Specific Considerations with Renal Disease - Renal Failure

The definition varies but has been reported as an increase in serum creatinine by 0.5 mg/dL, increase in serum creatinine by 50%, or serum creatinine greater than 2 mg/dL.

Acute Kidney Injury

Acute Kidney Injury. Incidence varies according to etiology, definition, and type of surgery but is 4% to 24% with mortality rates as high as 60% to 90%. Postoperative renal dysfunction is associated with higher incidence of gastrointestinal bleeding, respiratory infection, sepsis, and longer ICU and hospital length of stay.

  1. Epidemiology. From 2% to 5% of hospitalized patients; increases with age.
  2. Etiology
    1. Prerenal. Due to decreased circulating volume (hypovolemia) or a perceived decrease in circulating volume (decreased cardiac output or hypotension). Early correction of the underlying cause usually results in rapid reversal of renal dysfunction, but continued renal hypoperfusion may result in intrinsic renal damage.
    2. Intrarenal. The most common cause is ATN due to ischemia. Other intrarenal causes include toxins, acute glomerulonephritis, and interstitial nephritis.
    3. Postrenal. Obstructive lesions result in disrupted emptying and can be caused by renal calculi, neurogenic bladder, prostatic disease, or an encroaching tumor. Unilateral obstruction rarely causes AKI.
    4. Normotensive ischemic acute kidney injury. A low-perfusion state may arise in the absence of frank hypotension in a patient with “normal” appearing blood pressures. These patients typically have underlying risk factors for renal injury including early sepsis or exposure to nephrotoxic agents such as IV contrast or NSAIDs. Additionally, normotension in a patient with baseline chronic hypertension can actually herald a low-perfusion state.
  3. Classification. There are three widely used classification systems for AKI (Table 4.1):
    1. The RIFLE criteria classifies three levels of kidney injury (risk, injury, or failure) and two outcomes (loss and end-stage renal disease [ESRD]) based upon (1) a percentage increase in serum creatinine over 7 days or (2) a decrease in urine output (UOP).
    2. The AKIN criteria modifies the RIFLE criteria by including absolute increases in serum creatinine and limiting the period of injury to a 48-hour window.
    3. The KDIGO criteria fuses the RIFLE and AKIN criteria.
  4. Diagnosis. Clinical features occurring late in the course of the disease include hypervolemia due to an impaired ability to excrete water and sodium with resultant hypertension and peripheral edema, potential hypovolemia due to lack of urine concentrating ability, potassium retention, impaired excretion of drugs and toxins, and potential progression to CKD. Results of urine and serum indices can help to distinguish prerenal, intrarenal, and postrenal etiologies (Table 4.2).
  5. Prevention. Mainly based on tradition, anecdotes, or extrapolation from animal models. A modest goal is to keep UOP greater than 0.5 mL/kg/h and to avoid hypovolemia, hypoxia or decreased O2 delivery, renovascular constriction, increased renal O2 demand, and maintenance of renal vasodilation and renal tubular blood flow along with attenuation of renal ischemic reperfusion injury.
  6. Treatment
    1. Medications such as diuretics, dopamine, and fenoldopam can be used to increase UOP, treat hypertension, and manage electrolyte, fluid, and acid–base disturbances but have not been proven to prevent or treat AKI.
    2. Hemodialysis. Incidence of AKI patients requiring dialysis varies depending on the underlying surgical operation (e.g., coronary artery bypass grafting 1.1% versus general surgery 0.6%).
      1. Hemodialysis uses an artificial semipermeable membrane that separates the patient's blood from dialysate and allows the exchange of solutes by diffusion. Vascular access (via central venous catheters or a surgically created arteriovenous fistula) and systemic or regional anticoagulation are often required. Hemodialysis typically is performed three times a week, and serum electrolyte and volume abnormalities are corrected by adjusting the dialysis bath fluid. Blood samples taken immediately after dialysis will be inaccurate, because redistribution of fluid and electrolytes takes about 6 hours. Continuous arteriovenous or venovenous hemodialysis may also be performed. Complications include arteriovenous fistula infection or thrombosis, dialysis disequilibrium or dementia, hypotension, pericarditis, and hypoxemia.
      2. Hypotension can occur during hemodialysis with changes in preload, electrolyte changes, acid–base abnormalities, hemodynamic effects of buffering drugs, and impaired sympathetic response.
      3. Indications for dialysis in AKI and CKD include hyperkalemia, acidosis, volume overload, uremic complications (pericarditis, tamponade, and encephalopathy), and severe azotemia.
      4. Ultrafiltration and hemofiltration allow for the removal of volume with minimal removal of waste products. These techniques are useful in volume-overloaded patients. As with standard hemodialysis, anticoagulation may be required.
        1. Ultrafiltration uses hemodialysis equipment to create a hydrostatic driving force across the membrane without a dialysate on the opposing side. Thus, an ultrafiltrate of serum is removed, and this volume is not replaced. If large volumes of fluid are removed rapidly, hypotension may ensue.
        2. Hemofiltration uses the same principle as ultrafiltration; however, replacement fluid is given to the patient either before or after the membrane filter and solutes/electrolytes are removed by convection. Volume shifts are minimized so that patients can tolerate longer periods of continuous filtration.
    3. Continuous renal replacement therapy (CRRT) refers to any continuous mode of extracorporeal solute or fluid removal. Indications in addition to AKI include fluid clearance, electrolyte imbalances, and managing metabolic acidosis. Slower blood flow rates with CRRT improve hemodynamic stability compared with regular hemodialysis.

Chronic kidney disease (CKD)

Chronic kidney disease (CKD) is defined by kidney damage (structural or functional abnormalities of the kidney) for ≥3 months as manifested by abnormalities in the composition of blood or urine, abnormalities in imaging tests, or a glomerular filtration rate (GFR) less than 60 mL/minute/1.73 m2 for ≥3 months.

  1. Epidemiology. CKD affects more than 26 million adults in the United States (Table 4.3).
  2. Etiology. Common causes include hypertension, diabetes mellitus, chronic glomerulonephritis, tubulointerstitial disease, renovascular disease, and polycystic kidney disease.
  3. Clinical features
    1. Hypervolemia and hypertension, sometimes resulting in congestive heart failure and edema.
    2. Accelerated atherosclerosis, which may increase the risk of coronary artery disease.
    3. Uremic pericarditis and pericardial effusions, which may cause cardiac tamponade.
    4. Hyperkalemia, hypermagnesemia, and hyponatremia may occur.
    5. Hypocalcemia and hyperphosphatemia due to elevated parathyroid hormone, resulting in renal osteodystrophy.
    6. Metabolic acidosis due to retained sulfates and phosphates and an inability to excrete products of metabolism.
    7. Chronic anemia secondary to decreased erythropoietin production and decreased red blood cell survival.
    8. Platelet dysfunction, which can be temporarily treated with desmopressin acetate.
    9. Gastrointestinal dysfunction is common as a result of accumulated urea that may result in inflammation of the entire GI tract. Increased gastric volume, acid production, and delayed gastric emptying result in an increased incidence of peptic ulceration, and nausea and vomiting with increased risk of regurgitation and aspiration with anesthesia.
    10. Increased susceptibility to infection due to leukocyte and immune dysfunction from uremia, malnutrition, and inflammatory reaction to dialysis.
    11. Central nervous system changes range from mild changes in mentation to severe encephalopathy and coma. Peripheral and autonomic neuropathies are common.
    12. Glucose intolerance and hypertriglyceridemia.
  4. Treatment. When needed, 85% receive hemodialysis and 15% receive peritoneal dialysis. Transplantation is the preferred method of treatment for most CKD patients.
    1. Hemodialysis
    2. Peritoneal dialysis uses the capillaries of the peritoneum as a semipermeable exchange membrane with the dialysate infused into the peritoneal cavity via an indwelling peritoneal catheter. Advantages over hemodialysis include less hypotension or disequilibrium and no need for heparin treatment. However, peritoneal dialysis is less efficient and limited in catabolic states compared with hemodialysis. Complications include infection, hyperglycemia from the dextran in the dialysate, and increased protein loss into the dialysate.

Specific Causes of Renal Failure

Specific Causes of Renal Failure

  1. ATN may be produced by ischemic or toxin injuries and is the major intrinsic form of AKI. ATN is the most common cause of perioperative renal failure, and its development is associated with high mortality. The major risk factors for ATN are a history of preexisting renal insufficiency, administration of radiocontrast agents or aminoglycoside antibiotics, and advanced age. Anesthetic management of patients who are at risk for developing ATN includes meticulous management of fluids and hemodynamics with the goal of maintaining euvolemia, normal renal perfusion, and urinary output. No specific therapies have proved consistently beneficial in preventing or treating perioperative ATN.
  2. Glomerulonephropathies are a diverse family of diseases that may present insidiously or more acutely with fulminant renal failure. Nephrotic syndrome may be the initial presentation with severe proteinuria (3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema. Anesthetic concerns include depleted intravascular volume and protein, accelerated atherosclerotic disease, and increased risk of infection. Glomerulonephropathy may be secondary to autoimmune diseases such as systemic lupus erythematosus or vasculitides such as granulomatosis with polyangiitis. Therapy may include glucocorticoids and cytotoxic agents.
  3. Hypertensive nephrosclerosis is a major etiology in the development of ESRD and may account for up to 30% of patients beginning dialysis. Treatment of diastolic hypertension reduces disease progression and the associated morbidity and mortality.
  4. Diabetic nephropathy is the single largest cause of ESRD in the United States. The nephropathy presents with proteinuria, and there is a progressive decline in renal function over 10 to 30 years after the initial diagnosis. Diabetic nephropathy often manifests itself as a type IV renal tubular acidosis (hyporeninemic hypoaldosteronism) or as papillary necrosis. There is a high correlation between renal dysfunction and diabetic retinopathy. Aggressive control of blood glucose and blood pressure may forestall the development and prevent progression of nephropathy.
  5. Tubulointerstitial diseases primarily affect the renal tubules and interstitium and include acute and chronic forms of interstitial nephritis.
    1. Acute interstitial nephritis is most commonly caused by drugs (e.g., penicillins, cephalosporins, sulfonamides, rifampin, and NSAIDs) in adults. Systemic infections are the most common etiologies in children. Acute interstitial nephritis usually presents as oliguric renal failure with a variable degree of proteinuria. Symptoms of an inflammatory response, such as fever, rash, eosinophilia, and eosinophiluria, are suggestive of the diagnosis of acute interstitial nephritis. Treatment is supportive and includes discontinuation of suspect drugs.
    2. Chronic interstitial nephritis is most commonly due to obstruction of urine flow or reflux, analgesic abuse, or heavy metal intoxications. Early in the disease, patients lose the ability to concentrate urine and have polyuria and nocturia. Later manifestations depend on the specific anatomic lesions. The only specific therapy for chronic interstitial nephritis is treatment of the underlying cause.
  6. Polycystic kidney diseases are autosomal dominant diseases responsible for 5% to 8% of adult ESRD. Approximately 25% of patients at 50 years of age and 50% of patients at 75 years of age will manifest ESRD. Cystic disease may also affect the liver. Also, there is an association with intracranial and aortic aneurysms. Tuberous sclerosis and von Hippel-Lindau disease may also present as cystic renal disease.
  7. Obesity is associated with glomerular hyperfiltration, proteinuria, focal segmental glomerulosclerosis and other glomerulopathies. Additionally, obesity places patients at increased risk for hypertension, diabetes, activation of the renin–angiotensin–aldosterone system, and development of CKD. Perioperative renal considerations for the obese patient include altered pharmacokinetics, increased intra-abdominal pressures and associated oliguria, and difficulties in assessing volume status.

Tables

Criteria for Acute Kidney Injury (Table 4.1)

Serum Creatinine CriteriaUrine Output Criteria
RIFLEAKINKDIGO
DefinitionIncrease in serum creatinine of >50% developing over <7 daysIncrease in serum creatinine of 0.3 mg/dL or >50% developing over <48 hIncrease in serum creatinine of 0.3 mg/dL over 48 h or >50% developing over 7 daysUrine output of <0.5 mL/kg/h for > 6 h
Staging
RIFLE-Risk
AKIN/KDIGO stage 1
Increase in serum creatinine >50%Increase in serum creatinine of 0.3 mg/dL or >50%Increase in serum creatinine of 0.3 mg/dL or >50%Urine output of <0.5 mL/kg/h for >6 h
RIFLE-Injury
AKIN/KDIGO stage 2
Increase in serum creatinine >100%Increase in serum creatinine >100%Increase in serum creatinine >100%Urine output of <0.5 mL/kg/h for >12 h
RIFLE-Failure
AKIN/KDIGO stage 3
Increase in serum creatinine >200%Increase in serum creatinine >200%Increase in serum creatinine >200%Urine output of <0.3 mL/kg/h for >12 h or anuria for >12 h
RIFLE-LossNeed for RRT >4 wk
RIFLE-End-stageNeed for RRT >3 mo

Palevsky PM. Definition of acute kidney injury. In: Curhan GC, ed. UpToDate. Waltham: UpToDate. (Accessed August 13, 2014.)

Urine and Serum Diagnostic Indexes (Table 4.2)

PrerenalRenalPostrenal
Urine (Na)<10 mEq/L>20 mEq/L>20 mEq/L
Urine (Cl)<10 mEq/L>20 mEq/L
FENa<1%>2%>2%
Urine osmolarity>500<350<350
Urine/serum (creatinine)>40<20<20
Renal failure index<1%>2%>2%
Urine/serum (urea)>8<3<3
Serum (BUN)/creatinine>201010

BUN, blood urea nitrogen; FENa, fractional excretion of sodium.

National Kidney Foundation Classification of CKD (Table 4.3)

StageDescriptionGFRU.S. Prevalence (%)
INormal≥903.3
IIMild60–893.0
IIIModerate30–594.3
IVSevere15–290.2
VFailure<150.1

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