Dr. Ahmed Elberry provides an overview of acute kidney injury (AKI) including its definition, classification systems, causes, mechanisms, and clinical manifestations. AKI can be caused by prerenal, renal, or postrenal factors and results in a abrupt decrease in kidney function over hours to days. Common causes include ischemia, infections, drugs like NSAIDs, contrast media, and aminoglycosides. Patients with AKI may experience oliguria, azotemia, fluid overload, and electrolyte abnormalities.

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Dr. Ahmed A. Elberry, MBBCH, MSc, MD
Associate Professor of Clinical Pharmacy
Faculty of pharmacy,
KAU

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aelberry.kau.edu.sa
files
other
- Dyslipidemia
- Hypertension
- HF
- IHD
- Arrhythmia
- Thrombosis & DVT
- Shock
- Stroke

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10. Ahmed A. Elberry,MBBCH, MSc, MD
Associate Professor of Clinical Pharmacy,
Faculty of Pharmacy, KAU
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13. • Abrupt decrease in renal function over a period of hours
to days, resulting in the accumulation of nitrogenous
waste products (azotemia).
– ARF should now be restricted to patients who have AKI and
“need renal replacement therapy”.
• Definition & staging has been modified in 2004, 2007 &
2012
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14. Definition of decrease in renal function
-  in SCr of 0.5 mg/dL or more
or
-  in SCr 1.5-fold from
baseline
or
-  UO < 0.5 mL/kg/h for >6 h
or
-  GFR > 25%
-  in SCr of 0.3 mg/dL or more
or
-  in SCr 1.5-fold from
baseline
or
-  UO < 0.5 mL/kg/h for >6 h
-  in SCr of 0.3 mg/dL or more
within 48 h
or
-  in SCr 1.5-fold from
baseline within the last 7 days
or
-  UO < 0.5 mL/kg/h for >6 h
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ADQI group (2004): AKIN (2007): KDIGO (2012):
Definition of AKI
Abrupt (1-7 days)  in renal
function from base line
Abrupt (within 48 h)  in
renal function from base line
Abrupt (hours-days) in renal
function from base line

15. KDIGO criteria SCr criteria UO criteria
Statge 1 As AKIN As AKIN
Stage 2 As AKIN As AKIN
Stage 3 As AKIN
OR
eGFR < 35 mL/min. in patients < 18 years
As AKIN
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RIFLE category SCr & GFR criteria UO criteria
R SCr increased 1.5-2 times baseline
or
GFR decreased >25%
UO < 0.5 mL/kg/h >6 h
I SCr increased 2-3 times baseline
or
GFR decreased >50%
UO < 0.5 mL/kg/h >12 h
F SCr increased >3 times baseline
or
GFR decreased 75%
or
SCr ≥4 mg/dL with acute rise ≥0.5 mg/Dl
UO < 0.3 mL/kg/h 24 h
or
anuria >12 h
L Persistent failure: complete loss of kidney function >4 wk (requiring RRT)
E Complete loss of kidney function >3 mo (requiring RRT)
AKIN criteria SCr criteria UO criteria
Stage 1 SCr increased 1.5-2 times baseline
Or
SCr increased >0.3 mg/dL
As RIFLE (R)
Stage 2 SCr increased 2-3 times baseline As RIFLE (I)
Stage 3 SCr increased >3 times baseline
Or
SCr ≥4 mg/dL with acute rise ≥0.5 mg/dL
Or
Need RRT
As RIFLE (F)

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Community-
Acquired AKI
Hospital-
Acquired AKI
ICU-Acquired
AKI
Incidence Low (<1%) Moderate (7–20%) High (35–70%)
Cause Single Single or multiple Multifactorial
Overall mortality
rate (%)
15% 15–40% 30–90%
• Risk factors:
1. Renal ischemia: Elderly – Diabetics – Dehydration –
Diuretics – HF - Hepatic Cirrhosis - CKD, nephrotic
syndrome - Sepsis
2. Infections
3. Trauma
4. Drugs

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Prerenal (40-80 %)
 Intravascular
volume
 Intravascular
pressure
Hypovolemia
 Cardiac
output
Systemic
dilatation
- Burns
- Bleeding
- Excessive Sweat
- Diarrhea/vomiting
- Diuretic therapy
- DM: osmosis
- AMI
- HF
- Hypotension
- Septicemia
- Anaphylaxis
- Drugs
Afferent
constriction
Efferent
dilatation
- Sepsis
- Hypercalcemia
- Drugs: see later
- ACEIs/
ARBS
- CCB

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Afferent vasoconstrictors:
PGs inhibitors:
1- NSAIDS
2- COX-2 inhibitors
Direct vasoconstrictors:
1- Amphotericin-B
2- Pressors (NE)
3- Cyclosporine
4- Contrast media
Efferent vasodilators:
RAAS inhibitors::
1- ACEIs
2- ARBs
Direct vasodilators:
CCB (dihydropyridine,
Verapamil, diltiazem)

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Intrarenal (10-50%)
Glomerular
(5%)
Tubular
(85%)
Interstitial
(8-12%)
Vascular
(< 2%)
AGN
- post-
infectious,
- SLE
- NSAIDs
ATN
- Anoxic
(ischemia) 50%
- Toxic (30%)
Endo.: Hb,
Myoglobin
Exo: amph. B,
aminoglycosides
AIN
- Drug induced
NSAIDs,
antibiotics
- Infection related
pyelonephritis
- Infiltrative
lymphoma
- Granulomatous
sarcoidosis, TB
Vascular
occlusions
- Renal artery
occlusion
- Renal vein
thrombosis

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Postrenal (<10 %)
Obstruction Functional
Intrinsic Extrinsic
- Stone,
- Blood clots
- Stricture
- Fibrosis
- BPH, cancer prostate
- Bladder tumour
- Pelvic malignancies
- Prolapsed uterus
- Retroperitoneal
fibrosis
 Bladder
contractility
- Infection
- Anticholinergic
drugs

23. 1. Analgesics: NSAIDs
2. ACEIs/ARBs
3. Aminoglycosides
4. Amphotericicn B
5. Penicillins
6. Cyclosporin
7. Contrast media
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24. • Prerenal (mainly):
– due to afferent VC ( compensatory VD of PGs in cases of renal
ischemia that induces both PGs & RAAS [see before])
– Indomethacin has the highest risk, whereas aspirin has lowest risk.
Others are moderate. Sulindac may have “renal sparing” effect
– Selective COX-2 inhibitors: no benefit over non-selective NSAIDs
• Renal:
– AGN (glomerulonephropathy): due to increased leukotrienes
• The hall mark feature of NSAIDs-induced nephropathy is
nephrotic-range proteinuria. It resolves slowly over months once
stopped.
– ATN: due to peritubular ischemia
– AIN: due to immune mediated reaction
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25. • ACEIs/ARBs:
– as Prerenal mechanism of NSAIDs with the same
predisposing patients but acts on efferent causing
more efferent VD
• Penicillins, Cephalosporins, Sulfonamides,
Quinolones & Rifampin:
– as NSAIDs may cause immune mediated AIN
– Treatment:
1. Stop drug immediately
2. Maintain fluid & electrolyte balance
3. Corticosteroids (1mg/kg for a week, then
gradually taper)
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26. • Incidence:
– Affect 10% of all pts exposed to CM
– The incidence  in pts. with renal ischemia as in NSAIDs
• Mechanism:
– Prerenal VD followed by VC followed by
– ATN (main mechanism) due to peritubular medullary
ischemia
• Criteria:
– Progressive  in SCr 24-48 h after CM and this increase >
0.5 g/dL in 2-5 days
– Nonoliguric
– FENa is usually <1% (Unlike other causes of ATN >2%)
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27. • Prevention: 1 3 1 3 1 3
1. Avoid unnecessary procedure.
2. Avoid & Stop drugs: NSAIDs, COX-2 inhibitors, ACEIs,
ARBs, diuretics, and metformin (→lactic acidosis )
3. Volume expansion with isotonic saline (0.9% NaCl) 1
ml/kg/hr at least 12 hrs before imaging
4. Bicarbonate: 3 amps HCO3 in 5% dextrose;
– Preprocedure: bolus 3 mL/kg, 1 hour before,
– Postprocedure: 1mL/kg/hour for 6 hours
5. N-acetylcystiene, 600mg po BID (3doses before
imaging & 1 dose after) as it is antioxidant
6. Monitor SrCr for 48-72 hrs (3 days)
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28. • Incidence: Nephrotoxicity in 80% of cases
• Mechanism:
– ATN (mainly): direct cell membrane toxicity
– Prerenal: VC due to release of Thromboxane A2
• Prevention:
– Na+ loading (by IV saline)
– Use of lipid-based Am.B products
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• Taken by the macrophages present at the fungal
infection site, liberating AmB at site of infection 
preventing systemic AmB SE
• Affinity for fungal ergosterol > human ergosterol

29. • Incidence:
– The most common drug causing nephrotoxicity
– 10% and 25% of patients receiving a therapeutic
– neomycin> gentamicin = tobramycin = amikacin =
netilmicin> streptomycin
• Mechanism:
– ATN: 5% of filtered drug is actively reabsorbed by the PCT
cells  formation of myeloid bodies  tubular cells swell and
burst, releasing aminoglycoside & lysosomal enzymes into the
tubule lumen  further tubular destruction
• Extended-interval aminoglycoside dosing (One large daily dose)
– Advantages
1. Conc. Dependent killing activity
2. Postantibiotic effect observed with aminoglycoside
while minimizing time-dependent toxicity
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30. Patient factors:
1. Elderly
2. Underlying renal disease
3. Dehydration
4. Hypotension & shock
5. Hepatorenal syndrome
Aminoglycoside factors
1. Aminoglycoside choice: gentamicin >
tobramycin > amikacin
2. Therapy >3 days
3. Multiple daily dosing
4. Serum trough >2 mg/L
5. Recent aminoglycoside therapy
Concomitant therapy
1. Amphotericin B
2. Contrast media
3. Cisplatinum
4. Cyclosporine
5. Foscarnet
6. Furosemide
7. Vancomycin 30

31. • Pass in 3 phases:
1. Initial phase
2. Maintenance phase
3. Recovery phase
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32. • UO: (50% normal & 50% oliguria or anuria)
– Oliguria : UO ≤ 400 mL/day .
– Anuria: UO < 100 mL/day.
• Fluid overload
• Nitrogenous waste products accumulate in the blood due to impaired
glomerular filtration & concentrating capacity (Azotemia)
- SCr., sulfate, phosphate, & organic acid levels  rapidly.
• **Hyponatremia: dilutional hyponatremia.
• Hyperkalemia: Due to metabolic acidosis.
• Hyperphosphatemia due to phosphate excretion  hypocalcemia
 S& S of hypocalcemia (generally not seen in AKI ???
But seen in CKD)
• Metabolic acidosis
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34. • Diuretic phase: UO >500 mL/day ?? after several days of
oliguria. This “diuretic response” may not be seen in non-
oliguric patients
• Azotemia & associated laboratory findings may persist until UO
reaches 1000 -2000 mL/day.
• The maintenance phase carries a risk of fluid & electrolyte
abnormalities, GI bleeding, infection, & respiratory failure.
• Renal function gradually returns to normal (in
2 weeks; however, may continue for a year).
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35. • Non-specific: usually & Diagnosed accidently
• Symptomatic: in some patients
1. UO or anuria: from 20-500 mL/day. Complete anuria is rare.
2. S&S of hypervolemia (headache, confusion, blurred vision, N,V, HTN,
edema)
• S& S of hypovolemia may be in diuretic phase & if the cause is
prerenal
3. S&S of hyperkalemia, (resulting from metabolic acidosis & potassium
excretion):
4. Hyperphosphatemia
5. Hyponatremia.
6. Uremia caused by excessive nitrogenous waste retention
7. Metabolic acidosis 35

36. • Signs & symptoms of hyperkalemia: ???
• Hyponatremia
– Loss of concentration, impaired
consciousness, confusion, lethargy,
convulsions
– weakness
• Metabolic acidosis is evidenced by:
1.  CNS: lethargy & coma.
2.  CVS: hypotension, pulmonary edema,
ventricular fibrillation.
3. Respiration: Kussmaul’s respiration
(compensatory hyperventillation)
4. GIT: N, V
5. Skin: warm & flushed (VD)
6. Muscles: twitches & weakness
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37. • Hyperphosphatemia  hypocalcemia:
1. Confusion & convulsions.
2. Arrhythmia & Hypotension
3. Tetany & cramps
4. Stridor, spasm & soft tissue calcification.
• Uremia:
– A,N,V
– Astrexis (flapping tremors)
– Bleeding &
– Pericarditis
– Confusion, convulsions, coma
– Death
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38. • NB.:
–If the cause is prerenal 
Manifestations of Intravascular volume depletion:
• Hypotension, orthostatic hypotension,
• Dehydration, dry mm
–If the cause is postrenal 
• suprapubic or flank mass,
• costovertebral angle tenderness,
• bladder distention.
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40. 1. Conventional markers in Urine & blood
with calculation of CLcr, RFI, FENa
2. Novel biomarkers
3. Radiographic
4. Renal biopsy
5. ECG
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41. Prerenal Renal
1- Urine-specific gravity > 1018 < 1012
2- Urine osmolality. > 1.5 < 1.5
3- Urinary sediment
(Casts)
Hyaline casts • Epithelial or granular casts: in
ATN
• WBCs (eosinophilic) casts: AIN
• RBCs casts: AGN
4- Urinary Cr levels  Ucr  Ucr
5- Urinary Na Low <20 mEq/L High >40 mEq/L
6- FENa Low < 1% High > 2%
7- Renal failure index (RFI):
The ratio of UNa to
the Ucr -to- Scr. ratio.
< 1 > 2 (EXCEPT AGN < 1)
NB.: In post renal it is also > 2
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43. 1.  BUN
2.  SCr. (rapid increase >1 mg/dL/d)
3.  in Hb & Hct ( in cases of dehydration).
4. Abnormal serum electrolytes.
1. Hyperkalemia: Serum K above 5 mEq/L
2. Hyperphosphatemia: Serum phosphate above 2.6 mEq/L (4.8 mg/dL)
3. Hypocalcemia: Serum Ca below 4 mEq/L (8.5 mg/dL). (serum Ca level
must be correlated with the serum albumin level. Each rise or fall of 1
g/dL of serum albumin beyond its normal range is responsible for a
corresponding increase or decrease in serum calcium of approximately
0.8 mg/dL.)
4. Hyponatremia: Serum Na below 135 mEq/L
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44. • Cystatin C:
– cysteine proteinase, released into the plasma by all nucleated cells
in the body , then freely filtered by the glomeruli. It does not
undergo any secretion or reabsorption, but is completely
metabolized by PCT.
– Thus, a in GFR or tubular function   cystatin C in plasma &
urine conc.
• NGAL (neutrophil gelatinase–associated lipocalin ):
– Present on cell surfaces of neutrophils, freely filtered & reabsorbed
in PCT.
– Thus it increases in urine in tubular injury
• IL18: proinflammatory that  in urine in ATN
• KIM-1: biomarker that is  in urine in ATN 44

45. • Radiographic findings
– US may detect urinary tract obstruction.
– X- Ray may reveal urinary tract calculi.
– Radionuclide scan may reveal:
• slow radionuclide uptake, suggesting ATN.
– CT scan provide better visualization of obstruction.
• Renal biopsy: when other test results are
inconclusive.
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• Evidence of hyperkalemia: tall, peaked T waves;
widening QRS; prolonged PR interval, decreased
amplitude & disappearing P waves; ventricular
fibrillation & cardiac arrest.

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47. 1. Avoid dehydration
2. Avoid nephrotoxic drugs
3. Adequate hydration with isotonic solution
4. Na bicarb
5. Look for STOP (sepsis & hypotension, Toxins,
Obstruction, Parenchymal kidney disease)
• NB.: No role of the following despite theoretical benefits:
– Dopamine
– Fenoldopam
– Loop diuretics
– NAC
– Vit C 47

48. 1. Preventing further renal damage: through
correcting reversible causes
2. Prevention of complications & alleviation
of symptoms through correction of body
chemistry alteration & electrolyte imbalance
(may need dialysis).
3. Facilitate renal recovery through correction
& maintenance of fluid & electrolyte
balance.
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49. Treatment of AKI
Conservative
1- Fluid
management
2- Dietary
measures
Management of
body chemistry
alterations
1- Hyperkalemia
2- Hyperphosphatemia
3- Hypocalcemia
4- Hyponatremia
5- Metabolic acidosis
Management
of systemic
manifestation
Treatment of
fluid overload
& edema
RRT
1- hemodialysis
2- hemofiltration
3- hemodiafiltration
4- peritoneal
dialysis
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50. • Fluid management
– Fluid intake should match fluid losses (500-1000 mL/day). But
avoid overload (HTN & HF)
– Patient should be weighed daily to determine fluid volume
status.
• Dietary measures
– (1) High-calorie, low-protein diet
– (2)  Na If edema or HTN .
– (3)  K (Fruits, vegetables, & salt substitutes containing K).
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51. 1. Calcium chloride or calcium gluconate
2. Sodium bicarbonate
3. Sodium polystyrene sulfonate (SPS) (Kayexalate®)
4. Regular insulin with dextrose
5. Dialysis
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ACIDS

52. Hyperphosphatemia
Pharmacotherapy
1- Calcium carbonate, acetate, citrate:
2- Aluminum hydroxide (AlternaGel®)
3- Magnesium hydroxide, carbonate:
4- Sevelamer hydrochloride (Renagel®) or
carbonate (Renvela®):
5- Lanthanum carbonate (Fosrenol®):
Dialysis
In acute, life-threatening
hyperphosphatemia
accompanied by acute
hypocalcemia.
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53. • Calcium carbonate, acetate, citrate:
– IV calcium: first-line therapy for severe life-threatening
hyperphosphatemia.
– Oral: bind dietary phosphorus in the GIT.
• Aluminum hydroxide (AlternaGel®)
– Binds phosphate in the intestine (Onset of action is 6-12 hrs.)
– Orally as a tablet or 3-4 times daily with meals.
– SE: constipation& anorexia – osteomalacia – fatal neurological
symptoms (in dialysis patients (Dialysis encephalopathy))
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• Magnesium hydroxide, carbonate:
Not preferred as it is needed in high dose that may cause
severe diarrhea & hypermagnesemia (muscle weakness,
cardiac depression, CNS depression)

54. • Sevelamer hydrochloride (Renagel®)
or carbonate (Renvela®):
– binds dietary phosphorus in the GIT.
– In addition it decreases LDL level
– Sevelamer hydrochloride may increase
incidence of acidosis, while carbonate
may increase the bicarb level.
• Lanthanum carbonate (Fosrenol®):
– It dissociates into a trivalent cation with
similar binding capacity as aluminum
salts.
– Supplied as chewable tab. & excreted in
bile
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55. • New phosphate binders other
than sevelamer & lanthum??????
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56. • IV Calcium gluconate
• Oral calcium salts. Calcium carbonate, chloride, gluconate, or lactate
in mild hypocalcemia
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• Moderate or asymptomatic hyponatremia: fluid restriction.
• severe hyponatremia (serum Na < 120 mEq/L): 3% - 5% NaCl slow IV inf.
• Na bicarb. may be given if the arterial pH is < 7.35

57. • Diuretics (Mannitol or loop diuretic ) & dopamine
may be given to fluid volume excess & edema.
• Treatment should be initiated as soon as possible after
oliguria begins.
• NB.: Avoid Thiazides because
– they are ineffective when CLcr is less than 25 mL/min,
– they may worsen AKI.
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58. • Mechanism of action.
– Inhibit NaCl reabsorption at the loop of Henle,  water excretion
• Onset & duration of action
– Onset: orally (1 hr); IV (several minutes)
– Duration of action: orally (is 6 - 8 hrs); IV (2- 3 hrs).
58

59. Furosemide Bumetanide Torsemide Ethacrynic a.
• The most commonly
used,
• Used IV in AKI. The
usual initial dose is 1.0
- 1.5 mg/kg. If the 1st
dose does not
produce UO of 10-15
mL within 30 mins, a
dose of 2 - 3 mg/kg is
given; if the desired
response still does not
occur, a dose of 3-6
mg/kg is given 30
mins after the 2nd
dose.
• If unresponsive or
allergic to
furosemide.
• IV or IM in the ttt of
AKI, 0.5-1.0 mg/day;
up to 20 mg/day. A
2nd or 3rd dose may
be given at intervals
of 2-3 hrs.
• Orally, 0.5-2
mg/day, repeat up
to 2 times, if
needed, every 2 - 3
hrs.
•If unresponsive to or
allergic to
furosemide.
•IV, 20 mg, & may be
increased by
doubling up to 200
mg; 10-20 mg of
torsemide = 40 mg
of furosemide = 1
mg bumetanide.
•Better OBA
compared to other
loop diuretics; but,
it is more expensive.
• Less commonly
used because
ototoxicity.
given to patients
who are allergic
to sulfa.
• It may be given
IV (slowly for
several minutes)
50-100 mg.
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60. • Hpokalemia , Hyponatremia , Hypomagnesemia,
Hypochloremic alkalosis (monitor electrolytes)
• Hyper uricemia , Hyper glycemia (monitor glu in DM),
Hyper lipidemia , Hyper sensitivity
• Decrease calcium, Deafness (esp with rapid IV),
Dehydration (monitor BP), Disturbance of GIT
• Drug interaction:
1. Aminoglycoside potentiate the ototoxicity of loop diuretic.
2. NSAIDs antagonize the diuretic response.
3. Ethacrynic acid potentiate warfarin anticoagulants.
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61. • Mechanism of action.
–  the osmotic pressure in
• Blood  hypervolemia   RBF & GFR
• Glomerular filtrate   urine flow.
– Used to prevent AKI in high-risk patients, such as those
undergoing surgery.
• Onset of action:
– 15-30 mins. Duration of action is 3-4 hrs.
• Administration and dosage.
– is available in solutions ranging from 5% - 25%.
– Initial dose (12.5- 25.0 g) IV; the maximum daily
dose is 100 g.
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62. • SE. & MONITORING:
A. Hypervolemia & hyponatremia:
– due to osmotic effect in Bl.V.
– This effect can lead to water intoxication:
» complicate HF & pulmonary edema.
» Headache, confusion, blurred vision, nausea, & vomiting.
B. Dehydration, Hyperkalemia, & Hypernatremia
– Excessive use of mannitol can lead to severe
dehydration, hypernatremia & hyperkalemia. (monitor
electrolytes)
• CI:
1. anuria,
2. pulmonary edema or congestion,
3. intracranial hemorrhage.
4. severe dehydration,
62

63. Causes of Diuretic Resistance Potential Therapeutic Solutions
1-  Na intake (dietary, IV fluids, drugs) Remove Na from diet & medications
2- Inadequate diuretic dose or inappropriate
regimen
 dose, use continuous infusion or combination
3- Reduced OBA (usually furosemide) Use parenteral therapy;
Switch to oral torsemide or bumetanide
4- Nephrotic syndrome (loop diuretic protein binding
in tubule lumen)
 dose, switch diuretics, use combination therapy
5- Reduced renal blood flow
Drugs (NSAIDs, ACEIs, vasodilators)
Hypotension
Intravascular depletion
Discontinue these drugs if possible
Intravascular volume expansion and/or vasopressors
Intravascular volume expansion
6- sodium resorption
Nephron adaptation to chronic diuretic therapy
NSAID use
Heart failure
Cirrhosis
Combination diuretic therapy, sodium restriction
Discontinue NSAID
Treat HF,  diuretic dose, switch to better-absorbed
loop diuretic
Paracentesis
7- ATN  dose of diuretic, diuretic combination therapy;63

64. • Dosing of continuous inf.:
– Initial loading dose is given (equivalent to furosemide 40–80 mg) prior
to the initiation of a continuous infusion at 10 - 20 mg/h of furosemide
or its equivalent
• Advantage of continuous inf.:
– Less incidence of diuretic resistance
– Less incidence of SE as ototoxicity & myalgia
64

65. • Indications:
1. Anuria,
2. Acute fluid overload (acute pulmonary edema)
3. Metabolic Acidosis ( less than 7.2)
4. severe hyperkalemia,
5. BUN level above 100 mg/dL.
65

66. • Mortality rate:
– varies according to the cause (increase in intrinsic causes)
– The % increases in:
• multi-organ failure, (70%).
• over 60 years age.
• Cause of Death:
– Death resulting from uremia and hyperkalaemia are very
uncommon.
– The major causes of death are septicemia & intercurrent
acute vascular events (as MI & stroke).
66

67. •  in BUN or the SCr without  in GFR due to:
– Cross-reactivity with the assay used to measure the BUN or SCr
– Drugs inhibiting the secretion of Cr (eg. Clavulanic acid,
cephalexin, cephradin)
Or
•  in UO without real  in GFR due to:
– Inaccurate method of measurement
– Obesity
67

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