The kidneys are responsible for a number of vital homeostatic processes, including the excretion of nitrogenous waste products, the regulation of fluid volume and electrolytes, acid–base balance, and the production of hormones important for blood pressure regulation, erythropoiesis, and bone metabolism. They are frequently affected by disease, both acute (occurring over days to weeks) and chronic (occurring over months to years), and the prevalence and incidence of these disease processes in the United States and globally are rising. Acute kidney injury (AKI), formerly known as acute renal failure, has become an increasingly common cause of hospitalization with an incidence of 5–7% among hospitalized patients. Chronic kidney disease (CKD) reportedly affects 13% of adults in the United States1 and is associated with significant morbidity, mortality, and high costs of hospitalization. Furthermore, the recent advent of automatic reporting of estimated glomerular filtration rate (eGFR) with serum creatinine by hospital laboratories has resulted in more patients being identified as having impaired renal function. In order to provide the highest level of care for patients presenting with acute or CKD, the clinician should have a strong understanding of the fundamental issues relevant to their evaluation and management.

History and Physical Examination

The evaluation of the patient with kidney disease begins with a thorough history and physical examination. The clinician should identify early on whether the renal disease is an acute or chronic condition. If previous medical records are available for the patient, this can be determined by quickly reviewing prior laboratory testing, with particular attention given to serum creatinine, blood urea nitrogen, and urinalyses. Patients who present on admission with AKI should be questioned about recent symptoms (eg, vomiting, diarrhea, edema, difficulty voiding, decreased appetite, weight changes) and events (eg, changes in oral intake, new medications, history of nonsteroidal anti-inflammatory drug [NSAID] use, administration of intravenous contrast, recent colonoscopy) that may help narrow the differential diagnosis of AKI. The presence of symptoms such as fever, rashes, arthralgias, epistaxis, and hemoptysis may be suggestive of an underlying systemic disease process such as vasculitis or other inflammatory conditions. For patients who develop AKI during their hospitalization, a thorough review of the most recent hospital events—including episodes of hypotension, recent diagnostic and therapeutic procedures, and initiation of new medications—should be performed. All patients presenting with acute or CKD should be questioned about symptoms associated with uremia, including fatigue, nausea, vomiting, pruritus, metallic taste, lethargy, and confusion, since the presence of these symptoms may indicate the need for dialysis.

A past medical history should be elicited to identify a prior history of kidney disease or other systemic diseases that could be relevant to the current presentation. In patients with CKD, who may or may not be presenting with an acute kidney-related problem, the clinician should establish the underlying cause, chronicity, and severity of the kidney disease. If the patient has end-stage renal disease (ESRD), information about the patient’s nephrologist, outpatient dialysis unit, and regular dialysis schedule (including the timing of the last dialysis session) should be obtained and conveyed to the clinicians and other health care providers who will be facilitating the patient’s dialysis during the hospitalization. The clinician should also obtain a complete and current list of the patient’s medications, which should include prescription medications as well as all over-the-counter medications, herbal remedies, and supplements. A family history of kidney disease or other systemic illnesses should also be documented.

The physical examination starts with a careful assessment of the patient’s vital signs. The presence of a fever should always raise suspicion for an infection, particularly in dialysis patients or immunosuppressed patients, but can also be observed in the setting of acute kidney diseases such as acute glomerulonephritis, vasculitis, and allergic interstitial nephritis. Blood pressure may be elevated (eg, in acute nephritic syndrome, malignant hypertension, scleroderma, long-standing kidney disease), normal, or low (eg, in volume depletion, sepsis, cirrhosis, heart failure). The clinician should closely review the patient’s intake and output records to (1) ensure that the proper oral and intravenous fluids, if needed, are being administered to the patient at an appropriate frequency and rate depending on the patient’s clinical context, and (2) to evaluate the patient for evidence of positive or negative fluid balances that could contribute to volume overload or depletion, respectively.

Key aspects of the physical examination include (1) determination of the patient’s volume status, (2) identification of physical manifestations that can be associated with specific renal disease conditions, and (3) assessment for signs of uremia. Assessment of volume status is important for both the accurate diagnosis and management of most renal diseases. In the setting of prerenal acute kidney injury, for instance, the presence of hypervolemia (eg, elevated jugular venous pressure, pulmonary congestion, peripheral edema) could be suggestive of decreased renal perfusion from congestive heart failure or cirrhosis, whereas the presence of hypovolemia (postural pulse increase > 30 beats/min, severe postural dizziness, dry axilla and/or mucous membranes) would be more consistent with a diagnosis of volume depletion from bleeding or gastrointestinal losses. To best assess the jugular venous pulsation, the patient should be reclined with the head elevated at 30–45 degrees, and the elevation of the right internal jugular vein above the sternal angle should be measured. Certain physical findings (eg, edema, abdominal bruits, palpable purpura, warm and swollen joints) can be associated with specific renal diseases. Palpable purpura may be observed in vasculitic processes such as Wegener granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome. Abdominal bruits in the patient with refractory hypertension and progressive renal failure may be suggestive of renovascular disease. A funduscopic examination can reveal arteriolar narrowing, hemorrhages, exudates, or papilledema—findings consistent with chronic hypertension. Only a comprehensive physical examination will enable the clinician to identify these and other particular findings (see Table 57-1).

Patients with uremia can have a number of different physical examination findings. Evidence of uremic pericarditis or pleuritis may be present, as manifested by a pericardial or pleural friction rub, respectively. The pericardial friction rub classically has three components, one systolic and two diastolic, and a scratchy or grating quality. Skin and nail changes may include uremic frost (fine residue of excreted urea remaining on the surface of the skin), skin hyperpigmentation, or “half-and-half” nails (sharp demarcation between proximal and distal nail halves). Patients who have fluid retention may have pulmonary congestion or peripheral edema. Neurological findings can include confusion, coma, asterixis, and sensory deficits. As with the clinical symptoms of uremia, the presence of these physical findings, especially the pericardial friction rub and neurological abnormalities, may indicate the need for dialysis.

Laboratory Tests

Serum Electrolytes

Serum electrolytes are essential to the evaluation of the patient with both acute and chronic renal disease. Serum sodium concentration provides insight into the water balance of a patient and can identify patients with hyponatremia and hypernatremia, both of which can be seen in patients with kidney disease. Monitoring serum po tas sium levels is vital, since impaired renal function decreases renal po tas sium excretion and can lead to potentially life-threatening hyperkalemia in oliguric or anuric patients. The clinician should be aware that the serum potassium concentration might not be an accurate indicator of total body potassium stores, since the majority of total body potassium is confined to the intracellular fluid compartment. This is evident, for example, in patients with diabetic ketoacidosis whose labs reveal elevated serum potassium levels in spite of diminished total body potassium stores. Serum chloride and bicarbonate levels are useful to the assessment of volume and acid–base status. The serum anion gap can be calculated from serum sodium, chloride, and bicarbonate concentrations (AG = Na+ – [Cl– + HCO3–]) and used to narrow the differential diagnosis of metabolic acidosis. Serum calcium, phosphorus, and magnesium levels should also be monitored in patients with renal disease, as these electrolytes yield important information about renal tubular function and bone mineral metabolism. Hyperphosphatemia and hypocalcemia are commonly seen in patients with acute and chronic renal disease and contribute to the development of secondary hyperparathyroidism.

Blood Urea Nitrogen and Creatinine

Serum blood urea nitrogen (BUN) and creatinine are both nitrogenous end products of metabolism that generally rise in the setting of renal disease. Urea is formed from ammonia derived from the breakdown of dietary and tissue proteins, whereas creatinine is a by-product of muscle creatine metabolism. Urea and creatinine are both freely filtered by the kidneys but handled differently in the tubular system; whereas urea is partly reabsorbed by the proximal tubule and inner medullary collecting duct, creatinine is secreted to a small extent by the tubules. Despite these tubular alterations, BUN and creatinine are still the most commonly used biomarkers of renal function. Neither of these tests, however, is ideal for the early detection of renal disease. Elevations in serum BUN can be seen in other nonrenal factors, such as high protein intake, upper gastrointestinal tract bleeding, and states of high catabolism (fever, corticosteroids, and burns). Serum creatinine can also be affected by a variety of factors, including muscle mass and medications that impair tubular creatinine secretion (eg, trimethoprim, cimetidine, older cephalosporins). Though BUN and creatinine have traditionally been used as the primary biomarkers of renal injury, their use may decrease in the future in favor of more sensitive and specific biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), and cystatin C.

Estimated Glomerular Filtration Rate

All patients with kidney disease, both acute and chronic, should have their kidney function assessed by estimation of the glomerular filtration rate (GFR). GFR can be estimated by a few common methods, including (1) measurement of serum creatinine, (2) calculation of creatinine clearance, and (3) use of estimation equations such as the Cockcroft-Gault formula (creatinine clearance) or the Modification of Diet in Renal Disease (MDRD) equation (GFR). The normal GFR in a healthy adult is > 90 mL/min. There is an expected decrease in GFR with age, of approximately 1 mL/min/year after age 35. Elderly patients may also have lower creatinine levels due to decreased muscle mass. Measurement of serum creatinine is the simplest to perform and has been the most frequently used surrogate for GFR. However, given that serum creatinine concentration can be affected by several factors, including an individual’s muscle mass, dietary protein intake, and certain medications, it is not the most accurate method of estimating GFR. Both the Cockcroft-Gault and MDRD equations are relatively complex formulas that take into account serum creatinine as well as other defined factors such as age, race, gender, and weight. They were designed to estimate GFR in patients with established CKD and are most useful for this purpose. As these equations have yet to be well validated in specific populations, including individuals with normal or near-normal renal function, children and elderly individuals, and certain ethnic groups, they should be interpreted with caution in these patients. Furthermore, it is important to understand that serum creatinine and the estimation equations should only be used to approximate GFR in patients with stable kidney function (unchanging serum creatinine). If the clinician is uncertain about the accuracy of GFR estimation, a 24-hour urine collection can be performed to calculate creatinine clearance.

Proteinuria

Proteinuria, one of the hallmarks of kidney damage, is most frequently detected qualitatively by urine dipstick, which grades proteinuria on a scale of concentration: trace, 1+ (30 mg/dL), 2+ (100 mg/dL), 3+ (300 mg/dL). Normal urine may test slightly positive if very concentrated. The urine dipstick is only capable of detecting albumin in the urine, which is the most abundant protein seen with glomerular proteinuria; thus the presence of other proteins such as immunoglobulin light chains will not be detected by dipstick alone. The finding of proteinuria by dipstick should prompt a more accurate quantification, either by a single random measurement of urine protein and urine creatinine concentration to determine the urine protein-to-creatinine ratio or by a 24-hour urine collection for protein and creatinine excretion rate. Small amounts of urinary albumin (30–300 mg/L) that cannot be detected by dipstick can be quantified by measuring a urine microalbumin concentration and normalized to a creatinine measurement in the same sample.

Hematuria

Hematuria is defined as the presence of red blood cells in the urine. In the absence of gross bleeding, hematuria is most commonly discovered on a urine dipstick (which detects the pseudoperoxidase activity of hemoglobin) or urinalysis. False-positive dipstick results are seen in the setting of hemoglobinuria, myoglobinuria, menstrual blood in the urine, vigorous exercise, and concentrated urine. If significant proteinuria or renal dysfunction is also present, the kidney should be considered the source of hematuria until proven otherwise, and a renal biopsy should be considered to establish a diagnosis. In the absence of these findings, microscopic hematuria is considered to be isolated hematuria. The differential diagnosis of isolated microscopic hematuria can be divided into renal (glomerular) or extrarenal (nonglomerular) processes. Immunoglobulin A (IgA) nephropathy, thin basement membrane disease, and Alport syndrome are three of the most common causes of glomerular hematuria, though any form of acute or chronic glomerulonephritis can be a potential source. Common etiologies of nonglomerular hematuria include urinary tract infections, kidney stones, urinary tract tumors, trauma, bladder polyps, cystic kidney diseases (eg, polycystic kidney disease, medullary cystic disease), and metabolic abnormalities such as hypercalciuria and hyperuricosuria. Hematuria associated with exercise, especially running, is usually a benign condition in which the bleeding source is likely renal pelvis. Hematuria associated with glomerular bleeding may or may not be associated with flank pain, and ureteral causes that obstruct the urinary tract can be a source of severe pain and renal colic. Hematuria in other cases is usually painless. In extrarenal hematuria, the red blood cells typically appear normal on urinary sediment, round and uniform, whereas in glomerular hematuria, the red blood cells may appear dysmorphic due to distortion from the passage through the glomerular filtration barrier. Imaging studies are indicated to search for a structural cause of hematuria. Detection of persistent extrarenal hematuria should prompt further workup and consultation with a urologist to identify the source of bleeding. In older individuals particularly, bladder cancer should be considered. In cases of isolated glomerular hematuria, a renal biopsy is not typically indicated, since the pathologic diagnosis rarely has any effect on the management or outcome.

Abnormal Urinalysis

The examination of the urinary sediment by microscopy is one of the most valuable tests in the evaluation of the renal patient and can provide useful diagnostic information about both acute and CKD. Urine particles lyse easily after collection, and therefore urine samples should be examined within 2 to 4 hours of acquisition. Certain characteristic findings on urinalysis may point the clinician toward a specific diagnosis. The presence of red blood cells, when greater than 1–2 per high-power field, generally indicates hematuria (see Hematuria). White blood cells (pyuria), when greater than 2 per high-power field, can be observed with upper or lower urinary tract infections, contamination from genital secretions, or inflammation in the kidney, as in interstitial nephritis or acute glomerulonephritis. Urinary casts are cylindrical aggregates of protein and/or cells that form in the lumen of the distal convoluted tubule or collecting duct and are excreted into the urine. Hyaline casts, the most common type of cast, are acellular and consist primarily of Tamm-Horsfall mucoprotein produced by tubular epithelial cells. They can be seen in the setting of dehydration or vigorous exercise in normal patients who produce concentrated urine but can be seen in patients with proteinuria. Granular casts, the second most common type of cast, are usually formed from degenerating cellular casts or protein-containing lysosomes and can appear fine or coarse in texture. “Muddy brown” granular casts contain degenerating tubular epithelial cells and are commonly seen in acute tubular injury. Fatty casts are hyaline casts that contain lipid droplets and can be observed in patients with diseases causing lipiduria, such as the nephrotic syndrome. When red blood cells leak through the glomerular filtration barrier, they can form red blood cell casts in the tubular lumen, a finding that is consistent with acute glomerulonephritis. White blood cell casts are indicative of inflammation or infection in the kidney and can be seen in acute glomerulonephritis, interstitial nephritis, and acute pyelonephritis. Red blood cell casts and white blood cell casts are always pathologic findings and should prompt further evaluation of the patient for the clinical entities already mentioned.

Urine Chemistries

Urine chemistries, consisting primarily of the urinary sodium, potassium, chloride, and creatinine, can be useful in the evaluation of a number of renal conditions. In the setting of acute kidney injury, a fractional excretion of sodium (FENa) in combination with clinical history and other lab tests may help differentiate between prerenal etiologies and acute tubular necrosis (ATN). The FENa can be calculated by the following formula: (urine Na+ × plasma creatinine)/(plasma Na+ × urine creatinine) × 100. A FENa of < 1% is commonly seen in prerenal causes of oliguria, and a FENa > 2% is usually indicative of ATN. There are limitations to the use of the FENa, however, since a FENa of < 1% can also be seen in a number of other diseases, such as contrast-induced nephropathy, pigment nephropathy due to rhabdomyolysis, acute glomerulonephritis, hepatorenal syndrome, early urinary obstruction, acute interstitial nephritis, and even ATN. Furthermore, a FENa may be difficult to interpret in the setting of a patient taking diuretics. In such cases, calculating a fractional excretion of urea (FEurea) may be a more sensitive test to differentiate prerenal AKI (FEurea < 35%) from ATN (FEurea 50–65%).

In the setting of a nonanion gap metabolic acidosis, one can calculate a urine anion gap (UAG) to help differentiate between gastrointestinal losses of bicarbonate (eg, diarrhea) and renal tubular acidosis using the following formula: (urine Na+ + urine K+) – urine Cl–. A negative UAG is consistent with gastrointestinal losses, whereas a positive UAG is frequently seen with renal tubular acidosis.

Serum Enzymes

Serum enzyme levels should be interpreted cautiously in patients with impaired renal function, especially those with ESRD undergoing hemodialysis or peritoneal dialysis. These patients frequently have elevations in various serum enzyme levels due to decreased renal clearance, though abnormally low levels can occasionally be encountered. Such lab abnormalities can confound the diagnosis of certain diseases, which are often detected by increases in the levels of these serum enzymes. Cardiac enzymes, including cardiac troponin T (cTnT), cardiac troponin I (cTnI), and the MB isoenzyme of creatine kinase (CK-MB), are commonly used to detect acute coronary syndromes and to appropriately triage patients to coronary care units. This is particularly relevant to patients with CKD and ESRD, in which cardiovascular disease is highly prevalent. However, patients with impaired renal function often have elevated levels of cardiac troponins and CK-MB even in the absence of acute myocardial injury. A large percentage of false-positive elevations in cTnT and CK-MB are seen in patients with ESRD when these markers are used to diagnose acute myocardial infarction (MI). The use of cTnI is less likely to be associated with false-positive elevations, and serial measurements of cTnI are currently the most specific marker of myocardial damage in patients with renal failure and suspected acute MI.

The serum levels of liver and pancreatic enzymes can also be affected in patients with renal failure. Serum aminotransferase levels are frequently found to be in the lower range of normal values in patients with CKD and ESRD. In the absence of liver disease, gammaglutamyl transpeptidase (GGT) levels are most often normal but may be elevated in a small percentage of patients. Serum alkaline phosphatase levels are often elevated in dialysis patients, usually as a result of coexisting bone disease. An isolated elevation in serum alkaline phosphatase may not correlate well with hepatobiliary disease in ESRD patients; however, if a chronically elevated alkaline phosphatase level is accompanied by an elevation in serum GGT or 5′-nucleotidase, one should be more suspicious of an obstructive or infiltrative hepatobiliary process. Elevations in both serum amylase and lipase levels can be observed in patients with CKD and ESRD, even when acute pancreatitis is not present. The levels of these pancreatic enzymes in these patients are commonly threefold to fivefold higher (but typically less than three times the upper limit of normal) and may make the accurate diagnosis of acute pancreatitis more difficult. The elevations are due primarily to decreased renal clearance of these enzymes, though in the case of serum lipase, the use of heparin during hemodialysis has also been found to contribute to elevated levels.

Imaging Studies

Ultrasonography

Ultrasonography is a safe, noninvasive, rapid, and inexpensive diagnostic imaging modality used to study the kidneys. One distinct advantage of ultrasonography is that it requires neither ionizing radiation nor a potentially toxic intravenous contrast agent, which makes it a safe initial imaging study, especially for patients with known renal insufficiency. Renal ultrasonography can provide valuable information about kidney size, shape, and gross appearance. Normal adult kidneys are approximately 9–13 cm (4–5 inches) in length and 5–7.5 cm (2–3 inches) in width and should not differ by much more than 1 cm. With chronic injury, the renal parenchyma becomes replaced with fibrotic tissue and the renal cortex becomes thinner, causing diseased kidneys to shrink in size. In patients in which the chronicity of kidney disease is uncertain, the finding of smaller-sized kidneys on ultrasonography is suggestive of longstanding kidney disease. A number of conditions are associated with large kidneys, such as autosomal dominant polycystic kidney disease, urinary tract obstruction, HIV nephropathy, the early stages of diabetic nephropathy, and infiltrative diseases such as amyloidosis or kappa light chain nephropathy associated with multiple myeloma. Asymmetry in kidney size may indicate unilateral kidney disease, and the clinician must determine whether the smaller or larger kidney is abnormal. Increased echogenicity in the kidneys is a commonly reported and nonspecific finding, usually denoting medical renal disease. Renal ultrasonography can also identify the presence of cysts, stones, or masses in the kidney. In the patient presenting with acute kidney injury, renal ultrasonography can be useful in identifying obstructive uropathy, which usually manifests as hydronephrosis, although false-negative results can be seen in patients with early obstruction (less than 3–4 days), coexisting volume depletion, or obstruction caused by retroperitoneal fibrosis or compression by retroperitoneal or intraparenchymal tumor or blood.

Doppler Ultrasonography

Doppler ultrasonography can provide information about the presence and flow of blood through the vessels of the kidney. High-velocity or disorganized flow patterns can be seen in patients with hemodynamically significant renal artery stenosis. In addition, information about the vascular resistive indices can be obtained; elevated resistive indices (> 0.80) in a stenotic kidney are suggestive of severe parenchymal disease and a low likelihood of response to revascularization. Given the potential toxicities of using iodinated contrast agents or gadolinium, particularly in patients with impaired renal function, Doppler ultrasonography has recently become more widely used as the initial imaging study to evaluate renal artery stenosis. It is important to note that the sensitivity of Doppler ultrasonography is highly operator dependent and can be affected by factors such as patient anatomy.

Computed Tomography

Computed tomography (CT) can be instrumental to the evaluation of renal disease. In the evaluation of the patient with suspected renal colic, noncontrast helical CT scanning is currently the gold standard for diagnosing nephrolithiasis and can detect essentially all kidney stones with the exception of indinavir stones. Noncontrast can also be useful to detect ureteric obstruction in a patient with acute kidney injury, particularly when intravenous (IV) contrast is to be avoided due to nephrotoxicity. The administration of IV iodinated contrast permits the visualization of other disease processes. Imaging of the renal parenchyma is enhanced by IV contrast and facilitates the evaluation and detection of renal mass lesions such as renal cell carcinoma. CT angiography is one of the modalities of choice in evaluating the renal vasculature and can be used to diagnose suspected renal artery stenosis or aneurysms. CT urography allows imaging of the collecting system and can identify filling defects such as stones, blood clots, and tumors. The drawback to the use of iodinated contrast agents is the potential nephrotoxicity, especially in patients with preexisting renal impairment, diabetes, heart failure, or hypovolemia (see Contrast-Induced Nephropathy). In patients with ESRD who have residual renal function, administration of contrast dye can induce further tubular damage and lead to loss of the remaining renal function. As preservation of residual renal function in patients with ESRD has been shown to correlate with improved survival even after the initiation of dialysis, the use of contrast in these patients should be avoided if possible.

Magnetic Resonance Imaging

The primary role of magnetic resonance imaging (MRI) in renal imaging is in the evaluation of renal masses. MRI can effectively differentiate benign versus malignant lesions in the kidney, especially when CT scanning with intravenous iodinated contrast is contraindicated or if ultrasonographic and CT scans have been nondiagnostic. MR angiography (MRA), which involves the administration of intravenous gadolinium, has become the modality of choice in the evaluation of renovascular disease. According to one meta-analysis, gadolinium-enhanced MRA had a reported sensitivity of 97% and specificity of 85% for the detection of renal artery stenosis.2 However, the use of gadolinium-based contrast agents in patients with moderate to severe CKD, especially those on dialysis, has been associated with the development of nephrogenic systemic fibrosis (NSF), a debilitating condition characterized by fibrosis of the skin, joints, eyes, and other internal organs. Given the risk of NSF, patients with an estimated GFR < 30 mL/min or requiring dialysis should not be administered gadolinium-based contrast agents. In these patients, Doppler ultrasonography may be a safer alternative study.

Radionuclide Scans

Radionuclide studies are capable of providing functional information about the kidneys that is not detected by ultrasonography, CT, or MRI. Static radionuclide scans employ a radiolabeled tracer (eg, technetium 99m-DMSA) that binds to renal parenchymal cells but is not excreted into the tubules. These studies are most useful in quantifying the functional cortical tissue of each kidney and determining the percentage contribution of each kidney to total renal function. Dynamic radionuclide scans use tracers (eg, technetium 99m-DTPA, technetium 99m-MAG3) that are taken up by nephrons and then excreted into the collecting system. A diuretic such as furosemide is often administered just prior to injection of the tracer in order to ensure high levels of diuresis during the study. Dynamic scans can be used to evaluate potential renal tract obstructions as well as the response to treatment of the obstruction. Formerly used in the diagnosis of renovascular hypertension by providing a functional assessment, captopril renal scans have been more recently replaced by duplex Doppler ultrasonography, CT, and MRA, which have a higher sensitivity and specificity.

Acute kidney injury (AKI), formerly termed acute renal failure, is a sudden and sustained decline in renal function that results in the failure to excrete metabolic waste products, maintain fluid and electrolyte balance, and regulate acid–base homeostasis. AKI is an increasingly common cause of hospitalization, with 1% of all patients reported to have AKI upon admission to the hospital and 2–5% of inpatients subsequently developing AKI during their hospitalization. In spite of advances in intensive care and dialysis support over the last 50 years, the overall mortality rate of AKI continues to remain high, ranging from 20 to 90% depending on the severity of patient illness and the medical setting. The role of the hospitalist is to be able to acknowledge and diagnose common causes of AKI, to initiate management by identifying and treating reversible factors, to recognize when patients with AKI require dialysis as an intervention, and to know when to appropriately consult a nephrologist.

Numerous definitions covering the entire spectrum of severity of AKI have been previously proposed, but only recently have efforts been made to devise a more uniform definition for AKI. Two classification systems, the RIFLE and AKIN criteria, have defined and stratified AKI by stages of severity based on graded increases in serum creatinine and periods of decreased urine output (Table 57-2). The more recent AKIN criteria have proposed a definition for AKI that incorporates the prognostic significance associated with small changes in serum creatinine. The diagnosis of AKI can be established by (1) an abrupt (within 48 hours) absolute increase in serum creatinine of ≥ 0.3 mg/dL from baseline, (2) a percentage increase in serum creatinine of ≥ 50%, or (3) oliguria of ≤ 0.5 mL/kg/hour for > 6 hours. Although both the RIFLE and AKIN classification systems have been validated in a variety of clinical settings, their utility at this time appears to be greater for research use than for the bedside.