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Acute Kidney Injury (AKI)
Hasnein Mohamedali
Supervisor: Dr Ernest Mrema
Outline
• Definition
• Classification systems
• Pathophysiology
• Etiology
• Epidemiology
• Clinical Presentation
• Investigations
• Management
• Complications
• Prognosis
Definition
• Acute kidney injury (AKI) is defined as an abrupt or
rapid decline in renal function as measured by
serum urea and creatinine leading to a failure to
maintain fluid, electrolyte and acid – base
hemostasis.
• The KDIGO guidelines suggest the following
criteria for diagnosing AKI:
• Rise in creatinine >26 µmol/L in 48 hours
• Rise in creatinine >1.5 from baseline (best figure in
3/12)
• Urine output <0.5ml/kg/h for >6 consecutive hours
Categories
• AKI may be classified into 3 general categories, as
follows:
• Prerenal - As an adaptive response to severe
volume depletion and hypotension, with
structurally intact nephrons
• Intrinsic - In response to cytotoxic, ischemic, or
inflammatory insults to the kidney, with structural
and functional damage
• Postrenal - From obstruction to the passage of
urine
The RIFLE Classification system
• In 2004, the Acute Dialysis Quality Initiative
work group set forth a definition and
classification system for acute renal failure,
described by the acronym RIFLE (Risk of renal
dysfunction, Injury to the kidney, Failure or
Loss of kidney function, and End-stage kidney
disease)
Acute Kidney Injury Network
classification system
• The Acute Kidney Injury Network (AKIN) has developed
specific criteria for the diagnosis of AKI. The AKIN defines
AKI as abrupt (within 48 hours) reduction of kidney
function, manifested by any 1 of the following :
• An absolute increase in serum creatinine of 0.3 mg/dL or
greater (≥26.4 µmol/L)
• A percentage increase in serum creatinine of 50% or
greater (1.5-fold from baseline)
• A reduction in urine output, defined as less than 0.5
mL/kg/h for more than 6 hours
Pathophysiology
• Regardless of the cause of AKI, reductions in
Renal Blood Flow (RBF) represent a common
pathologic pathway for decreasing glomerular
filtration rate (GFR).
• The etiology of AKI consists of 3 main
mechanisms: prerenal, intrinsic, and
obstructive.
• In prerenal failure, GFR is depressed by compromised renal
perfusion. Tubular and glomerular function remain normal.
• Intrinsic renal failure includes diseases of the kidney itself.
Ischemic renal injury is the most common cause of intrinsic
renal failure.
• Obstruction of the urinary tract initially causes an increase
in tubular pressure, which decreases the filtration driving
force.
Etiology
• Prerenal AKI: most common form and can be due to:
1. Volume loss – GI, renal, cutaneous or hemorrhage
2. Decreased renal perfusion for e.g. in patients with
heart failure or shock
3. Medications inducing AKI in volume depleted states
including ACEI and ARBs, amphotericin B,
aminoglycosides and radio contrast agents.
4. Arteriolar vasoconstriction e.g. hepatorenal
syndrome
Intrinsic AKI
• Structural injury in the kidney is the hallmark
of intrinsic AKI; the most common form is
ATN, either ischemic or cytotoxic
• Vascular causes e.g. thrombosis, emboli,
vasculitis, microangiopathies
• Glomerular causes e.g. anti-GBM disease,
ANCA – associated glomerulonephritis
• Tubular causes – cytotoxic or ischemic
• Drugs, infections and systemic causes
Postrenal AKI
• Mechanical obstruction of the urinary
collecting system, including the renal pelvis,
ureters, bladder, or urethra.
• Causes of obstruction include the following:
Stone disease, stricture,intraluminal,
extraluminal, or intramural tumors,
thrombosis or compressive hematoma,
fibrosis.
Epidemiology
• In the United States, approximately 1% of patients
admitted to hospitals have AKI at the time of
admission.
• The estimated incidence rate of AKI during
hospitalization is 2-5%.
• AKI develops within 30 days postoperatively in
approximately 1% of general surgery cases and
arises in up to 67% of intensive care unit (ICU)
patients.
• Approximately 95% of consultations with
nephrologists are related to AKI.
History and Clinical presentation
• Hx of etiologic factors
• Co – morbid conditions which have high risk of
developing AKI
• Urine output history – Oliguria or abrupt
anuria or gradually diminishing urine output.
Pre renal failure
• Symptoms related to hypovolemia – thirst,
dizziness, decreased urine output, orthostasis
Intrinsic renal failure
• Can be divided into glomerular and tubular
etiologies.
• Nephritic syndrome suggest glomerular
etiology
• Query about prior throat or skin infections
• ATN should be suspected in pts presenting
after a period of hypotension
• Hx of exposure to nephrotoxins
Postrenal failure
• Usually older men with symptoms of urgency,
frequency and hesitancy.
• Previous hx of pelvic surgery or malignancy
• Flank pain and hematuria which could be due
to renal calculi
• Use of acyclovir, methotrexate, triamterene,
indinavir, or sulfonamides implies the
possibility that crystals of these medications
have caused tubular obstruction.
Physical examination
• The most important part of the physical
examination is the assessment of
cardiovascular and volume status.
• Pulse rate and blood pressure recordings
measured in the supine and the standing
position
• Careful examination of the heart and lungs,
skin turgor, and mucous membranes
• Assessment for peripheral edema
• Obtaining a thorough physical examination is
extremely important when collecting evidence
about the etiology of AKI. Clues may be found
in any of the following:
• Skin e.g. butterfly rash, purpura
• Eyes eg. Hypertensive or diabetic changes
• Cardiovascular system (signs of heart failure)
• Abdomen (costoverterbral angle tenderness)
Investigations
• Renal function tests
• Normal ranges; Urea: 2.5 – 6.7 mmol/L
Creatinine: 70 – 150 µmol/L
eGFR: 90 – 120 ml/min/1.73m2
• The ratio of BUN to creatinine is an important
finding. The ratio can exceed 20:1 in
conditions in which enhanced reabsorption of
urea is favored (eg, in volume contraction);
this suggests prerenal AKI.
Urinalysis
• Granular, muddy brown casts
• Sloughing of cells
• Presence of RBCs – Eumorphic vs Dysmorphic
• Presence of WBCs
CBC and peripheral smear
• To define the etiology e.g. the peripheral
smear may show schistocytes in conditions
such as hemolytic uremic syndrome (HUS) or
thrombotic thrombocytopenic purpura (TTP)
Ultrasonography
• For evaluating existing renal disease and
obstruction of the urinary collecting system.
• Use of IVCD in evaluating the volume status of
the body (normal 15 – 25 mm)
Renal Biopsy
• Useful in identifying intrarenal causes of AKI
• Can be justified if the results may change
management (eg, initiation of
immunosuppressive medications)
• may also be indicated when renal function
does not return for a prolonged period
Management:
• Maintenance of volume homeostasis and correction of
biochemical abnormalities remain the primary goals of
treatment and may include the following measures:
Correction of fluid overload with furosemide (rule out
obstructive causes first!!)
Correction of severe acidosis with bicarbonate
administration, which can be important as a bridge to
dialysis
Correction of hyperkalemia
Correction of hematologic abnormalities (eg, anemia,
uremic platelet dysfunction) with measures such as
transfusions.
Dialysis
• The indications for dialysis (AEIOU) includes:
• Volume expansion that cannot be managed
with diuretics
• Hyperkalemia refractory to medical therapy
(K > 7mmol/L)
• Severe metabolic acidosis (pH < 7.2)
• Drug overdose – BLAST
• Uremia
Dietary Modification
• Restriction of salt and fluid
• Because potassium and phosphorus are not
excreted optimally in patients with AKI, blood
levels of these electrolytes tend to be high.
Restriction of these elements in the diet may
be necessary.
Complications
• Cardiovascular complications – Fluid overload
leading to HF, cardiac arrest secondary to
hyperkalemia
• GI complications - Nausea, vomiting, and
anorexia are frequent complications of AKI and
represent one of the cardinal signs of uremia.
• Neurologic complications - Neurologic sequelae
include lethargy, somnolence, reversal of the
sleep-wake cycle, and cognitive or memory
deficits
Prognosis
• Age
• Cause of renal failure e.g. burns (80%) and,
• The presence or absence of preexisting kidney
disease (estimated GFR [eGFR] < 60 mL/min),
• The duration of renal dysfunction prior to
therapeutic intervention.
• Hypotension and the need for inotropic
support during renal replacement therapy are
significant poor predictors for patient
survival

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Acute kidney injury

  • 1. Acute Kidney Injury (AKI) Hasnein Mohamedali Supervisor: Dr Ernest Mrema
  • 2. Outline • Definition • Classification systems • Pathophysiology • Etiology • Epidemiology • Clinical Presentation • Investigations • Management • Complications • Prognosis
  • 3. Definition • Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal function as measured by serum urea and creatinine leading to a failure to maintain fluid, electrolyte and acid – base hemostasis. • The KDIGO guidelines suggest the following criteria for diagnosing AKI: • Rise in creatinine >26 µmol/L in 48 hours • Rise in creatinine >1.5 from baseline (best figure in 3/12) • Urine output <0.5ml/kg/h for >6 consecutive hours
  • 4. Categories • AKI may be classified into 3 general categories, as follows: • Prerenal - As an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons • Intrinsic - In response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage • Postrenal - From obstruction to the passage of urine
  • 5. The RIFLE Classification system • In 2004, the Acute Dialysis Quality Initiative work group set forth a definition and classification system for acute renal failure, described by the acronym RIFLE (Risk of renal dysfunction, Injury to the kidney, Failure or Loss of kidney function, and End-stage kidney disease)
  • 6.
  • 7. Acute Kidney Injury Network classification system • The Acute Kidney Injury Network (AKIN) has developed specific criteria for the diagnosis of AKI. The AKIN defines AKI as abrupt (within 48 hours) reduction of kidney function, manifested by any 1 of the following : • An absolute increase in serum creatinine of 0.3 mg/dL or greater (≥26.4 µmol/L) • A percentage increase in serum creatinine of 50% or greater (1.5-fold from baseline) • A reduction in urine output, defined as less than 0.5 mL/kg/h for more than 6 hours
  • 8.
  • 9. Pathophysiology • Regardless of the cause of AKI, reductions in Renal Blood Flow (RBF) represent a common pathologic pathway for decreasing glomerular filtration rate (GFR). • The etiology of AKI consists of 3 main mechanisms: prerenal, intrinsic, and obstructive.
  • 10. • In prerenal failure, GFR is depressed by compromised renal perfusion. Tubular and glomerular function remain normal. • Intrinsic renal failure includes diseases of the kidney itself. Ischemic renal injury is the most common cause of intrinsic renal failure. • Obstruction of the urinary tract initially causes an increase in tubular pressure, which decreases the filtration driving force.
  • 11. Etiology • Prerenal AKI: most common form and can be due to: 1. Volume loss – GI, renal, cutaneous or hemorrhage 2. Decreased renal perfusion for e.g. in patients with heart failure or shock 3. Medications inducing AKI in volume depleted states including ACEI and ARBs, amphotericin B, aminoglycosides and radio contrast agents. 4. Arteriolar vasoconstriction e.g. hepatorenal syndrome
  • 12. Intrinsic AKI • Structural injury in the kidney is the hallmark of intrinsic AKI; the most common form is ATN, either ischemic or cytotoxic • Vascular causes e.g. thrombosis, emboli, vasculitis, microangiopathies • Glomerular causes e.g. anti-GBM disease, ANCA – associated glomerulonephritis • Tubular causes – cytotoxic or ischemic • Drugs, infections and systemic causes
  • 13. Postrenal AKI • Mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra. • Causes of obstruction include the following: Stone disease, stricture,intraluminal, extraluminal, or intramural tumors, thrombosis or compressive hematoma, fibrosis.
  • 14. Epidemiology • In the United States, approximately 1% of patients admitted to hospitals have AKI at the time of admission. • The estimated incidence rate of AKI during hospitalization is 2-5%. • AKI develops within 30 days postoperatively in approximately 1% of general surgery cases and arises in up to 67% of intensive care unit (ICU) patients. • Approximately 95% of consultations with nephrologists are related to AKI.
  • 15. History and Clinical presentation • Hx of etiologic factors • Co – morbid conditions which have high risk of developing AKI • Urine output history – Oliguria or abrupt anuria or gradually diminishing urine output.
  • 16. Pre renal failure • Symptoms related to hypovolemia – thirst, dizziness, decreased urine output, orthostasis
  • 17. Intrinsic renal failure • Can be divided into glomerular and tubular etiologies. • Nephritic syndrome suggest glomerular etiology • Query about prior throat or skin infections • ATN should be suspected in pts presenting after a period of hypotension • Hx of exposure to nephrotoxins
  • 18. Postrenal failure • Usually older men with symptoms of urgency, frequency and hesitancy. • Previous hx of pelvic surgery or malignancy • Flank pain and hematuria which could be due to renal calculi • Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility that crystals of these medications have caused tubular obstruction.
  • 19. Physical examination • The most important part of the physical examination is the assessment of cardiovascular and volume status. • Pulse rate and blood pressure recordings measured in the supine and the standing position • Careful examination of the heart and lungs, skin turgor, and mucous membranes • Assessment for peripheral edema
  • 20. • Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of AKI. Clues may be found in any of the following: • Skin e.g. butterfly rash, purpura • Eyes eg. Hypertensive or diabetic changes • Cardiovascular system (signs of heart failure) • Abdomen (costoverterbral angle tenderness)
  • 21. Investigations • Renal function tests • Normal ranges; Urea: 2.5 – 6.7 mmol/L Creatinine: 70 – 150 µmol/L eGFR: 90 – 120 ml/min/1.73m2 • The ratio of BUN to creatinine is an important finding. The ratio can exceed 20:1 in conditions in which enhanced reabsorption of urea is favored (eg, in volume contraction); this suggests prerenal AKI.
  • 22. Urinalysis • Granular, muddy brown casts • Sloughing of cells • Presence of RBCs – Eumorphic vs Dysmorphic • Presence of WBCs
  • 23. CBC and peripheral smear • To define the etiology e.g. the peripheral smear may show schistocytes in conditions such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP)
  • 24. Ultrasonography • For evaluating existing renal disease and obstruction of the urinary collecting system. • Use of IVCD in evaluating the volume status of the body (normal 15 – 25 mm)
  • 25. Renal Biopsy • Useful in identifying intrarenal causes of AKI • Can be justified if the results may change management (eg, initiation of immunosuppressive medications) • may also be indicated when renal function does not return for a prolonged period
  • 26. Management: • Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment and may include the following measures: Correction of fluid overload with furosemide (rule out obstructive causes first!!) Correction of severe acidosis with bicarbonate administration, which can be important as a bridge to dialysis Correction of hyperkalemia Correction of hematologic abnormalities (eg, anemia, uremic platelet dysfunction) with measures such as transfusions.
  • 27.
  • 28. Dialysis • The indications for dialysis (AEIOU) includes: • Volume expansion that cannot be managed with diuretics • Hyperkalemia refractory to medical therapy (K > 7mmol/L) • Severe metabolic acidosis (pH < 7.2) • Drug overdose – BLAST • Uremia
  • 29. Dietary Modification • Restriction of salt and fluid • Because potassium and phosphorus are not excreted optimally in patients with AKI, blood levels of these electrolytes tend to be high. Restriction of these elements in the diet may be necessary.
  • 30. Complications • Cardiovascular complications – Fluid overload leading to HF, cardiac arrest secondary to hyperkalemia • GI complications - Nausea, vomiting, and anorexia are frequent complications of AKI and represent one of the cardinal signs of uremia. • Neurologic complications - Neurologic sequelae include lethargy, somnolence, reversal of the sleep-wake cycle, and cognitive or memory deficits
  • 31. Prognosis • Age • Cause of renal failure e.g. burns (80%) and, • The presence or absence of preexisting kidney disease (estimated GFR [eGFR] < 60 mL/min), • The duration of renal dysfunction prior to therapeutic intervention. • Hypotension and the need for inotropic support during renal replacement therapy are significant poor predictors for patient survival

Editor's Notes

  1. However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production A rise in the creatinine level can result from medications (eg, cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion, while a rise in the BUN level can also occur without renal injury, resulting instead from such sources as gastrointestinal (GI) or mucosal bleeding, steroid use, or protein loading. Therefore, a careful inventory must be taken before concluding that a kidney injury is present.
  2. The driving force for glomerular filtration is the pressure gradient from the glomerulus to the Bowman space. Glomerular pressure depends primarily on renal blood flow (RBF) and is controlled by the combined resistances of renal afferent and efferent arterioles
  3. involve a reduction in renal blood flow secondary to systemic arterial vasodilation and concomitant intrarenal vasoconstriction. This results in renal hypoperfusion and ischemia.The kidneys receive higher blood flow per unit mass compared to any other organ in the body but the actual fraction of extracted oxygen is less. This makes the kidney very sensitive to conditions of hypoperfusion. Ischemia and toxins result in vasoconstriction, endothelial injury, and the activation of innate and acquired inflammatory immune responses.2,5 The oxygen supply to the renal tissues can be impaired due to acute blood loss from trauma or during acute hemodilution during resuscitation with large quantities of crystalloids in trauma or septic shock
  4. To summarize, volume depletion can be caused by the following: Renal losses - Diuretics, polyuria GI losses - Vomiting, diarrhea Cutaneous losses - Burns, Stevens-Johnson syndrome Hemorrhage Pancreatitis Decreased cardiac output can be caused by the following: Heart failure Pulmonary embolus Acute myocardial infarction Severe valvular disease Abdominal compartment syndrome - Tense ascites Systemic vasodilation can be caused by the following: Sepsis Anaphylaxis Anesthetics Drug overdose Afferent arteriolar vasoconstriction can be caused by the following: Hypercalcemia Drugs - NSAIDs, amphotericin B, calcineurin inhibitors, norepinephrine, radiocontrast agents Hepatorenal syndrome
  5. To summarize, vascular (large- and small-vessel) causes of intrinsic AKI include the following: Renal artery obstruction - Thrombosis, emboli, dissection, vasculitis Renal vein obstruction - Thrombosis Microangiopathy - TTP, HUS, disseminated intravascular coagulation (DIC), preeclampsia Malignant hypertension Scleroderma renal crisis Transplant rejection Atheroembolic disease Glomerular causes include the following: Anti-glomerular basement membrane (GBM) disease - As part of Goodpasture syndrome or renal limited disease Anti-neutrophil cytoplasmic antibody-–associated glomerulonephritis (ANCA-associated glomerulonephritis) - Wegener granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis Immune complex glomerulonephritis - Lupus, postinfectious glomerulonephritis, cryoglobulinemia, primary membranoproliferative glomerulonephritis Tubular etiologies may include ischemia or cytotoxicity. Cytotoxic etiologies include the following: Heme pigment - Rhabdomyolysis, intravascular hemolysis Crystals - Tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, methotrexate Drugs - Aminoglycosides, lithium, amphotericin B, pentamidine, cisplatin, ifosfamide, radiocontrast agents Interstitial causes include the following: Drugs - Penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides Infection - Pyelonephritis, viral nephritides Systemic disease - Sjögren syndrome, sarcoid, lupus, lymphoma, leukemia, tubulonephritis, uveitis
  6. If the site of obstruction is unilateral, then a rise in the serum creatinine level may not be apparent, because of preserved function of the contralateral kidney. Nevertheless, even with unilateral obstruction a significant loss of GFR occurs, and patients with partial obstruction may develop progressive loss of GFR if the obstruction is not relieved. Bilateral obstruction is usually a result of prostate enlargement or tumors in men and urologic or gynecologic tumors in women. Patients who develop anuria typically have obstruction at the level of the bladder or downstream to it. To summarize, causes of postrenal AKI include the following: Ureteric obstruction - Stone disease, tumor, fibrosis, ligation during pelvic surgery Bladder neck obstruction - Benign prostatic hypertrophy (BPH), cancer of the prostate (CA prostate or prostatic CA), neurogenic bladder, tricyclic antidepressants, ganglion blockers, bladder tumor, stone disease, hemorrhage/clot Urethral obstruction - Strictures, tumor, phimosis Intra-abdominal hypertension - Tense ascites Renal vein thrombosis Diseases causing urinary obstruction from the level of the renal tubules to the urethra include the following: Tubular obstruction from crystals - Eg, uric acid, calcium oxalate, acyclovir, sulfonamide, methotrexate, myeloma light chains Ureteral obstruction - Retroperitoneal tumor, retroperitoneal fibrosis (methysergide, propranolol, hydralazine), urolithiasis, or papillary necrosis Urethral obstruction - Benign prostatic hypertrophy; prostate, cervical, bladder, or colorectal carcinoma; bladder hematoma; bladder stone; obstructed Foley catheter; neurogenic bladder; stricture
  7. It is important to elicit a history of any of the following etiologic factors:   Volume restriction (eg, low fluid intake, gastroenteritis) Nephrotoxic drug ingestion Trauma or unaccustomed exertion Blood loss or transfusions Exposure to toxic substances, such as ethyl alcohol or ethylene glycol Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners People with the following comorbid conditions are at a higher risk for developing AKI:   Hypertension Chronic heart failure Diabetes Multiple myeloma Chronic infection Myeloproliferative disorder Connective tissue disorders Autoimmune diseases Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.
  8. Prerenal failure Patients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced cardiac failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.   Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.
  9. Intrinsic renal failure Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI. Nephritic syndrome of hematuria, edema, and hypertension indicates a glomerular etiology for AKI. Query about prior throat or skin infections. Acute tubular necrosis (ATN) should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.   A careful search for exposure to nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents). Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis (muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood transfusion). Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.
  10. Postrenal failure Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of urgency, frequency, and hesitancy. Patients may present with asymptomatic, high-grade urinary obstruction because of the chronicity of their symptoms. A history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of obstruction.   Flank pain and hematuria should raise a concern about renal calculi or papillary necrosis as the source of urinary obstruction. Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility that crystals of these medications have caused tubular obstruction.
  11. Skin examination may reveal the following:   Livido reticularis, digital ischemia, butterfly rash, palpable purpura - Systemic vasculitis Maculopapular rash - Allergic interstitial nephritis Track marks (ie, intravenous drug abuse) - Endocarditis Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AK. Infectious diseases, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), and embolic phenomena can produce typical cutaneous changes.   Eyes and ears Eye examination may reveal the following:   Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune vasculitis Jaundice - Liver diseases Band keratopathy (ie, hypercalcemia) - Multiple myeloma Signs of diabetes mellitus Signs of hypertension Atheroemboli - Retinopathy Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis. Findings suggestive of severe hypertension, atheroembolic disease, and endocarditis may be observed on careful examination of the eyes.   Ear examination may reveal the following:   Hearing loss - Alport disease and aminoglycoside toxicity Mucosal or cartilaginous ulcerations - Wegener granulomatosis Cardiovascular system The most important part of the physical examination is the assessment of cardiovascular and volume status. The physical examination must include the following:   Pulse rate and blood pressure recordings measured in the supine and the standing position Close inspection of the jugulovenous pulse Careful examination of the heart and lungs, skin turgor, and mucous membranes Assessment for peripheral edema Cardiovascular examination may reveal the following:   Irregular rhythms (ie, atrial fibrillation) - Thromboemboli Murmurs - Endocarditis Pericardial friction rub - Uremic pericarditis Increased jugulovenous distention, rales, S 3 - Heart failure In hospitalized patients, accurate daily records of fluid intake and urine output, as well as daily measurements of patient weight, are important. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia.   Severe heart failure may also cause hypotension. Although patients with heart failure may have low blood pressure, volume expansion is present and effective renal perfusion is poor, which can result in AKI.   Severe hypertension with renal failure suggests one of the following disorders:   Renovascular disease Glomerulonephritis Vasculitis Atheroembolic disease Abdomen Abdominal examination may reveal the following:   Pulsatile mass or bruit - Atheroemboli Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis Pelvic, rectal masses; prostatic hypertrophy; distended bladder – Urinary obstruction Limb ischemia, edema - Rhabdomyolysis Abdominal examination findings can be useful in helping to detect obstruction at the bladder outlet as the cause of renal failure; such obstruction may be due to cancer or to an enlarged prostate.   The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI. The presence of an epigastric bruit suggests renal vascular hypertension, which may predispose to AKI.   Pulmonary system Pulmonary examination may reveal the following:   Rales - Goodpasture syndrome, Wegener granulomatosis Hemoptysis - Wegener granulomatosis
  12. Serum BUN/creatinine ratio — serum BUN/creatinine ratio is normal at 10-15:1 in ATN, and may be greater than 20:1 in prerenal Thus, a high ratio is highly suggestive of prerenal disease Although increased levels of blood urea nitrogen (BUN) and creatinine are the hallmarks of renal failure, the rate of rise depends on the degree of renal insult and, with respect to BUN, on protein intake. BUN may be elevated in patients with gastrointestinal (GI) or mucosal bleeding, steroid treatment, or protein loading.   The ratio of BUN to creatinine is an important finding. The ratio can exceed 20:1 in conditions in which enhanced reabsorption of urea is favored (eg, in volume contraction); this suggests prerenal AKI.   Assuming that the patient has no renal function, the rise in BUN over 24 hours can be roughly predicted using the following formula:   24-hour protein intake in milligrams ´ 0.16 divided by total body water in mg/dL added to the BUN value   Assuming no renal function, the rise in creatinine can be predicted using the following formulas:   For males: Weight in kilograms ´ [28 - 0.2(age)] divided by total body water in mg/dL added to the creatinine value For females: Weight in kilograms ´ [23.8 - 0.17(age)] divided by total body water added to the creatinine value As a general rule, if serum creatinine increases to more than 1.5 mg/dL/day, rhabdomyolysis must be ruled out.
  13. Findings of granular, muddy brown casts are highly suggestive of tubular necrosis (see the image below). The presence of tubular cells or tubular cell casts also supports the diagnosis of ATN. Sloughing of cells, which is responsible for the formation of granular casts, is a feature of acute tubular necrosis. Reddish brown or cola-colored urine suggests the presence of myoglobin or hemoglobin, especially in the setting of a positive dipstick for heme and no red blood cells (RBCs) on the microscopic examination. The dipstick assay may reveal significant proteinuria as a result of tubular injury.The presence of RBCs in the urine is always pathologic. Eumorphic RBCs suggest bleeding along the collecting system. Dysmorphic RBCs or RBC casts indicate glomerular inflammation, suggesting glomerulonephritis is present.   The presence of white blood cells (WBCs) or WBC casts suggests pyelonephritis or acute interstitial nephritis. The presence of urine eosinophils is helpful in establishing a diagnosis but is not necessary for allergic interstitial nephritis to be present.
  14. CBC, Peripheral Smear, and Serology   The peripheral smear may show schistocytes in conditions such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). A finding of increased rouleaux formation suggests multiple myeloma, and the workup should be directed toward immunoelectrophoresis of serum and urine.   The presence of the following, along with related findings, may help to further define the etiology of AKI:   Myoglobin or free hemoglobin - Eg, pigment nephropathy Increased serum uric acid level - Eg, tumor lysis syndrome Serum lactate dehydrogenase (LDH) - Eg, renal infarction Although serologic tests can be informative, the costs can be prohibitive if these tests are not ordered judiciously. Possible tests include the following:   Complement levels Antinuclear antibody (ANA) Antineutrophil cytoplasmic antibody (ANCA) Anti-glomerular basement membrane (anti-GBM) antibody Hepatitis B and C virus studies Antistreptolysin (ASO)
  15. Renal ultrasonography is useful for evaluating existing renal disease and obstruction of the urinary collecting system. Obtaining images of the kidneys can be technically difficult in patients who are obese, however, as well as in those with abdominal distention from ascites, gas, or retroperitoneal fluid collection.   The degree of hydronephrosis found on an ultrasonogram does not necessarily correlate with the degree of obstruction. Mild hydronephrosis may be observed with complete obstruction if found early. Small kidneys suggest chronic renal failure.
  16. Volume overload Furosemide can be used to correct volume overload when patients are still responsive; this often requires high intravenous (IV) doses. Furosemide plays no role in converting an oliguric AKI to a nonoliguric AKI or in increasing urine output when a patient is not hypervolemic. However, response to furosemide can be taken as a good prognostic sign.   Hyperkalemia Hyperkalemia in patients with AKI can be life-threatening. Approaches to lowering serum potassium include the following:   Decreasing the intake of potassium in diet or tube feeds Exchanging potassium across the gut lumen using potassium-binding resins Promoting intracellular shifts in potassium with insulin, dextrose solutions, and beta agonists Instituting dialysis Nephrotoxic agents In AKI, the kidneys are especially vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, nonsteroidal anti-inflammatory drugs [NSAIDs]) should be avoided or used with extreme caution. Similarly, all medications cleared by renal excretion should be avoided, or their doses should be adjusted appropriately.
  17. Cardiovascular complications Cardiovascular complications (eg, heart failure, myocardial infarction, arrhythmias, cardiac arrest) have been observed in as many as 35% of patients with AKI. Fluid overload secondary to oliguric AKI is a particular risk for elderly patients with limited cardiac reserve. In cardiac patients who experience AKI either in the setting of acute decompensated heart failure or cardiac surgery, AKI is associated with worse morbidity and mortality.[5]   Pericarditis is a relatively rare complication of AKI. When pericarditis complicates AKI, consider additional diagnoses, such as systemic lupus erythematosus (SLE) and hepatorenal syndrome.   AKI also can be a complication of cardiac diseases, such as endocarditis, decompensated heart failure, or atrial fibrillation with emboli. Cardiac arrest in a patient with AKI always should arouse suspicion of hyperkalemia. Many authors recommend a trial of intravenous calcium chloride (or gluconate) in all patients with AKI who experience cardiac arrest.
  18. The prognosis for patients with AKI is directly related to the cause of renal failure and, to a great extent, to the presence or absence of preexisting kidney disease (estimated GFR [eGFR] &amp;lt; 60 mL/min), as well as to the duration of renal dysfunction prior to therapeutic intervention.