Renal Failure

Foundations

The hallmark of AKI (formerly termed acute renal failure [ARF]) is progressive azotemia, which commonly is accompanied by a wide range of other disturbances, depending on the severity and duration of renal dysfunction. These include metabolic derangements (e.g., metabolic acidosis, hyperkalemia), disturbances of body fluid balance (particularly volume overload), and a variety of effects on almost every organ system ( Box 83.1 ).

The causes of AKI are divided into those that decrease renal blood flow (prerenal), produce a renal parenchymal insult (intrarenal), or obstruct urine flow (obstructive, or postrenal). Identification of a prerenal or postrenal cause of AKI generally makes it possible to initiate specific corrective therapy; if these two broad categories of AKI can be excluded, an intrarenal cause is implicated. The renal parenchymal causes of AKI can be usefully subdivided into those primarily affecting the glomeruli, intrarenal vasculature, or renal interstitium. The term acute tubular necrosis denotes another broad category of intrinsic renal failure that cannot be attributed to a specific glomerular, vascular, or interstitial cause ( Fig. 83.1 ).

Renal failure can lead to numerous other systemic and organ-specific effects. Uremia impairs host defenses, particularly leukocyte function, and infection is a significant cause of morbidity and mortality in AKI. Pericarditis, which has a prevalence of 10% to 20% in dialyzed patients with CKD, also may occur in patients with AKI. Urgent dialysis is indicated when there is associated pericardial effusion and tamponade. Neurologic abnormalities in AKI may be precipitated by electrolyte abnormalities, medications, or uremia. Anorexia, nausea, vomiting, gastritis, and pancreatitis also are associated with AKI and significant gastrointestinal (GI) hemorrhage is seen in about 10% of patients.

Impaired erythropoiesis, shortened red blood cell (RBC) survival, hemolysis, hemodilution, and GI blood loss all play a role in the normocytic normochromic anemia that usually accompanies AKI. Although mild thrombocytopenia may be present, it is the qualitative defect in platelet function thought to be caused by the effect of circulating uremic toxins that contributes to these patients’ bleeding tendencies.

Clinical Features

When the presence of azotemia or renal failure has been discovered, the first consideration in the ED evaluation should be the possibility of potentially life-threatening complications (e.g., hyperkalemia, pulmonary edema). Assuming that these have been satisfactorily ruled out, the next step is to determine whether the condition represents AKI or is the result of preexisting renal disease. The clinical distinction between AKI and CKD often is difficult, especially if prior records and laboratory results are not available. The finding of small kidneys on abdominal imaging or bone changes of secondary hyperparathyroidism on hand films demonstrating abnormal calcifications suggests that the renal failure is chronic. Anemia, hypocalcemia, and hyperphosphatemia, however, should not be relied on to identify patients who have CKD because these abnormalities can develop rapidly in AKI.

In evaluating the patient with azotemia, the emergency clinician uses history, physical examination, and laboratory studies to seek clues to the cause and to identify signs and symptoms of uremia, volume overload, or other complications of renal failure. In attempting to identify the cause, the general strategy is to rule out prerenal and postrenal causes before considering the many intrinsic renal causes. First, potential sources of volume loss and causes of decreased cardiac output are sought in the history, and the patient should be questioned about lightheadedness, bleeding, GI fluid loss, abnormal polyuria, or symptoms of congestive heart failure (CHF). In men, a history of nocturia, frequency, hesitancy, or decreased urinary stream suggests prostatic obstruction. A history of lower tract symptoms or of abdominal or pelvic tumor in either gender is sought, as is a history of kidney stones or chronic urinary tract infection (UTI). A history of acute anuria, defined as the production of less than 100 mL of urine/day, is most often the result of high-grade urinary tract obstruction, although it also may accompany severe volume depletion, severe acute glomerulonephritis, cortical necrosis, or bilateral renal vascular occlusion. Intermittent anuria, on the other hand, is characteristic of obstructive disease. Medication use and possible exposure to radiographic contrast agents or other exogenous toxins are other key components of the history. A history of hypertension, dark-colored urine, rash, fever, or arthritis suggests intrinsic renal disease or a multisystem disorder.

The physical examination focuses on signs of volume depletion, such as tachycardia and decreased skin turgor. Documented short-term changes in body weight also offer a valuable clue in assessing volume status, particularly in patients who are chronically ill. Volume overload is suggested by findings of jugular vein distention and the presence of rales or peripheral edema.

A distended bladder is percussible when it contains at least 150 mL of urine, and the dome is palpable abdominally when the bladder contains 500 mL. Ultrasonography can be used to detect bladder distention or postvoid residual volume if there is a question of urinary retention. A prostate examination in men and pelvic examination in women are also necessary components of the examination. The presence of rash, purpura, pallor, or petechiae on skin examination may be noted, as is arthritis, musculoskeletal tenderness, and findings suggestive of infection or malignancy.

Differential Diagnosis

The management of AKI requires a systematic approach to the potential underlying causes. Once prerenal and postrenal causes are considered, the diagnostic and management strategies focus on the intrarenal pathologies.