Joan C. Delto, MD
Fernando J. Bianco, Jr., MD
BASICS
DESCRIPTION
• The term acute kidney injury (AKI) has replaced the older descriptor of acute renal failure (ARF)
– Rapid decline in renal function characterized by progressive azotemia, with or without oliguria (<500 mL/d)
– Decreased glomerular filtration rate
• Attempts to standardize the definition of AKI have been proposed by different groups as noted below. However, their utility in daily clinical care has not been confirmed (1)
– Acute dialysis quality initiative (ADQI) group RIFLE criteria
– Acute kidney injury network (AKIN)
– Kidney Disease/Improving Global Outcomes (KDIGO) Clinical Practice Guidelines
EPIDEMIOLOGY
Incidence
• 5% of hospital admissions
• 30% of ICU admissions
• 25% of hospital patients develop AKI
– 50% are iatrogenic
RISK FACTORS
• Preoperative risk factors for development of AKI:
– Age >56
– Male
– Emergency surgery
– Intraperitoneal surgery
– Diabetes mellitus
– Active CHF
– Ascites
– Hypertension
– Preoperative renal insufficiency
Genetics
No genetic association
PATHOPHYSIOLOGY
• Pre-renal
– Transient renal hypoperfusion (reversible)
– Stimulation of sympathetic nervous system and RAS causing renal vasoconstriction and sodium reabsorption; stimulation of antidiuretic hormone
– Water reabsorption, low urine output, concentrated urine
• Intrarenal
– Acute tubular necrosis (ATN)
Renal ischemia
Depletion of ATP
Dysfunction of plasma membrane
Reperfusion injury
Oxidative stress leading to tubular cell damage
Rhabdomyolysis and hemolysis
• Postrenal (obstruction)
– Intrinsic obstruction
– Extrinsic compression
• Iatrogenic (urinary extravasation, fistula)
– Reabsorption of BUN, Cr
ASSOCIATED CONDITIONS
• Dehydration
• Trauma
• Burns
• Sepsis
• Urinary tract infection
• Chronic renal insufficiency
• Hypertension
• Congestive heart failure
• Liver disease, cirrhosis
• Nephrolithiasis
• BPH
• Advanced prostate or bladder cancer, malignancy
• Malignant hypertension
GENERAL PREVENTION
• Hydration
• Proper renal dosing of medication; daily dosing of aminoglycosides
• Avoidance of nephrotoxic agents
• Adequate voiding (timed, double voiding)
• Risk of contrast-induced AKI may be reduced by N-acetylcysteine 600 mg PO BID on day prior to and day of contrast and isotonic NaHCO3 3 mL/kg/h × 1 hr before and 1 mL/kg/h × 6 hr after contrast administration
ALERT
Determine if the patient is on any nephrotoxic medication? Has there been recent contrast injection? Is the foley draining?
DIAGNOSIS
• HISTORY
– Urination history—frequency, urgency, strength of stream, hematuria
– Fever, chills
– Nausea, vomiting, diarrhea
– Flank or abdominal pain
– Recent strenuous activity
– Review medications—nephrotoxic agents, diuretics
– Comorbidities
Renal disease
Diabetes
Hypertension
Liver disease
– Infections
– Nephrolithiasis
– BPH
– Malignancies, metastatic disease
– Previous abdominal or pelvic surgeries
– Radiation
– Chemotherapy
– Prior ureteroscopy or endoscopy
• Social History
– Smoking
– Alcohol
– Drug use
PHYSICAL EXAM
• Vital signs: Blood pressure, heart rate, orthostatic changes
• Volume status, body weight
• Urinary output, drain output
• Neck vein distention, lung rales
• Abdominal exam
– Bruits
– Palpable mass
– Distention, palpable bladder
– Costovertebral angle tenderness
• Digital rectal exam—prostate size/nodularity
• Patency of urinary catheters, stents
• Peripheral edema, rash
DIAGNOSTIC TESTS & INTERPRETATION
Lab
• CBC, BUN, creatinine, electrolytes (including Ca/Mg/Phos), consider arterial blood gases (ABGs)
• AKI
– Rise in serum creatinine (SCr) of at least 0.3 mg/dL over a 48-hr period
– Over 1.5 times the baseline SCr value within the 7 previous days
• Common lab abnormalities in AKI:
– Increased: K+, phosphate, Mg, uric acid
– Decreased: Hematocrit (Hct), Na, Ca
• NephroCheckTM detects the presence of insulin-like growth-factor binding protein 7 (IGFBP7) and tissue inhibitor of met alloproteinases (TIMP-2) in the urine (both AKI associated); the test provides a risk score of developing AKI within 12 hrs
• Creatinine kinase (rhabdomyolysis)
• Immune antibodies (vasculitis)
• Urine
– Urinalysis: Blood, protein, cells, casts, crystals
Transparent hyaline casts—prerenal etiology; pigmented granular/muddy brown casts—ATN; WBC casts—acute interstitial nephritis; RBC casts—glomerulonephritis
– Urine eosinophils: ≥1% eosinophils by Hansel’s stain suggestive of acute interstitial nephritis (sensitivity, 67%; specificity, 83%)
– Urine electrolytes (Urine Na; UNa)
– Urine osmolality (Uosm)
– Fractional excretion of sodium (FENA)
• Prerenal
– FENA <1%; BUN/Cr >20
– UNa <10; Uosm >500
• Intrarenal
– FENA >2%; BUN/Cr <15
– UNa >20; Uosm <350
• Postrenal
– FENA >4%; BUN/Cr >15
– UNa >40; Uosm <350
Imaging
• Renal/bladder ultrasound
– Hydronephrosis
– Stones
– Bladder volume, post void residual
– Prostatic size
– Bladder masses causing obstruction
– Ureteral jets, resistive indices
• Abdominal x-ray (KUB)
– Calcifications
– Stent location
• CT abdomen/pelvis
– Obstructing stones
– Obstructing masses
• Renal scan
– Obstruction
– Kidney function
Diagnostic Procedures/Surgery
• Cystoscopy with retrograde pyelography
• Renal biopsy (acute glomerular nephritis)
Pathologic Findings
• Acute interstitial nephritis
– Interstitial edema, marked interstitial infiltrate of T cells and monocytes
– Eosinophilic plasma cells
– PMN cells
– Granulomata
DIFFERENTIAL DIAGNOSIS (4)
• Prerenal (∼55%): Hypotension; volume depletion (GI losses, excessive sweating, dehydration, hemorrhage); renal artery stenosis/embolism; burns; heart failure; liver failure
• Intrarenal (∼40%): ATN (from prolonged prerenal insufficiency, radiographic contrast material, aminoglycosides, NSAIDs, or other nephrotoxic substances); glomerulonephritis; acute interstitial nephritis (drug-induced); arteriolar insults; vasculitis; accelerated hypertension; cholesterol embolization (common after arterial procedures); intrarenal deposition/sludging (uric acid nephropathy and multiple myeloma [Bence Jones proteins])
• Postrenal (∼5%): Extrinsic compression (eg, BPH, carcinoma, pregnancy); intrinsic obstruction (eg, calculus, tumor, clot, stricture, sloughed papillae); decreased function (eg, neurogenic bladder)
• Pseudo-AKI: Endogenous chromogens (eg, bilirubin, ascorbic acid, uric acid) and exogenous chromogens (eg, cephalosporins, trimethoprim, cimetidine) may interfere with the creatinine assay and cause falsely elevated results
TREATMENT
GENERAL MEASURES
• AKI requires close management of fluid, acid–base, and electrolyte balance and the removal of uremic toxins
• Fenoldopam, a dopamine agonist, may decrease dialysis and mortality in AKI (4)
• Furosemide is ineffective in preventing and treating AKI
• Prerenal
– Restoration of renal perfusion; isotonic fluid
• Intrarenal
– Cessation of nephrotoxic drugs
– Renal dosing of medications
• Postrenal
– Foley or suprapubic tube drainage
– Ensure patency of drains
Ensure proper placement within bladder
Rule out catheter obstruction (mucus, clot)
– Percutaneous nephrostomy tube
• Treatment of hyperkalemia (3)
– Monitor EKG when K+ >6 mmol/L
IV calcium
Sodium bicarbonate (if acidotic)
Insulin and glucose
Kayexalate
Hemodialysis for severe hyperkalemia or refractory to treatment
• Control of urinary extravasation
• Dietary considerations
– Maintain carbohydrate and protein intake
– Restrict: Phosphorus, potassium, sodium
MEDICATION
First Line
See above
Second Line
N/A
SURGERY/OTHER PROCEDURES
• Postrenal
– If cannot drain bladder per urethra, consider suprapubic tube
– Ureteral stent
– Percutaneous nephrostomy
– If clot retention, removal of clots. May require cystoscopy, clot evacuation
– If BPH, consideration for outpatient TURP
• Indications for dialysis (called renal replacement therapy can be hemo or peritoneal dialysis: For these urgent and potentially life-threatening indications:
– Metabolic disturbances refractory to medical management such as hyperkalemia, metabolic acidosis, hypo/hypercalcemia, hyperphosphatemia
– Pericarditis or pleuritis
– Uremic encephalopathy
– Uremia-related bleeding diathesis
– Volume overload refractory to diuretics
– Severe refractory hypertension
ONGOING CARE
PROGNOSIS
• Prerenal
– Good if renal function improvement within 24–72 hr after fluid repletion
• ATN
– Mortality rate of ATN generally 50%
– Mortality rate of ATN in ICU 75%
– Of those who survive ATN, 50% have complete resolution of renal function
– 5% of AKI patients will require chronic renal replacement therapy
• Postrenal
– Great recovery once obstruction and insult are resolved
COMPLICATIONS
• Postobstructive diuresis
• Sepsis post relief of obstruction with instrumentation
• Stent inflammation, crusting, and pain
• Chronic renal failure
FOLLOW-UP
Patient Monitoring
• Blood pressure control
• Monitoring of creatinine, potassium, calcium, and phosphorus
• Repeat imaging (US) to re-evaluate hydronephrosis
• If question of stent migration, obtain KUB or US
• Ureteral stents will need to eventually be exchanged or removed
• Consideration of internalization of percutaneous nephrostomy tubes
Patient Resources
National Kidney Foundation: www.kidney.org
REFERENCES
1. Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet. 2005;365:417–430.
2. Pannu N, Klarenbach S, Wiebe N, et al. Renal replacement therapy in patients with acute renal failure: A systematic review. JAMA. 2008;299:793–805.
3. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36:3246–3251
4. White HF, Kurland JM. Acute kidney injury. In: Domino FJ, ed. The Five Minute Clinical Consult. Philadelphia, PA: Wolters Kluwer; 2014.
ADDITIONAL READING
• Duty BD, Kavoussi LR. Assessment and Management of Incidentally Detected Unilateral Hydronephrosis in Adults. AUA Update Series. 2012;31:30.
• Van Wert R, Friedrich JO, Scales DC, et al. High-dose renal replacement therapy for acute kidney injury: Systematic review and meta-analysis. Crit Care Med. 2010;38:1360–1369.
See Also (Topic, Algorithm, Media)
• Acute Kidney Injury, Pediatric (Renal Failure, Acute)
• Acute Glomerulonephritis
• Acute Tubular Necrosis
• Contrast-Induced Nephropathy (CIN)
• Postobstructive Diuresis
CODES
ICD9
• 584.5 Acute kidney failure with lesion of tubular necrosis
• 584.9 Acute kidney failure, unspecified
• 593.81 Vascular disorders of kidney
ICD10
• N17.0 Acute kidney failure with tubular necrosis
• N17.9 Acute kidney failure, unspecified
• N28.0 Ischemia and infarction of kidney
CLINICAL/SURGICAL PEARLS
• Maximize urinary drainage.
• Avoid nephrotoxic agents.
• Upper tract obstructive uropathy should be acutely managed by stent vs. percutaneous nephrostomy.