114 Renal Failure
Key Points• Management of renal failure in the emergency department should be aimed at identifying and treating life-threatening abnormalities associated with the disorder, identifying reversible causes of renal failure, and preventing further injury to the kidneys.
• Acute pulmonary edema and hyperkalemia are potentially life-threatening complications of renal failure.
• Severe hyperkalemia should be suspected as the cause of cardiac arrest in patients with a possible history of renal failure.
• An electrocardiogram should be obtained for all patients with renal failure on arrival at the emergency department to screen for hyperkalemia.
Definitions
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).
1. Prerenal failure results from the kidneys not receiving enough blood via a cause external to the kidneys themselves; it results in a reduced GFR, buildup of toxic waste products, and damage to the kidneys persisting after the underlying cause has been corrected. Causes of prerenal failure include hypovolemia, decreased cardiac output, and septic shock.
2. Renal failure may be caused by diseases intrinsic to the kidneys, including genetic syndromes such as polycystic kidney disease, infections, vascular diseases, and toxins or drugs.
3. Postrenal failure may result from obstruction to urinary flow external to the kidneys themselves. The obstruction causes increased fluid pressure within the nephron, which ultimately leads to loss of function. Ureteral stones, prostatic hypertrophy, tumors, and anticholinergic medications are some possible causes of postrenal kidney failure.
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
| 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 |
