, Microscopic analysis, Urine electrolytes
  2. EKG – evaluate for changes secondary to electrolyte changes
  3. CXR – volume status, infection
  4. KUB – displaced ureteral stents, nephrolithiasis
  5. U/S – hydronephrosis, hydroureter, bladder distention, flow doppler of the kidney
  6. CT – nephrolithiasis, abdominal/pelvic masses

ED Management

Patients meeting the KDIGO definition for AKI typically require admission to the hospital (if etiology is identified/addressed and close follow-up established then reliable patients can be discharged – shared decision-making). Since there are various causes of AKI, simultaneous attempts should be made to treat the direct and indirect causes of AKI. As such, for all pre-renal causes of AKI, IV fluid resuscitation should not be delayed. Similarly, patients with rhabdomyolysis should receive aggressive fluid resuscitation to avoid new or worsening AKI. Likewise, relieving obstruction in post-renal AKI should be done without delay. Patient’s may require suprapubic catheterization if urethral catheterization fails. For more proximal obstruction, nephrostomy tube may be required until the obstruction is relieved. Patients with prolonged obstruction can have postobstructive diuresis and should be admitted if they have persistent diuresis of about 250 mL/hr or more for two hours. Eliminate any nephrotoxic substances, including any medications and treatments that can worsen AKI. Patients with fluid overload may demonstrate hypoxia and require positive pressure ventilation. Consider dialysis for severe acidosis, electrolyte abnormalities, ingestion of toxins like ASA, methanol, lithium and ethylene glycol, volume overload and uremia with pericarditis, encephalopathy, or BUN > 100.

References / Further Reading:

  1. Palevsky, P. Definition of acute kidney injury (acute renal failure). Available at: www.uptodate.com+definition-of-acute-kidney-injury-acute-renal-failure. Last accessed: Feb 19, 2015
  2. Rosenberg, M. Overview of the management of chronic kidney disease in adults. Available at: www.uptodate.com+overview-of-the-management-of-chronic-kidney-disease-in-adults. Last accessed: Feb 19, 2015
  3. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8.
  4. Erdbruegger, U., Okusa, M. Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure). Available at: www.uptodate.com+etiology-and-diagnosis-of-prerenal-disease-and-acute-tubular-necrosis-in-acute-kidney-injury-acute-renal-failure. Last accessed: Feb 19, 2015
  5. Pazhayattil, G. S., Shirali, A. C. (2014). Drug-induced impairment of renal function. International Journal of Nephrology and Renovascular Disease, 7, 457–68. doi:10.2147/IJNRD.S39747
  6. Tögel, F., Westenfelder, C. (2014). Recent advances in the understanding of acute kidney injury. F1000Prime Reports, 6, 83. doi:10.12703/P6-83
  7. Pickering, J. W., Endre, Z. H. (2014). The definition and detection of acute kidney injury. Journal of Renal Injury Prevention, 3(1), 21–5. doi:10.12861/jrip.2014.08
  8. AKI, lifeinthefastlane, Critical Care Compendium

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