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Renal Failure.

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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

47

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

56

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

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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


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