Renal Failure

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114 Renal Failure

Definitions

Renal failure can be the result of a wide variety of conditions that cause injury to the kidneys. Recently, there has been a change in terminology with respect to kidney disease: the entities previously known as acute renal failure and chronic renal failure are now known as acute kidney injury and chronic kidney disease, respectively.

The Acute Kidney Injury Network (AKIN) provides the following criteria for the diagnosis of acute kidney injury: an abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of 0.3 mg/dL or greater (≥26.4 µmol/L), a 50% or greater increase in serum creatinine of (1.5-fold higher than baseline), or a reduction in urine output (documented oliguria of less than 0.5 mL/kg/hr for more than 6 hours).1

Two classification systems describe the stage of renal disease. The first, created by the Acute Dialysis Quality Initiative, is the RIFLE (risk, injury, failure, loss, and end-stage kidney disease) classification system, which bases severity on the degree of change in serum creatinine or urine output from a baseline measurement (Table 114.1).2 The second was created by AKIN. Although it is modeled on the RIFLE classification, it does not require the physician to know the patient’s baseline creatinine level. Its ease of use in the emergency department (ED) is improved by the fact that it does not use the glomerular filtration rate (GFR) as one of the criteria for staging kidney injury. The AKIN criteria are to be applied after adequate fluid resuscitation has taken place, and the authors of the criteria also recommend excluding easily reversible causes of kidney failure, such as urinary outflow obstruction (Table 114.2).1

Table 114.1 RIFLE Classification System

  GFR CRITERIA URINE OUTPUT CRITERIA
Risk Increased Cr × 1.5 UO < 0.5 mL/kg/hr × 6 hr
or
GFR decreased >25%
Injury Increased Cr × 2 UO < 0.5 mL/kg/hr × 12 hr
or
GFR decreased >50%
Failure Increased Cr × 3 UO < 0.5 mL/kg/hr × 12 hr
or or
GFR decreased >75% anuria × 12 hr
Loss Persistent ARF = complete loss of renal function for >4 wk None
End-stage kidney disease End-stage kidney disease > 4 mo None

Cr, Creatinine; GFR, glomerular filtration rate; UO, urine output.

Table 114.2 AKIN Criteria for Staging Acute Kidney Injury

  CREATININE CRITERIA URINE OUTPUT CRITERIA
Stage 1 Increased Cr × 1.5 UO < 0.5 mL/kg/hr > 6 hr
or
Increased ≥0.3 mg/dL
Stage 2 Increased Cr × 2 UO < 0.5 mL/kg/hr > 12 hr
Stage 3 Increased Cr × 3 UO < 0.5 mL/kg/hr > 24 hr or anuria for 12 hr
or
≥4 mg/dL with acute increase of 0.5 mg/dL
or
Patient receiving renal replacement therapy

AKIN, Acute Kidney Injury Network, Cr, creatinine; UO, urine output.

The National Kidney Foundation’s clinical practice guidelines define patients with chronic kidney disease as meeting one of the following criteria: (1) kidney damage for 3 or more months, defined as structural or functional abnormalities of the kidney, with or without an increased GFR, and demonstrated by either pathologic abnormalities or markers of kidney damage, including abnormalities in blood or urine or abnormal findings on imaging tests; or (2) a GFR lower than 60 mL/min/1.73 m2 for 3 or more months, with or without kidney damage.3 The complicated definition of chronic kidney disease plus the need to monitor kidney function over an extended period means that it is unlikely that chronic kidney disease will be convincingly diagnosed in the ED. However, it is useful for the emergency physician (EP) to understand what it means when a patient has preexisting chronic kidney disease, as well as to be vigilant for suspected, but previously undiagnosed chronic kidney disease in a patient with the appropriate signs and symptoms.

Epidemiology

The prevalence and incidence of kidney failure in the United States are rising. The prevalence of chronic kidney disease is estimated to be greater than 10%.4 The annual incidence of acute kidney injury is 100 per 1 million population. The incidence of acute kidney injury in the community varies widely depending on the population, but hospital-acquired rates can be quite high, with as many as 30% of critical care patients in some studies developing acute kidney injury.5

Pathophysiology

The kidneys are located in the retroperitoneal space and are composed of three basic structures: vasculature, parenchyma, and the collecting system. The kidneys receive about a quarter of the body’s total cardiac output through the renal arterial system and an extensive network of arteries, arterioles, and capillaries that eventually drain into the renal vein. The renal parenchyma is composed of the medulla and cortex, which houses the functional unit of the kidney, the nephron. A single nephron consists of a glomerulus, proximal tubule, thin limbs of Henle, and a distal tubule. The connecting tubule joins the nephron to the collecting system, including the renal pelvis, minor and major calyces, and the ureter, bladder, and urethra (Fig. 114.1).

The kidney is responsible for maintaining the volume and ionic composition of body fluids, excreting metabolic waste products such as urea, and eliminating exogenous drugs, hormones, and toxins. The kidneys also serve as a major endocrine organ through the production of renin, erythropoietin, 1,25-dihydroxycholecalciferol, prostaglandins, and kinins. Metabolic functions of the kidney include catabolism of small-molecular-weight proteins and anabolic roles in ammoniagenesis and gluconeogenesis.

In a person weighing 70 kg, the kidney forms approximately 180 L of glomerular filtrate each day. Cardiac output in combination with effective intravascular volume generates hydraulic pressure that drives fluid from the capillaries into the urinary space, which represents the main mechanism of urine formation. The final urinary filtrate is determined by a complex interaction between hydraulic and oncotic pressure, molecular size and charge, absorption, reabsorption, and secretion under hormonal control.

Renal failure can be the result of dysfunction in any part of this system. It is helpful to understand the pathophysiology of renal disease as a set of three etiologic categories: prerenal, intrinsic renal, and postrenal causes.

Renal failure can be divided into two categories: primary disturbances and secondary disturbances. Primary disturbances reflect a direct failure of the kidneys to perform critical functions, such as failure to excrete sodium (leading to volume overload) or a decrease in erythropoietin production (leading to anemia). Secondary disturbances result from an accumulation of metabolic products in other organ systems, as when hyperphosphatemia causes hyperparathyroidism or when nitrogenous waste products promote platelet dysfunction. The combination of primary and secondary disturbances disrupts the homeostatic balance of almost every organ system.

Presenting Signs and Symptoms

Manifestations may vary greatly depending on the cause of the renal failure, but patients may describe a history of volume overload or decreased urine output. They may also have one or many of a long list of end-organ effects (Table 114.3). Renal failure is not a diagnosis that is necessarily obvious on initial encounter and is often made only after screening laboratory data are obtained.

Table 114.3 Organ System Effects of Renal Failure

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ABNORMALITY CAUSED BY RENAL FAILURE PHYSICAL FINDINGS, END-ORGAN EFFECT
Cardiovascular
Pulmonary edema Crackles
Hypertension  
Pericardial effusion  
Metabolic
Hyperkalemia Peaked T waves, arrhythmias, bradycardia, cardiac arrest
Hypocalcemia Tetany, cardiac arrhythmias
Hypermagnesemia Nausea and vomiting, arrhythmias
Neurologic
Uremia Seizures
Acute and chronic neurologic changes HyperreflexiaEncephalopathy, including asterixisSensory neuropathy
Hyponatremia or hypernatremia Altered mental status, seizures
Dialysis-associated dementia Loss of cognitive function
Immunologic
Immunosuppression Recurrent infections
Pulmonary
Fluid overload: pleural effusions, pulmonary edema Shortness of breath, hypoxia, crackles, dullness to percussion, peripheral edema
Gastrointestinal
Gastritis Abdominal pain
Bleeding Melena
Malnutrition Cachexia, anemia
Endocrine
Glucose intolerance Hyperglycemia
Renal osteodystrophy Myopathy Amyloid arthropathySecondary hyperparathyroidism Bone and joint pain, myalgias
Skin
Uremia Pruritus, uremic frost (urea crystals from sweat on skin)
Cardiovascular
Uremic pericarditis Pericardial friction rub, chest pain worse with lying down, ECG changes: ST elevation and PR depression (only some or none of these may be seen)
Myocardial infarction ST elevation in anatomic distribution or elevated enzymes
Acidosis Hypotension
Hematologic
Uremic platelets Bleeding