1. Renal Failure

2. Renal Failure
Results when kidney’s cannot remove wastes or perform regulatory functions
Systemic disorder resulting from many different causes
ARF : Reversible syndrome that results in decreased GFR and oliguria (Fast & Days )
CRF : Progressive ( Slow & Years ); Irreversible deterioration of renal function resulting in azotemia
Both types result in loss of ability to maintain normal volume and composition of body fluids

3. Assessment of Renal Function
Glomerular Filtration Rate (GFR)
= The volume of water filtered from the plasma per unit of time.
Gives a rough measure of the number of functioning nephrons
Normal GFR:
Men: 130 mL/min./1.73m2
Women: 120 mL/min./1.73m2
Cannot be measured directly, so we use creatinine and creatinine clearance to estimate.

4. Assessment of Renal Function
Creatinine
As plasma creatinine increases, the GFR exponentially decreases.
Limitations to estimate GFR:
Patients with decrease in muscle mass,, malnutrition, advanced age, may have low/normal creatinine despite underlying kidney disease
Medications may artificially elevate creatinine:
Trimethroprim
Cimetidine

5. Assessment of Renal Function
Creatinine Clearance
Best way to estimate GFR
GFR = (creatinine clearance) x (body surface area in m2/1.73)
Ways to measure:
24-hour urine creatinine:
Creatinine clearance = (Ucr x Uvol)/ plasma Cr
Cockcroft-Gault Equation:
                             (140 - age)  x  lean body weight [kg] CrCl (mL/min)    =    ——————————————— x 0.85 if                                          Cr [mg/dL]  x   female

6. Major causes of Kidney Failure
Prerenal Disease
Vascular Disease
Glomerular Disease
Interstitial/Tubular Disease
Obstructive Uropathy

7. Acute Renal Failure
Relatively sudden onset of renal failure that is potentially reversible

8. Acute Renal Failure Risk factor for acute renal failure
An abrupt decrease in renal function sufficient to cause retention of metabolic waste such as urea and creatinine.
Most community acquired acute renal failure (70%) is prerenal
Most hospital acquired acute renal failure (60%) is due to ischemia or nephrotoxic tubular epithelial injury (acute tubular necrosis).
Mortality rate 50-70%
Risk factor for acute renal failure
Advanced age
Preexisting renal parenchymal disease
Diabetes mellitus
Underlying cardiac or liver disease
Early sign of ARF is oliguria.
Only seen in 2/3 of ARF pts.
Frequently have:
Metabolic acidosis
Hyperkalemia
Disturbance in body fluid homeostasis
Secondary effects on other organ systems

9. Definition of Acute Renal Failure Based on “Acute Kidney Injury Network”
Stage
Increase in Serum Creatinine
Urine Output 1
1.5-2 times baseline OR
0.3 mg/dl increase from baseline
<0.5 ml/kg/h for >6 h 2
2-3 times baseline
<0.5 ml/kg/h for >12 h 3
3 times baseline OR
0.5 mg/dl increase if baseline>4mg/dl
Any RRT given
<0.3 ml/kg/h for >24 h
Anuria for >12 h

10. RIFLE criteria for diagnosis of ARF based on The “Acute Dialysis Quality Initiative”
Increase in SCr
Urine output
Risk of renal injury
Injury to the kidney
Failure of kidney function
0.3 mg/dl increase
2 X baseline
3 X baseline OR
> 0.5 mg/dl increase if SCr >=4 mg/dl
< 0.5 ml/kg/hr for > 6 h
< 0.5 ml/kg/hr for >12h
Anuria for >12 h
Loss of kidney function
End-stage disease
Persistent renal failure for > 4 weeks
Persistent renal failure for > 3 months

11. Classification of ARF Acute Renal Failure Pre-renal Intrinsic
Post-renal
Glomerular
Interstitial
Tubular
Vascular

12. Acute Renal Failure Intrinsic causes Post Renal Causes
Pre Renal Causes
Intrinsic causes
Post Renal Causes
Tubular Interstitial Acute
Necrosis Nephritis Glomerulonephritis
(10% of cases) (5% of cases)
Ischemia Toxins
(50% of cases) (35% of cases)

13. Ischemic Acute Renal Failure
Intravascular volume depletion and hypotension
Gastrointestinal, renal, dermal losses, hemorrhage, shock
Decreased effective intravascular volume: CHF, cirrhosis, nephrosis, peritonitis
Large vessel renal vascular disease: Renal artery thrombosis or embolism, Renal artery stenosis
Generalized
or localized reduction in
renal blood flow
Medications: ACE inhibitors, NSAIDS, radiocontrast agents, Ampho B, Cyclosporin
Small vessel renal vascular disease:
Atheroembolism, vasculitis, malignant
hypertension, hypercalcemia,
transplant rejection
Hepatorenal syndrome
Sepsis
Ischemic
Acute Renal Failure

14. Blocked by ACE inhibitors
Effects of NSAIDS and ACE inhibitors on Glomerular Hydrostatic Pressure
Prostaglandins cause
afferent vaso dilation
Locally produced AII causes efferent vaso constriction
Blocked by ACE inhibitors
Blocked by NSAIDS

15. Most common causes of ACUTE Renal Failure
Prerenal ( Community )
Acute Tubular Necrosis (ATN) – ( Hospitals )
Acute on chronic renal failure (usually due to ATN or prerenal)
Obstructive uropathy
Glomerulonephritis/Vasculitis
Acute Interstitial nephritis
Atheroemboli

16. Major Disease Categories Causing ARF
Disease Category
Incidence
Prerenal Azotemia caused by acute renal hypoperfusion
55-60%
Intrinsic Renal Azotemia caused by acute diseases of renal parenchyma:
-Large renal vessels dis.
-Small renal vessels and glomerular dis.
-ATN (ischemic and toxic)
-Tubulo-interestitial dis.
-Intratubular obstruccttion
35-40%
*>90%*
Postrenal Azotemia caused by acute obstruction of the urinary tract
<5%

17. Prerenal Azotemia Intravascular volume depletion
Bleeding, GI loss, Renal loss, Skin loss, Third space loss
Decreased cardiac output
CHF
Renal vasoconstriction
Liver Disease, Sepsis, Hypercalcemia
Pharmacologic impairment of Autoregulation and GFR in specific settings
ACEI in bilateral RAS, NSAIDS in any renal hypoperfusion setting

18. Renal Acute Renal Failure
Acute Tubular Necrosis(ischaemic or toxic) [ATN]
Interstitial nephritis
Glomerular disease
Renal Vascular Disease
Microvascular
Vasoconstriction
Tubular Obstruction
70% ATN
Drugs (Aminoglycosides,NSAIDs, Amphotericin)
Rhabdomyolysis
Iodinated contrast agents
Heavy metals
Prolonged ischaemia
Combination of the above

19. Intrinsic Renal Azotemia
Large Renal Vessel Disease
Thrombo-embolic disease
Renal Microvasculature and Glomerular Disease
Inflammatory: glomerulonephritis, allograft rejection
Vasospastic: malignant hypertension, scleroderma crisis, pre-eclampsia, contrast
Hematologic: HUS-TTP, DIC
Acute Tubular Necrosis (ATN)
Ischemic
Toxic
Tubulo-interestitial Disease
Acute Interestitial Nephritis (AIN), Acute cellular allograft rejection, viral (HIV, BK virus), infiltration (sarcoid)
Intratubular Obstruction
myoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)

20. Acute Tubular Necrosis
Most common form of “Renal” ARF
Tubular damage, loss of tubular function with direct effect on GFR
U/P osmol =1, U/P creatinine 10-20, UNa+ > 40 mmol/l
Duration days to 6 weeks
Oliguria most common but anuria and polyuria possible
Diuretics do not change course of ATN but can increase water excretion
High mortality even with dialysis (ATN associated with other organ failure

21. Postrenal Azotemia Stones Blood clots Papillary necrotic tissue
Urethral disease
Anatomic: posterior valve
Functional: anticholinergics, L-DOPA
Prostate disease
Bladder disease
Anatomic: cancer, schistosomiasis
Functional: neurogenic bladder

22. Urine Output in Acute Renal failure
Oliguria
= Daily urine output < 400 mL
When present in acute renal failure, associated with a mortality rate of 75% (versus 25% mortality rate in non-oliguric patients)
Most deaths are associated with the underlying disease process and infectious complications
Anuria
No urine production
Probably time for dialysis

23. Phases of Acute Renal Failure
Phases of rapid decrease in renal function lead to the collection of metabolic wastes in the body.
Phases include:
Oliguric
Diuretic
Recovery
Acute syndrome may be reversible with prompt intervention.

24. Oliguric Phase
Clinical picture dominated by surgical, medical or obstetric problem causing ARF
Oliguria within hours of initial injury
May take several days to develop with nephrotoxic chemicals
Azotemia accompanies oliguria
Critical to recognize, determine cause and begin treatment
Oliguria caused by acute-on-chronic RF usually easy to detect from history
Post renal obstruction must be ruled out
Prerenal oliguria most common condition leading to ARF and must be distinguished from ATN

25. Diuretic Phase Begins when urine output increases to >400 ml/day
Usually lasts 2-3 weeks
Urine output rarely exceeds 4 L/day
Caused partly by osmotic diuresis due to high blood urea and partly by impaired ability of recovering tubules to conserve salts and water
May develop K+, Na+ and water deficits
Must replace loses or death
BUN may continue to rise as clearance does not keep up with production
With continued diuresis azotemia gradually disappears and get clinical improvement

26. Recovery Phase Lasts up to one year
Anemia and concentrating ability gradually improve
Some have permanent reduction in GFR
ATN serious condition (still 50% mortality – down from 90% 30 years ago)
About 2/3 die during oliguric stage and about 1/3 during diuretic stage
Mortality related to cause
60% after surgery, crushing injuries
25% after CCl4, bad transfusion
10-15% in obstetric cases
With non-oliguric ARF – 25% mortality

27. Natural Clinical Course of ATN
Initiation Phase (hours to days)
Continuous ischemic or toxic insult
Evolving renal injury
ATN is potentially preventable at this time
Maintenance Phase (typically 1-2 wks)
May be prolonged to 1-12 months
Established renal injury
GFR < 10 cc/min, The lowest UOP
Recovery Phase
Gradual increase in UOP toward post-ATN diuresis
Gradual fall in SCr (may lag behind the onset of diuresis by several days)

28. ARF: Systemic Complications
Infections of urinary tract & lungs due to uremia
Up to 70% of pts. with ARF.
#1 cause of ARF morbidity/mortality
Anemia
Kidney makes EPO, ↓ EPO anemia (HCT 20-30)
“3rd space disease”
Salt and Water retention (esp. in prerenal failure)
Pulmonary edema, Pleural effusion, & ascites
Hypocalcemia
↓ Excretion of phosphate impaired GI absorption of Calcium.
Hyperkalemia
↓ Glomerular filtration, ↓ Tubular secretion
Malaise, nausea, and muscle weakness.
A cardiac emergency
Metabolic Acidosis w/ ↑ Anion Gap
↓ Excretion of acids & ↓ tubular reabsorption of bicarbonate results in metabolic acidosis with a high anion gap.
Hypotension, Kussmaul’s respirations

29. Initial Diagnostic Tools in ARF
History and Physical examination
Detailed review of the chart, drugs administered, procedures done, hemodynamics during the procedures.
Urinalysis (SG, PH, protein, blood, crystals, infection )
Urine microscopy {casts, cells (eosinophils)}
Urine Electrolytes
Renal imaging (US, CT Scan ,Retrograde Pyelogram )
Markers of CKD (iPTH, size<9cm, anemia, high phosphate, low bicarbbonate
Renal biopsy

30. Assessing the patient with ARF
History:
Cancer?
Recent Infections?
Blood in urine?
Change in urine output?
Flank Pain?
Recent bleeding?
Dehydration? Diarrhea? Nausea? Vomiting?
Blurred vision? Elevated BP at home? Elevated sugars?

31. Assessing the patient with ARF
Family History:
Cancers?
Polycystic kidney disease?
Medications:
Any non-compliance with diabetic or hypertensive meds?
Any recent antibiotic use?
Any NSAID use?

32. Assessing the patient with ARF Physical Exam
Vital Signs:
Elevated BP: Concern for malignant hypertension
Low BP: Concern for hypotension/hypoperfusion (acute tubular necrosis)
Neuro:
Confusion: hypercalcemia, uremia, malignant hypertension, infection, malignancy
HEENT:
Dry mucus membranes: Concern for dehydration (pre-renal)
Abdomen:
Ascites: Concern for liver disease (hepatorenal syndrome), or nephrotic syndrome
Extremities:
Edema: Concern for nephrotic syndrome
Skin:
Tight skin, sclerodactyly – Sclerodermal renal crisis
Malar rash - Lupus

33. Assessing the patient with ARF Laboratory Analysis
Fractional Excretion of Sodium:
(UrineNa+ x PlasmaCreatinine)
FENa= ______________________ x 100
(PlasmaNa+ x UrineCreatinine)
FENa < 1% → Prerenal
FENa > 2% → (Acute Tubular Necrosis), obstructive uropathy
If patient receiving diuretics, can check FE of urea.

34. Assessing the patient with ARF Radiology
Renal Ultrasound
Look for signs of hydronephrosis as sign of obstructive uropathy.

35. Assessing the patient with ARF Urinalysis
Hematuria
Non-glomerular:
Urinary sediment: intact red blood cells
Causes:
Infection
Cancer
Obstructive Uropathy
Rhabdomyolysis
Myoglobinuria; Hematuria with no RBCs
Glomerular:
Urine sediment: dysmorphic red blood cells, red cell casts
Glomerulonephritis
Vasculitis
Atheroembolic disease
TTP/HUS (Thombotic Microangiopathy)

36. Assessing Patient with ARF Urinalysis (cont.)
Protein
Need microscopic urinalysis to see microabluminemia
Can check 24-hour urine protein collection
Nephrotic syndrome - ≥ 3.5 g protein in 24 hours
Albuminuria
Glomerulonephritis
Atheroembolic disease
(TTP/HUS) Thrombotic microangiopathy
Nephrotic syndrome
Tubular proteinuria
Tubular epithelial injury (acute tubular necrosis)
Interstitial nephritis

37. Assessing patient with acute renal failure Urinary Casts
Red cell casts
Glomerulonephritis
Vasculitis
White Cell casts
Acute Interstitial nephritis
Fatty casts
Nephrotic syndrome, Minimal change disease
Muddy Brown casts
Acute tubular necrosis

38. Urine Indices in ARF > 500 < 350 < 20 > 40 > 20:1
Pre Renal
Intrinsic ATN
Post Renal
> 500
< 350
< 20
> 40
> 20:1
< 10:1
< 1%
<35%
>3%
>55%
Hyaline casts
Brown, Granular casts,
Bland
Uosm
Na (meq/L)
Bun/Cr (mg/dL)
FENa
FEUrea
Sediment

39. When to do Renal Biopsy in ARF?
If unable to discover cause of renal disease
Any evidence of glomerular disease
-Nephrotic range proteinuria
-Sub-nephrotic range proteinuria with hematuria
-RBC cast
ARF in renal allograft
Determine the prognosis and chance of recovery of renal function in dialysis dependent ARF.
Whenever potential Biopsy result can change the management or prognosis.

40. Treatment of Acute Renal Failure
Treat underlying cause
Blood pressure
Infections
Stop inciting medications
Nephrostomy tubes/ureteral stents if obstruction
Treat scleroderma renal crisis with ACE inhibitor
Hydration
Diuresis (Lasix)
Renal Replacement Therapy : Dialysis & Renal Transplant
Pharmacologic treatments under study:
Dopamine: no benefit
Atrial Natriuretic Peptide (ANP) or ANP-analogue (Anaritide): promising

41. When to initiate RRT in a patient with ARF?
1) Renal Replacement Therapy:
Electrolytes imbalances
Acid-base disturbances
Uremic complications
-Encephalopathy
-Pericarditis
-Gastropathy
2) Renal/Multiorgan Support Therapy
-Protects other organs by improving overall body milieu (balance of inflammatory mediators)
-Allowing therapies for other organs that pt could not otherwise tolerate
-Volume resuscitation
-Aggressive nutrition

42. 3) Removal of toxic agents in overdose
-Ethylene Glycol
-Methanol
-Salicylates
-Lithium
-Theophylline

43. Indications for Hemodialysis
Refractory fluid overload
Hyperkalemia (plasma potassium concentration >6.5 meq/L) or rapidly rising potassium levels
Metabolic acidosis (pH less than 7.1)
Azotemia (BUN greater than 80 to 100 mg/dL )
Signs of uremia, such as pericarditis, neuropathy, or an otherwise unexplained decline in mental status
Severe dysnatremias (sodium concentration greater than 155 meq/L or less than 120 meq/L)
Hyperthermia
Overdose with a dialyzable drug/toxin

44. Chronic Renal Failure
Chronic renal failure: Slowly progressive and non- reversible loss of kidney function
Uraemia: Metabolic outcome of chronic renal failure
End-stage renal disease: Requirement for renal replacement therapy

45. Chronic Kidney Disease
= a GFR of < 60 for 3 months or more.
Most common causes:
Diabetes Mellitus
Hypertension
Management:
Blood pressure control!
Diabetic control!
Smoking cessation
Dietary protein restriction
Phosphorus lowering drugs/ Calcium replacement
Most patients have some degree of hyperparathyroidism
Erythropoietin replacement
Start when Hgb < 10 g/dL
Bicarbonate therapy for acidosis
Dialysis?

46. Stages of Chronic Kidney Disease
Description
GFR (mL/min/1.73 m2) 1
Kidney damage with normal or increased GFR
≥ 90 2
Kidney damage with mildly decreased GFR
60-89 3
Moderately decreased GFR
30-59 4
Severely decreased GFR
15-29 5
Kidney Failure ( ESRD )
< 15

48. Progression of Chronic Renal Failure
Factors causing progression
Sustaining primary disease
Systemic hypertension
Proteinuria
Nephrocalcinosis
Dyslipidaemia
Imbalance between renal energy demands and supply

49. What is ESRD?
The deterioration of nephrons resulting in loss of ability to excrete wastes, concentrate urine, and regulate electrolytes.
Occurs as chronic or acute renal failure progressing to the point where function is less than 15% of normal.
Function is so low that without dialysis or kidney transplantation, death will occur from accumulation of fluids and waste products in the body.
ESRD almost always follows chronic kidney failure, which may exist for years or more before progression to ESRD.

50. Chronic Renal Failure Percentage incidence Common causes of ESRD
Diabetes mellitus 50
Glumerulonephritis 10
Hypertension 20
Polycycstic kidney disease 5
Vesicouretic reflux
Analgesic nephropahty
Other

51. Diabetes (most common cause) Congestive Heart Failure
Causes
Hypertension
Diabetes (most common cause)
Congestive Heart Failure
Chronic Glomerulonephritis

52. Aminoglycoside nephrotoxicity
Causes
Aminoglycoside nephrotoxicity
(Gentamycin)
IV contrast medium
Long term use of NSAIDS

53. Causes
Prostate Cancer
Nephrolithiasis

54. Systemic Lupus Erythrematosus Polycystic Kidney Disease
Causes
Systemic Lupus Erythrematosus
Polycystic Kidney Disease
Amyloidosis
Atherosclerosis

55. Decreased biosynthesis
Chronic Renal Failure
Main consequences
Mechanism
Example
Consequence
Decreased excretion
Uraemic toxins
Salt and water
Phosphate
Acid
Potassium
Uraemic syndrome
Volume overload, hypertension
Hyperparathyroidism
Metabolic acidose
Hyperkalaemia
Decreased biosynthesis
Erythropoietin
Activation of vitamin D
Anaemia
Osteomalacia, Hyperparathyroidism
Altered metabolism
Dyslipidaemia
Sex hormones
Atherogenesis
Abnormal reproductive function

57. Symptoms of ESRD Unintentional weight loss Nausea or vomiting Fatigue
Headache
Generalized itching
Greatly decreased urine output
Easy bruising or bleeding
Decreased alertness
drowsiness, somnolence, lethargy
confusion, delirium , coma
Muscle twitching or cramps
Seizures
Increased skin pigmentation
Skin may appear yellow or brown
Nail abnormalities
Decreased sensation in the hands, feet, or other areas

58. Chronic Renal Failure : Treatment
Differentiate from ARF
Establish aetiology
Establish severity
Treat reversible factors
Treat complication
Changes in lifestyle
Avoid or treat factors causing progression
Dialysis
Transplantation

59. Dialysis or kidney transplantation are the only treatments for ESRD
Diseases that cause or result from chronic renal failure must be controlled.
Hypertension, congestive heart failure, urinary tract infections, kidney stones, obstructions of the urinary tract, glomerulonephritis, and other disorders should be treated appropriately
Dialysis or kidney transplantation are the only treatments for ESRD

60. Pre-Dialysis Treatment
Maintain normal electrolytes
Potassium, calcium, phosphate are major electrolytes affected in CRF
ACE inhibitors may be acceptable in many patients with creatinine >3.0mg/dL
ACE inhibitors may slow the progression of diabetic and non-diabetic renal disease , Reduce or discontinue other renal toxins (including NSAIDS)
Diuretics (eg. furosemide) may help maintain potassium in normal range
Renal diet including high calcium and low phosphate

61. Permanent Vascular Access

62. Dialysis Method of removing toxic substances from the blood
Dialysis Method of removing toxic substances from the blood. Blood is diverted from the access through a filter. The blood flows counter-current to a special solution called the dialysate. The electrolyte imbalances and toxins in the blood are corrected and returned to the body.
Hemodialysis
Peritoneal

63. Hemodialysis
Works by circulating the blood, from an access in the body, through a semi-permeable filter in the dialysis machine that helps remove toxins. The cleansed blood is then returned to the body.
Typically, most patients undergo hemodialysis for three sessions every week. Each session lasts 3-4 hours
Patients on hemodialysis are always heparinized to prevent clotting of the AV access.
Indicated in chronic tx and obese patients

64. Hemodialysis : Indications
Uremia - azotemia with symptoms and/or signs
Severe Hyperkalemia
Volume Overload - usually with congestive heart failure (pulmonary edema)
Toxin Removal - ethylene glycol poisoning, theophylline overdose, etc.
An arterio-venous fistula in the arm is created surgically
Catheters are inserted into the fistula for blood flow to dialysis machine

65. Complications of Hemodialysis
Dialysis disequilibrium syndrome
Infectious diseases
Hepatitis B and C infections
HIV exposure—poses some risk for patients undergoing dialysis
S&P

66. Peritoneal
Works by using the body's peritoneal membrane, inside the abdomen, as a semi-permeable membrane.
Solutions that help to remove toxins are infused in, remain in the abdomen for a certain time period, and are eventually drained out.
This can be done at home on a continuous basis. (CAPD )
Indicated in patients with ARF, require occasional dialysis, or those who are young and have the capability of doing this at home.
Types of peritoneal dialysis:
Continuous ambulatory peritoneal
Automated peritoneal
Intermittent peritoneal
Continuous-cycle peritoneal

67. Complications Peritonitis Pain Exit site and tunnel infections
Poor dialysate flow
Dialysate leakage
Other complications

68. Renal Transplantation
Candidate selection criteria
Donors
Preoperative care
Immunologic studies
Surgical team
Operative procedure

70. Differentiation between ARF & CRF
Renal Failure
Differentiation between ARF & CRF
Acute
Chronic
History
Short (days-week)
Long (month-years)
Haemoglobin concentration
Normal
Low
Renal size
Reduced
Renal osteodystrophy
Absent
Present
Peripheral neuropathy
Serum Creatinine concentration
Acute reversible increase
Chronic irreversible

71. Acute Interstitial/Tubular Disease
Acute Tubular Necrosis:
One of the most causes of acute renal failure in hospitalized patients
Causes:
Hypotension, Sepsis
Toxins: Aminoglycosides, Amphotericin,, Pentamadine, IV contrast
Rhabdomyolysis (heme-pigments are toxins)
Urine sediment: muddy brown granular casts
Acute Interstitial Nephritis:
Drugs: Antibiotics, Proton-pump inhibitors, NSAIDS, allopurinol
Infections: Legionella, Leptospirosis
Auto-immune disorders
Urine sediment: urine eosinophils (but not always present), white blood cells, red blood cells, white cell casts
Cast Nephropathy – Multiple Myeloma
Tubular casts – PAS-negative, and PAS-positive (Tamm-Horsefall mucoprotein)

72. Chronic Interstitial Tubular Disease
Polycystic Kidney Disease
Hypercalcemia
Autoimmune disorders
Sarcoidosis
Sjögren’s syndrome

73. Increase in Creatinine without ARF
Inhibition of tubular creatinine secretion
Trimethoprim, Cimetidine, Probenecid
Interference with creatinine assays in the lab (false elevation)
glucose, acetoacetate, ascorbic acid, cefoxitin
flucytosine

74. Increase in BUN without ARF
Increased production
GI Bleeding
Catabolic states (Prolonged ICU stay)
Corticosteroids
Protein loads (TPN-Albumin infusion)

75. New Biomarkers in ARF Alternatives to Serum Creatinine
Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL)
Urinary Interleukin 18
Urinary Kidney Injury Molecule 1 (KIM-1)

76. Is there a role for Dopamine in prevention or treatment of ARF in ICU setting?
Clinical Outcomes:
No effect on mortality
No effect on the need for or incidence of Renal Replacement Therapy (RRT)
Renal Physiologic Outcomes:
Diuretic effect and increased creatinine clearance on the first day which was not significant on the following days.
Adverse effect:
on the immune, respiratory, and endocrine system.

77. Role of ANP analogues in ARF ?
61 patients in 2 cardiothoracic ICU with post-op ARF assigned to receive recombinent ANP (50ng/kg/min) or placebo
The need for RRT before day 21 after development of ARF was significantly lower in ANP group (21% vs 47%)
The need for RRT or death after day 21 was significantly lower in ANP group (28% vs 57%)

78. Is there a role for Fenoldepam in prevention or treatment of AKI in ICU setting?
Dopamine-1 receptor agonist, lack of Dopamine-2, and alpha-1 receptor effect, make it a potentially safer drug than Dopamine!
Reduces in hospital mortality and the need for RRT in ARF
Reverses renal hypoperfusion more effectively than renal dose Dopamine
So far so good specially in cardiothoracic ICU patients, awaiting more powered trials in other groups!

79. Is there a role for diuretics in the treatment of ARF in ICU setting?
PICARD Study:
Cohort study of 552 pts in 4 UC hospitals:
Odds Ratio
In-hospital Mortality
Non-recovery of renal function
Improved urine output and shorter duration of RRT (none has clinical relevance in ICU pts)
But diuretics continue to be used for volume control in ARF in ICU setting!

80. CRRT vs SLED (Sustained low efficiency dialysis)
SLED became popular because of CRRT disadvantages:
Expensive, continuous pt immobilization, need for specialized machines and pre-mixed commercial solutions, and anticoagulation
Only 2 small studies compared these 2 in hemodynamically unstable pts with ARF
They did not see significant differences in hemodynamic parameters and solute clearance
They did not look at any patient-relevant outcomes, so the jury is still out there

81. Overall conclusion on RRT modality benefit in ARF
CRRT does not confer a survival advantage as compared to IHD
SLED may replace CRRT although there is no outcome benefit study up to this date
There is limited data regarding the ideal timing of RRT initiation and the preferred mode of solute clearance
No evidence to support a more intensive strategy of RRT in the setting of AKI