Family Medicine 8600 Chicago Rd Warren, Mi 48093
Am Fam Physician. 2012 October ane;86(7):631-639.
Article Sections
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
Astute kidney injury is characterized by abrupt deterioration in kidney function, manifested by an increment in serum creatinine level with or without reduced urine output. The spectrum of injury ranges from mild to avant-garde, sometimes requiring renal replacement therapy. The diagnostic evaluation can be used to classify astute kidney injury every bit prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to identify the use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or straight impair renal role. Concrete examination should assess intravascular volume condition and identify pare rashes indicative of systemic affliction. The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in most patients, particularly in older men, to dominion out obstruction. Management of astute kidney injury involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; book overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of chance factors (eastward.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early on diagnosis, and aggressive direction are critical for improving outcomes.
The incidence of acute kidney injury has increased in recent years, both in the customs and in infirmary settings.1,2 The estimated incidence of acute kidney injury is two to iii cases per ane,000 persons.3 7 percent of hospitalized patients and about two-thirds of patients in intensive intendance units develop acute kidney injury,2 often every bit part of the multiple organ dysfunction syndrome.four
SORT: Key RECOMMENDATIONS FOR Practice
| Clinical recommendation | Evidence rating | References |
|---|---|---|
| The diagnosis of acute kidney injury is based on serum creatinine levels, urine output, and the need for renal replacement therapy. | C | 8 |
| Renal ultrasonography should be performed in most patients with acute kidney injury to rule out obstruction. | C | 17 |
| Adequate fluid balance should be maintained in patients with acute kidney injury by using isotonic solutions (e.chiliad., normal saline) instead of hyperoncotic solutions (e.g., dextrans, hydroxyethyl starch, albumin). | C | 19 |
| Dopamine use is non recommended for the prevention of acute kidney injury. | A | 21 |
| Diuretics do not improve morbidity, mortality, or renal outcomes, and should not be used to foreclose or treat astute kidney injury in the absence of book overload. | A | 22 |
| Consider therapy with immunosuppressive agents (e.yard., cyclophosphamide, prednisone) in patients with rapidly progressive glomerulonephritis. | C | 23 |
Astute kidney injury is associated with a high charge per unit of adverse outcomes; bloodshed rates range between 25 and 80 percent, depending on the cause and the clinical status of the patient.5–seven These data highlight the importance of recognition and appropriate direction, usually in collaboration with nephrologists and other subspecialists.
Definition
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
Acute kidney injury is divers as an abrupt (inside 48 hours) reduction in kidney part based on an elevation in serum creatinine level, a reduction in urine output, the need for renal replacement therapy (dialysis), or a combination of these factors. Information technology is classified in iii stages (Table one).8 The term acute kidney injury should supervene upon terms such as acute renal failure and acute renal insufficiency, which previously have been used to depict the same clinical condition.
Tabular array one.
Stages of Acute Kidney Injury
| Phase | Change in serum creatinine level | Urine output | Other |
|---|---|---|---|
| 1 | Increase ≥ 0.iii mg per dL (26.52 μmol per Fifty) or ≥ ane.5- to twofold from baseline | < 0.5 mL per kg per hour for more vi hours | — |
| 2 | Increase > two- to threefold from baseline | < 0.5 mL per kg per hour for more than than 12 hours | — |
| 3 | Increase > threefold from baseline or ≥ 4.0 mg per dL (353.60 μmol per L) with an acute rise of at least 0.5 mg per dL (44.twenty μmol per L) | < 0.three mL per kg per hour for 24 hours or anuria for 12 hours | Renal replacement therapy required |
Etiology
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Direction
- Prognosis
- Prevention
- References
The causes of acute kidney injury can be divided into three categories (Table 2ix): prerenal (caused by decreased renal perfusion, often considering of book depletion), intrinsic renal (caused by a process inside the kidneys), and postrenal (caused past inadequate drainage of urine distal to the kidneys). In patients who already have underlying chronic kidney affliction, any of these factors, but especially volume depletion, may cause acute kidney injury in addition to the chronic harm of renal part.
Table 2.
Causes of Astute Kidney Injury
| Prerenal | |
| Intrarenal vasoconstriction (hemodynamically mediated) | |
| Medications: nonsteroidal anti-inflammatory drugs,* angiotensin-converting enzyme inhibitors,* angiotensin receptor blockers,* cyclosporine (Sandimmune), tacrolimus (Prograf) | |
| Cardiorenal syndrome* | |
| Hepatorenal syndrome | |
| Intestinal compartment syndrome | |
| Hypercalcemia | |
| Systemic vasodilation (e.m., sepsis,* neurogenic shock) | |
| Book depletion | |
| Renal loss from diuretic overuse,* osmotic diuresis (e.g., diabetic ketoacidosis*) | |
| Extrarenal loss from airsickness, diarrhea,* burns, sweating, blood loss | |
| Intrinsic renal | |
| Glomerular (eastward.g., postinfectious and other glomerulonephritis) | |
| Interstitial | |
| Medications: penicillin analogues,* cephalosporins,* sulfonamides, ciprofloxacin (Cipro), acyclovir (Zovirax), rifampin, phenytoin (Dilantin), interferon, proton pump inhibitors, nonsteroidal anti-inflammatory drugs | |
| Infections (e.g., direct infection of renal parenchyma or associated with systemic infections) | |
| Viruses: Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus | |
| Bacteria: Streptococcus species, Legionella species | |
| Fungi: candidiasis, histoplasmosis | |
| Systemic affliction: sarcoidosis, lupus | |
| Tubular | |
| Ischemic: prolonged hypotension* | |
| Nephrotoxic: exogenous toxins (e.g., radiographic contrast agents,* aminoglycosides,* cisplatin, methotrexate, ethylene glycol, amphotericin B) and endogenous toxins (e.1000., hemolysis and rhabdomyolysis [pigment nephropathy], tumor lysis syndrome, myeloma) | |
| Vascular | |
| Renal vein thrombosis, malignant hypertension, scleroderma renal crunch, renal atheroembolic illness,* and renal infarction | |
| Postrenal | |
| Extrarenal obstacle: prostate hypertrophy*; neurogenic bladder; retroperitoneal fibrosis; float, prostate, or cervical cancer | |
| Intrarenal obstruction: stones,* crystals (acyclovir, indinavir [Crixivan]), clots, tumors | |
PRERENAL CAUSES
Approximately 70 pct of community-acquired cases of astute kidney injury are attributed to prerenal causes.10 In these cases, underlying kidney role may be normal, only decreased renal perfusion associated with intravascular volume depletion (east.1000., from vomiting or diarrhea) or decreased arterial pressure (e.g., from heart failure or sepsis) results in a reduced glomerular filtration charge per unit. Autoregulatory mechanisms often can compensate for some caste of reduced renal perfusion in an endeavour to maintain the glomerular filtration rate. In patients with preexisting chronic kidney disease, however, these mechanisms are dumb, and the susceptibility to develop acute-on-chronic renal failure is higher.11
Several medications can cause prerenal acute kidney injury. Notably, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers tin can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular force per unit area. Nonsteroidal anti-inflammatory drugs also tin decrease the glomerular filtration rate past changing the residuum of vasodilatory/vasoconstrictive agents in the renal microcirculation. These drugs and others limit the normal homeostatic responses to volume depletion and can be associated with a reject in renal function. In patients with prerenal acute kidney injury, kidney office typically returns to baseline after acceptable book condition is established, the underlying cause is treated, or the offending drug is discontinued.
INTRINSIC RENAL CAUSES
Intrinsic renal causes are also important sources of acute kidney injury and can be categorized by the component of the kidney that is primarily affected (i.eastward., tubular, glomerular, interstitial, or vascular).
Astute tubular necrosis is the nigh mutual blazon of intrinsic acute kidney injury in hospitalized patients. The cause is usually ischemic (from prolonged hypotension) or nephrotoxic (from an amanuensis that is toxic to the tubular cells). In contrast to a prerenal etiology, acute kidney injury caused by acute tubular necrosis does not improve with adequate repletion of intravascular volume and blood flow to the kidneys. Both ischemic and nephrotoxic acute tubular necrosis can resolve over time, although temporary renal replacement therapy may be required, depending on the degree of renal injury and the presence of preexisting chronic kidney illness.
Glomerular causes of acute kidney injury are the consequence of astute inflammation of blood vessels and glomeruli. Glomerulonephritis is commonly a manifestation of a systemic affliction (due east.m., systemic lupus erythematosus) or pulmonary renal syndromes (eastward.g., Goodpasture syndrome, Wegener granulomatosis). History, concrete examination, and urinalysis are crucial for diagnosing glomerulonephritis (Table 39 and Figure 1 12). Because management frequently involves administration of immunosuppressive or cytotoxic medications with potentially severe adverse effects, renal biopsy is often required to confirm the diagnosis before initiating therapy.
Tabular array 3.
History and Physical Examination Findings for Categorizing Acute Kidney Injury
| Type of astute kidney injury | History findings | Physical examination findings | |
|---|---|---|---|
| Prerenal | Volume loss (e.g., history of vomiting, diarrhea, diuretic overuse, hemorrhage, burns) | Weight loss, orthostatic hypotension and tachycardia | |
| Thirst and reduced fluid intake | Poor skin turgor | ||
| Cardiac affliction | Dilated cervix veins, S3 heart sound, pulmonary rales, peripheral edema | ||
| Liver disease | Ascites, caput medusae, spider angiomas | ||
| Intrinsic renal | |||
| Astute tubular necrosis | History of receiving nephrotoxic medications (including over-the-counter, illicit, and herbal), hypotension, trauma or myalgias suggesting rhabdomyolysis, recent exposure to radiographic contrast agents | Muscle tenderness, compartment syndrome, cess of book condition | |
| Glomerular | Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, hepatitis C virus infection, human immunodeficiency virus infection, hematuria, foamy urine, cough, sinusitis, hemoptysis | Periorbital, sacral, and lower-extremity edema; rash; oral/nasal ulcers | |
| Interstitial | Medication utilise (e.grand., antibiotics, proton pump inhibitors), rash, arthralgias, fever, infectious illness | Fever, drug-related rash | |
| Vascular | Nephrotic syndrome, trauma, flank hurting, anticoagulation (atheroembolic disease), vessel catheterization or vascular surgery | Livedo reticularis, funduscopic examination (showing cancerous hypertension), abdominal bruits | |
| Postrenal | Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer | Bladder distention, pelvic mass, prostate enlargement | |
Diagnosis and Treatment of Acute Kidney Injury
Figure one.
Algorithm for the diagnosis and treatment of acute kidney injury.
Adapted with permission from Smith MC. Acute renal failure. In: Resnick MI, Elder JS, Spirnak JP, eds. Clinical Decisions in Urology. tertiary ed. Hamilton, Ontario, Canada: BC Decker, Inc.; 2004:61.
Astute interstitial nephritis can exist secondary to many weather condition, merely most cases are related to medication use, making patient history the key to diagnosis. In about one-third of cases, there is a history of maculopapular erythematous rash, fever, arthralgias, or a combination of these symptoms.13 Eosinophiluria may be found in patients with acute interstitial nephritis, simply it is not pathognomonic of this illness. A kidney biopsy may exist needed to distinguish between allergic interstitial nephritis and other renal causes of acute kidney injury. In addition to discontinuing offending agents, steroids may be beneficial if given early in the course of disease.14
Astute events involving renal arteries or veins tin can as well atomic number 82 to intrinsic acute kidney injury. Renal atheroembolic disease is the most common cause and is suspected with a contempo history of arterial catheterization, the presence of a status requiring anticoagulation, or after vascular surgery. Physical test and history provide of import clues to the diagnosis (Tabular array iiinine). Vascular causes of acute kidney injury usually require imaging to confirm the diagnosis.
POSTRENAL CAUSES
Postrenal causes typically result from obstruction of urinary flow, and prostatic hypertrophy is the most common cause of obstruction in older men. Prompt diagnosis followed by early on relief of obstruction is associated with improvement in renal function in most patients.
Clinical Presentation
- Abstruse
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Direction
- Prognosis
- Prevention
- References
Clinical presentation varies with the cause and severity of renal injury, and associated diseases. Most patients with balmy to moderate astute kidney injury are asymptomatic and are identified on laboratory testing. Patients with severe cases, however, may exist symptomatic and present with listlessness, defoliation, fatigue, anorexia, nausea, airsickness, weight gain, or edema.fifteen Patients can also present with oliguria (urine output less than 400 mL per day), anuria (urine output less than 100 mL per twenty-four hour period), or normal volumes of urine (nonoliguric acute kidney injury). Other presentations of acute kidney injury may include evolution of uremic encephalopathy (manifested by a pass up in mental condition, asterixis, or other neurologic symptoms), anemia, or bleeding caused by uremic platelet dysfunction.
Diagnosis
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
A patient history and physical examination, with an emphasis on assessing the patient's volume status, are crucial for determining the crusade of acute kidney injury (Table three9). The history should identify employ of nephrotoxic medications or systemic illnesses that might crusade poor renal perfusion or direct impair renal function. Concrete examination should assess intravascular volume status and any skin rashes indicative of systemic disease. The initial laboratory evaluation should include urinalysis, complete claret count, and measurement of serum creatinine level and fractional excretion of sodium (IronNa). Imaging studies can help rule out obstruction. Useful tests are summarized in Table 4.16 Figure 1 presents an overview of the diagnosis and direction of acute kidney injury.12
Table 4.
Diagnostic Test Results and Corresponding Diseases in Patients with Acute Kidney Injury
| Test result | When to order | Associated diseases/conditions |
|---|---|---|
| Elevated antineutrophil cytoplasmic antibiotic, antiglomerular basement membrane antibody | Suspected astute glomerulonephritis, pulmonary renal syndromes | Vasculitis, Goodpasture syndrome |
| Elevated antistreptolysin O titer | Contempo infection and clinical picture of acute glomerulonephritis | Poststreptococcal glomerulonephritis |
| Elevated creatine kinase level, elevated myoglobin level, dipstick positive for blood but negative for red claret cells | Contempo trauma, muscle injury | Rhabdomyolysis |
| Elevated prostate-specific antigen level | Older men with symptoms suggestive of urinary obstacle | Prostate hypertrophy, prostate cancer |
| Elevated uric acid level | History of chop-chop proliferating tumors, recent chemotherapy | Malignancy, tumor lysis syndrome |
| Eosinophiluria | Fever, rash | Allergic interstitial nephritis |
| Evidence of hemolysis (schistocytes on peripheral smear, decreased haptoglobin level, elevated indirect bilirubin level, elevated lactate dehydrogenase level) | Fever, anemia, thrombocytopenia, neurologic signs | Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, other autoimmune diseases |
| Hydronephrosis on renal ultrasonography | Suspected obstruction | Malignancy, prostate hypertrophy, uterine fibroids, nephrolithiasis, ureterolithiasis |
| Increased anion gap with increased osmolar gap* | Suspected poisoning, unresponsive patient | Ethylene glycol or methanol poisoning |
| Low complement level | Suspected acute glomerulonephritis | Systemic lupus erythematosus, endocarditis, postinfectious glomerulonephritis |
| Monoclonal spike on serum poly peptide electrophoresis | Anemia, proteinuria, acute kidney injury in older patients | Multiple myeloma |
| Positive antinuclear antibody, double-stranded Dna antibody | Proteinuria, skin rash, arthritis | Autoimmune diseases, systemic lupus erythematosus |
| Positive claret cultures | Intravenous drug use, contempo infection, new cardiac murmur | Endocarditis |
| Positive HIV test | Risk factors for HIV infection | HIV nephropathy |
SERUM CREATININE LEVEL
Information technology is important to compare the patient's current serum creatinine level with previous levels to determine the duration and acuity of the disease. The definition of astute kidney injury indicates that a rise in creatinine has occurred within 48 hours, although in the outpatient setting, it may be difficult to define when the rise actually happened. A high serum creatinine level in a patient with a previously normal documented level suggests an acute procedure, whereas a rise over weeks to months represents a subacute or chronic procedure.
URINALYSIS
Urinalysis is the almost important noninvasive test in the initial workup of astute kidney injury. Findings on urinalysis guide the differential diagnosis and direct farther workup (Figure 1 12).
Consummate Claret COUNT
The presence of acute hemolytic anemia with the peripheral smear showing schistocytes in the setting of acute kidney injury should raise the possibility of hemolytic uremic syndrome or thrombotic thrombocytopenic purpura.
URINE ELECTROLYTES
In patients with oliguria, measurement of FENa is helpful in distinguishing prerenal from intrinsic renal causes of astute kidney injury. IronNa is defined past the following formula: 
Online calculators are also available. A value less than 1 percent indicates a prerenal cause of acute kidney injury, whereas a value greater than 2 percent indicates an intrinsic renal cause. In patients on diuretic therapy, however, a FENa higher than 1 percent may exist caused by natriuresis induced past the diuretic, and is a less reliable measure out of a prerenal country. In such cases, fractional excretion of urea may be helpful, with values less than 35 per centum indicating a prerenal cause. IronNa values less than one percent are not specific for prerenal causes of acute kidney injury considering these values can occur in other weather condition, such equally contrast nephropathy, rhabdomyolysis, acute glomerulonephritis, and urinary tract obstruction.
IMAGING STUDIES
Renal ultrasonography should exist performed in most patients with acute kidney injury, particularly in older men, to dominion out obstruction (i.e., a postrenal cause).17,18 The presence of postvoid residuum urine greater than 100 mL (determined by a bladder browse or via urethral catheterization if bladder scan is unavailable) suggests postrenal acute kidney injury and requires renal ultrasonography to detect hydronephrosis or outlet obstruction. To diagnose extrarenal causes of obstruction (east.chiliad., pelvic tumors), other imaging modalities, such as computed tomography or magnetic resonance imaging, may exist required.
RENAL BIOPSY
Renal biopsy is reserved for patients in whom prerenal and postrenal causes of acute kidney injury have been excluded and the cause of intrinsic renal injury is unclear. Renal biopsy is specially of import when clinical cess and laboratory investigations advise a diagnosis that requires confirmation before disease-specific therapy (e.g., immunosuppressive medications) is instituted. Renal biopsy may need to be performed urgently in patients with oliguria who have rapidly worsening acute kidney injury, hematuria, and red claret cell casts. In this setting, in addition to indicating a diagnosis that requires immunosuppressive therapy, the biopsy may support the initiation of special therapies, such as plasmapheresis if Goodpasture syndrome is nowadays.
Management
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
Optimal management of acute kidney injury requires shut collaboration among primary care physicians, nephrologists, hospitalists, and other subspecialists participating in the care of the patient. After acute kidney injury is established, management is primarily supportive.
Patients with astute kidney injury generally should exist hospitalized unless the status is mild and clearly resulting from an easily reversible cause. The key to management is assuring adequate renal perfusion by achieving and maintaining hemodynamic stability and avoiding hypovolemia. In some patients, clinical assessment of intravascular book status and avoidance of volume overload may exist difficult, in which example measurement of central venous pressures in an intensive care setting may be helpful.
If fluid resuscitation is required because of intravascular book depletion, isotonic solutions (e.k., normal saline) are preferred over hyperoncotic solutions (e.yard., dextrans, hydroxyethyl starch, albumin).xix A reasonable goal is a mean arterial pressure greater than 65 mm Hg, which may require the utilise of vasopressors in patients with persistent hypotension.20 Renal-dose dopamine is associated with poorer outcomes in patients with acute kidney injury; it is no longer recommended.21 Cardiac part tin exist optimized every bit needed with positive inotropes, or afterload and preload reduction.
Attention to electrolyte imbalances (e.1000., hyperkalemia, hyperphosphatemia, hypermagnesemia, hyponatremia, hypernatremia, metabolic acidosis) is important. Severe hyperkalemia is defined as potassium levels of 6.5 mEq per Fifty (six.5 mmol per L) or greater, or less than 6.five mEq per L with electrocardiographic changes typical of hyperkalemia (e.yard., tall, peaked T waves). In severe hyperkalemia, 5 to 10 units of regular insulin and dextrose 50% given intravenously can shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused intravenously over 5 minutes) is also used to stabilize the membrane and reduce the risk of arrhythmias when there are electrocardiographic changes showing hyperkalemia. In patients without electrocardiographic bear witness of hyperkalemia, calcium gluconate is not necessary, but sodium polystyrene sulfonate (Kayexalate) tin can be given to lower potassium levels gradually, and loop diuretics tin can be used in patients who are responsive to diuretics. Dietary intake of potassium should be restricted.
The primary indication for use of diuretics is direction of volume overload. Intravenous loop diuretics, equally a bolus or continuous infusion, can be helpful for this purpose. However, information technology is of import to notation that diuretics do not improve morbidity, bloodshed, or renal outcomes, and should not be used to forestall or treat acute kidney injury in the absence of volume overload.22
All medications that may potentially affect renal role by direct toxicity or past hemodynamic mechanisms should exist discontinued, if possible. For example, metformin (Glucophage) should non be given to patients with diabetes mellitus who develop acute kidney injury. The dosages of essential medications should be adjusted for the lower level of kidney role. Avoidance of iodinated contrast media and gadolinium is of import and, if imaging is needed, noncontrast studies are recommended.
Supportive therapies (e.1000., antibiotics, maintenance of adequate nutrition, mechanical ventilation, glycemic control, anemia management) should exist pursued based on standard management practices. In patients with chop-chop progressive glomerulonephritis, treatment with pulse steroids, cytotoxic therapy, or a combination may be considered, often after confirmation of the diagnosis past kidney biopsy.23 In some patients, the metabolic consequences of acute kidney injury cannot be adequately controlled with conservative management, and renal replacement therapy will exist required. The indications for initiation of renal replacement therapy include refractory hyperkalemia, volume overload refractory to medical management, uremic pericarditis or pleuritis, uremic encephalopathy, intractable acidosis, and certain poisonings and intoxications (e.g., ethylene glycol, lithium).24
Prognosis
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
Patients with acute kidney injury are more probable to develop chronic kidney illness in the future. They are too at college risk of end-stage renal affliction and premature death.25–27 Patients who take an episode of acute kidney injury should be monitored for the evolution or worsening of chronic kidney affliction.
Prevention
- Abstract
- Definition
- Etiology
- Clinical Presentation
- Diagnosis
- Management
- Prognosis
- Prevention
- References
Because of the morbidity and mortality associated with acute kidney injury, it is of import for primary care physicians to identify patients who are at loftier run a risk of developing this type of injury and to implement preventive strategies. Those at highest risk include adults older than 75 years; persons with diabetes or preexisting chronic kidney illness; persons with medical bug such every bit cardiac failure, liver failure, or sepsis; and those who are exposed to contrast agents or who are undergoing cardiac surgery.28 Preventive strategies tin can exist tailored to the clinical circumstances of the individual patient (Table 5).19–21,27,29–31
Table 5.
Preventive Strategies for Patients at High Take chances of Acute Kidney Injury
| Gamble factors | Preventive strategies |
|---|---|
| Cancer chemotherapy with chance of tumor lysis syndrome27 | Hydration and allopurinol (Zyloprim) assistants a few days before chemotherapy initiation in patients at high gamble of tumor lysis syndrome to forbid uric acid nephropathy |
| Exposure to nephrotoxic medications | Avert nephrotoxic medications if possible |
| Measure and follow drug levels if bachelor | |
| Use advisable dosing, intervals, and duration of therapy | |
| Exposure to radiographic contrast agents29 | Avoid apply of intravenous dissimilarity media when risks outweigh benefits |
| If use of contrast media is essential, use iso-osmolar or low-osmolar contrast agent with lowest book possible | |
| Optimize book status before administration of contrast media; use of isotonic normal saline or sodium bicarbonate may exist considered in high-run a risk patients who are not at risk of volume overload | |
| Use of N-acetylcysteine may be considered | |
| Hemodynamic instability | Optimal fluid resuscitation; although at that place is no consensus, a hateful arterial pressure goal of > 65 mm Hg is widely used; isotonic solutions (e.g., normal saline) are preferred over hyperoncotic solutions (east.g., albumin)nineteen |
| Vasopressors are recommended for persistent hypotension (mean arterial pressure < 65 mm Hg) despite fluid resuscitation; pick of vasoactive agent should exist tailored to patients' needs20 | |
| Dopamine is non recommended21 | |
| Hepatic failure30 | Avoid hypotension and gastrointestinal bleeding |
| Early recognition and handling of spontaneous bacterial peritonitis; use albumin, 1.5 g per kg at diagnosis and i g per kg at 48 hours | |
| Early on recognition and management of ascites | |
| Albumin infusion during large book paracentesis | |
| Avoid nephrotoxic medications | |
| Rhabdomyolysis20 | Maintain acceptable hydration |
| Alkalinization of the urine with intravenous sodium bicarbonate in select patients (normal calcium, bicarbonate less than 30 mEq per L [30 mmol per L], and arterial pH less than vii.v) | |
| Undergoing surgery | Adequate volume resuscitation/prevention of hypotension, sepsis, optimizing cardiac function Consider holding renin-angiotensin system antagonists preoperatively31 |
Data Sources: We searched PubMed (also with the Clinical Queries role), the Cochrane Database of Systematic Reviews, and the National Guidelines Clearinghouse using the primal words AKI, acute kidney injury, and acute renal failure. Search date: February 2012.
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REFERENCES
evidence all references
ane. Hsu CY, McCulloch CE, Fan D, Ordoñez JD, Chertow GM, Get Equally. Community-based incidence of acute renal failure. Kidney Int. 2007;72(2):208–212. ...
2. Nash K, Hafeez A, Hou Southward. Hospital-acquired renal insufficiency. Am J Kidney Dis. 2002;39(5):930–936.
3. Hoste EA, Schurgers One thousand. Epidemiology of acute kidney injury: how big is the problem? Crit Care Med. 2008;36(iv suppl):S146–S151.
4. Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically sick patients: a cohort analysis. Crit Care. 2006;10(iii):R73.
5. Ympa YP, Sakr Y, Reinhart Chiliad, Vincent JL. Has mortality from astute renal failure decreased? A systematic review of the literature. Am J Med. 2005;118(8):827–832.
6. Gruberg L, Weissman NJ, Pichard Ad, et al. Bear upon of renal role on morbidity and mortality afterwards percutaneous aortocoronary saphenous vein graft intervention. Am Heart J. 2003;145(3):529–534.
7. Uchino Southward, Kellum JA, Bellomo R, Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators, et al. Acute renal failure in critically ill patients: a multinational, multicenter written report. JAMA. 2005;294(7):813–818.
eight. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in astute kidney injury. Crit Care. 2007;eleven(2):R31.
9. Holley JL. Clinical approach to the diagnosis of acute renal failure. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, Pa.: National Kidney Foundation; 2009.
10. Kaufman J, Dhakal Grand, Patel B, Hamburger R. Community-acquired acute renal failure. Am J Kidney Dis. 1991;17(two):191–198.
eleven. Christensen PK, Hansen HP, Parving HH. Dumb autoregulation of GFR in hypertensive non-insulin dependent diabetic patients. Kidney Int. 1997;52(v):1369–1374.
12. Smith MC. Acute renal failure. In: Resnick MI, Elder JS, Spirnak JP, eds. Clinical Decisions in Urology. 3rd ed. Hamilton, Ontario, Canada: BC Decker, Inc.; 2004:lx–63.
xiii. Clarkson MR, Giblin L, O'Connell FP, et al. Astute interstitial nephritis: clinical features and response to corticosteroid therapy. Nephrol Punch Transplant. 2004;19(11):2778–2783.
fourteen. González E, Gutiérrez Due east, Galeano C, Grupo Madrileño De Nefritis Intersticiales, et al. Early steroid treatment improves the recovery of renal office in patients with drug-induced acute interstitial nephritis. Kidney Int. 2008;73(8):940–946.
15. Meyer TW, Hostetter TH. Uremia. N Engl J Med. 2007;357(13):1316–1325.
16. Agrawal Yard, Swartz R. Astute renal failure [published correction appears in Am Fam Doctor. 2001;63(3):445]. Am Fam Dr.. 2000;61(7):2077–2088.
17. Lewington A, Kanagasundaram South. Clinical practice guidelines: acute kidney injury. 2011. http://www.renal.org/clinical/guidelinessection/AcuteKidneyInjury.aspx. Accessed September vii, 2012.
18. O'Neill WC. Sonographic evaluation of renal failure. Am J Kidney Dis. 2000;35(6):1021–1038.
xix. Schortgen F, Lacherade JC, Bruneel F, et al. Furnishings of hydroxyethylstarch and gelatin on renal role in severe sepsis: a multicentre randomised study. Lancet. 2001;357(9260):911–916.
20. Brochard L, Abroug F, Brenner K, et al. An Official ATS/ERS/ESICM/SCCM/SRLF Statement: Prevention and Direction of Astute Renal Failure in the ICU Patient: an international consensus conference in intensive care medicine. Am J Respir Crit Care Med. 2010;181(10):1128–1155.
21. Friedrich JO, Adhikari Northward, Herridge MS, Beyene J. Meta-analysis: low-dose dopamine increases urine output but does not foreclose renal dysfunction or death. Ann Intern Med. 2005;142(vii):510–524.
22. Ho KM, Sheridan DJ. Meta-assay of frusemide to prevent or treat astute renal failure. BMJ. 2006;333(7565):420.
23. Walters Thou, Willis NS, Craig JC. Interventions for renal vasculitis in adults Cochrane Database Syst Rev. 2008(iii):CD003232.
24. Mehta RL. Indications for dialysis in the ICU: renal replacement vs. renal support. Blood Purif. 2001;xix(2):227–232.
25. Goldberg R, Dennen P. Long-term outcomes of acute kidney injury. Adv Chronic Kidney Dis. 2008;fifteen(iii):297–307.
26. Coca SG, Yusuf B, Shlipak MG, Garg AX, Parikh CR. Long-term hazard of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53(6):961–973.
27. Pession A, Masetti R, Gaidano One thousand, et al. Risk evaluation, prophylaxis, and treatment of tumor lysis syndrome: consensus of an Italian skilful panel. Adv Ther. 2011;28(8):684–697.
28. Leblanc M, Kellum JA, Gibney RT, Lieberthal W, Tumlin J, Mehta R. Take a chance factors for acute renal failure: inherent and modifiable risks. Curr Opin Crit Care. 2005;11(half-dozen):533–536.
29. Rundback JH, Nahl D, Yoo V. Contrast-induced nephropathy. J Vasc Surg. 2011;54(2):575–579.
30. Nadim MK, Kellum JA, Davenport A, et al. Hepatorenal syndrome: the 8th international consensus conference of the Astute Dialysis Quality Initiative (ADQI) group. Crit Care. 2012;xvi(one):R23.
31. Auron Thousand, Harte B, Kumar A, Michota F. Renin-angiotensin organization antagonists in the perioperative setting: clinical consequences and recommendations for practice. Postgrad Med J. 2011;87(1029):472–481.
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