ACUTE KIDNEY INJURY AKI laboratory investigation


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ACUTE KIDNEY INJURY AKI laboratory investigation

  1. 1. ACUTE KIDNEY INJURY (AKI) LABORATORY INVESTIGATION BY ABDULLAH S . K . AL-ANZI 4th year – medical student NBU – medical college Twitter on: @ASKAnzi
  2. 2. KIDNEY FUNCTION STUDIES 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
  3. 3. ACUTE OR CHRONIC URAEMIA? The distinction between acute and chronic uraemia depends in part on the history, duration of symptoms and previous urinalysis or measurements of renal function. A rapid rate of change of serum urea and creatinine with time suggests an acute process. A normochromic, normocytic anaemia suggests chronic disease, but anaemia may complicate many of the diseases that cause AKI, owing to a combination of haemolysis, haemorrhage and deficient erythropoietin production.
  4. 4. Several laboratory tests, including the following, are useful for assessing the etiology of acute kidney injury (AKI) and can aid in proper management of the disease: Complete blood count (CBC) Serum biochemistries Urine analysis with microscopy Urine electrolytes In some cases, renal imaging is useful, especially if renal failure is secondary to obstruction. The American College of Radiology recommends ultrasonography, preferably with Doppler methods, as the most appropriate imaging method in AKI.
  5. 5. CBC, PERIPHERAL SMEAR 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 The peripheral smear may show schistocytes in conditions such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP).
  6. 6. SEROLOGIC TESTS Possible tests include the following: Complement levels ( C3-C4 for SLE ) Antinuclear antibody (ANA) Antineutrophil cytoplasmic antibody (ANCA) Anti-glomerular basement membrane (anti-GBM) antibody Hepatitis B and C virus studies Antistreptolysin (ASO)
  7. 7. URINALYSIS 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. Often, oxalate crystals are observed in cases of ATN.
  8. 8. URINALYSIS Reddish brown or cola-colored urine suggests thepresence 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 The presence of white blood cells (WBCs) or WBC casts suggests pyelonephritis or acute interstitial nephritis.
  9. 9. URINALYSIS The presence of urine eosinophils is helpful in establishing a diagnosis but is not necessary for allergic interstitial nephritis to be present. However, this finding can also be seen in urinary tract infections, glomerulonephritis, and atheroembolic disease. The presence of uric acid crystals may represent ATN associated with uric acid nephropathy. Calcium oxalate crystals are usually present in cases of ethylene glycol poisoning
  10. 10. FRACTIONAL EXCRETION FENA ))OF SODIUM Urine electrolyte findings also can serve as valuable indicators of functioning renal tubules. FENa is the commonly used indicator. the interpretation of results from patients in nonoliguric states, those with glomerulonephritis, and those receiving or ingesting diuretics can lead to an erroneous diagnosis FENa can be a valuable test for hepatorenal syndrome & useful in AKI only in the presence of ????
  11. 11. FRACTIONAL EXCRETION OF UREA In patients who are receiving diuretics, (FEUrea) can be obtained, since urea transport is not affected by diuretics. (FEUrea of less than 35% is suggestive of a prerenal state.) The formula for calculating the FEUrea is as follows:
  12. 12. EMERGING BIOMARKERS Creatinine elevation is a late marker for renal dysfunction and, once elevated, reflects a severe reduction in GFR The most promising biomarker to date is urinary neutrophil gelatinase-associated lipocalin (NGAL), which has been shown to detect AKI in patients undergoing cardiopulmonary bypass surgery the markers plasma B-type natriuretic peptide (BNP) and NGAL and found it to be a strong predictor of early AKI in patients with lower respiratory tract infection. The presence of a BNP level of over 267 pg/mL or an NGAL level of greater than 231 ng/mL correctly identified 15 of 16 early AKI patients, with a sensitivity of 94% and a specificity of 61%. the cystatin C level was less sensitive than the creatinine level for detecting AKI. (confirmation )