Pandian M
Dept. of Physiology
Overview
 Definitions
 Classification and causes
 Presentation
 Treatment
Definition Acute Renal failure (ARF)
 Inability of kidney to maintain homeostasis leading to
a buildup of nitrogenous wastes
 Different to renal insufficiency where kidney function
is deranged but can still support life
 Exact biochemical/clinical definition not clear – 26
studies – no 2 used the same definition
ARF
 Occurs over hours/days
 Lab definition
 Increase in baseline creatinine of more than 50%
 Decrease in creatinine clearance of more than 50%
 Deterioration in renal function requiring dialysis
ARF definitions
 Anuria – no urine output or less than 100mls/24 hours
 Oliguria - <500mls urine output/24 hours or
<20mls/hour
 Polyuria - >2.5L/24 hours
ARF
 Pre renal (functional)
 Renal-intrinsic (structural)
 Post renal (obstruction)
ARF Pirouz Daeihagh, M.D.Internal medicine/Nephrology Wake Forest University School of Medicine. Downloaded 4.6.09
Causes of ARF
 Pre-renal:
Inadequate perfusion
 check volume status
 Renal:
ARF despite perfusion & excretion
 check urinalysis, FBC & autoimmune screen
 Post-renal:
Blocked outflow
 check bladder, catheter & ultrasound
Causes of ARF
Pre-renal Renal Post-renal
Absolute
hypovolaemia
Glomerular
(RPGN)
Pelvi-calyceal
Relative
hypovolaemia
Tubular
(ATN)
Ureteric
Reduced
cardiac output
Interstitial
(AIN)
VUJ-bladder
Reno-vascular
occlusion
Vascular
(atheroemboli)
Bladder neck-
urethra
ARF Pre renal
 Decreased renal perfusion without cellular injury
 70% of community acquired cases
 40% hospital acquired cases
ARF Intrinsic
 Acute tubular necrosis (ATN)
 Ischaemia
 Toxin
 Tubular factors
 Acute interstitial Necrosis (AIN)
 Inflammation
 oedema
 Glomerulonephritis (GN)
 Damage to filtering mechanisms
 Multiple causes as per previous presentation
ARF Post renal
 Post renal obstruction
 Obstruction to the urinary outflow tract
 Prostatic hypertrophy
 Blocked catheter
 Malignancy
Prerenal Failure 1
•Often rapidly reversible if we can identify this early.
•The elderly at high risk because of their predisposition to
hypovolemia and renal atherosclerotic disease.
•This is by definition rapidly reversible upon the restoration of
renal blood flow and glomerular perfusion pressure.
•THE KIDNEYS ARE NORMAL.
•This will accompany any disease that involves hypovolemia,
low cardiac output, systemic dilation, or selective intrarenal
vasoconstriction.
ARF Anthony Mato MD Downloaded 5.8.09
Differential Diagnosis 2
 Hypovolemia
 GI loss: Nausea, vomiting, diarrhea (hyponatraemia)
 Renal loss: diuresis, hypo adrenalism, osmotic diuresis
(DM)
 Sequestration: pancreatitis, peritonitis,trauma, low
albumin (third spacing).
 Hemorrhage, burns, dehydration (intravascular loss).
ARF Anthony Mato MD Downloaded 5.8.09
Differential Diagnosis 3
 Renal vasoconstriction: hypercalcaemia,
adrenaline/noradrenaline, cyclosporin, tacrolimus,
amphotericin B.
 Systemic vasodilation: sepsis, medications, anesthesia,
anaphylaxis.
 Cirrhosis with ascites
 Hepato-renal syndrome
 Impairment of autoregulation: NSAIDs, ACE, ARBs.
 Hyperviscosity syndromes: Multiple Myeloma,
Polycyaemia rubra vera
Differential Diagnosis 4
 Low CO
 Myocardial diseases
 Valvular heart disease
 Pericardial disease
 Tamponade
 Pulmonary artery hypertension
 Pulmonary Embolus
 Positive pressure mechanical ventilation
The only organ with
entry and exit arteries
Glomerular blood flow
Afferent arteriole Efferent art
Glomerular
Capillaries &
Mesangium
Constrictors: endothelin,
catecholamines, thromboxane
Compensatory
Constrictor:
Angiotensin II
Blocker:
ACE-I
Compensatory
Dilators:
Prostacyclin, NO
Blocker:
NSAID
Pre-Renal Azotemia
Pathophysiology 7
 Renal hypoperfusion
 Decreased renal blood flow and GFR
 Increased filtration fraction (GFR/RBF)
 Increased Na and H2O reabsorption
 Oliguria, high Uosm, low UNa
 Elevated BUN/Cr ratio
Malcolm Cox
Acute Tubular Necrosis (ATN)
Classification
 Ischemic
 Nephrotoxic
Acute Renal Failure
Nephrotoxic ATN
 Endogenous Toxins
 Heme pigments (myoglobin, hemoglobin)
 Myeloma light chains
 Exogenous Toxins
 Antibiotics (e.g., aminoglycosides, amphotericin B)
 Radiocontrast agents
 Heavy metals (e.g., cis-platinum, mercury)
 Poisons (e.g., ethylene glycol)
Acute Interstitial Nephritis
Causes
 Allergic interstitial nephritis
 Drugs
 Infections
 Bacterial
 Viral
 Sarcoidosis
Allergic Interstitial Nephritis(AIN)
Clinical Characteristics
 Fever
 Rash
 Arthralgias
 Eosinophilia
 Urinalysis
 Microscopic hematuria
 Sterile pyuria
 Eosinophiluria
Contrast-Induced ARF
Risk Factors
 Renal insufficiency
 Diabetes mellitus
 Multiple myeloma
 High osmolar (ionic) contrast media
 Contrast medium volume
Contrast-induced ARF
Clinical Characteristics
 Onset - 24 to 48 hrs after exposure
 Duration - 5 to 7 days
 Non-oliguric (majority)
 Dialysis - rarely needed
 Urinary sediment - variable
 Low fractional excretion of Na
Pre-Procedure Prophylaxis
1. IV Fluid (N/S)
1-1.5 ml/kg/hour x12 hours prior to procedure and 6-12 hours
after
2. Mucomyst (N-acetylcysteine)
Free radical scavenger; prevents oxidative tissue damage
600mg po bd x 4 doses (2 before procedure, 2 after)
3. Bicarbonate (JAMA 2004)
Alkalinizing urine should reduce renal medullary damage
5% dextrose with 3 amps HCO3; bolus 3.5 mL/kg 1 hour
preprocedure, then 1mL/kg/hour for 6 hours
postprocedure
4. Possibly helpful? Fenoldopam, Dopamine
5. Not helpful! Diuretics, Mannitol
ARF Post-renal Causes 1
 Intra-renal Obstruction
 Acute uric acid nephropathy
 Drugs (e.g., acyclovir)
 Extra-renal Obstruction
 Renal pelvis or ureter (e.g., stones, clots, tumors,
papillary necrosis, retroperitoneal fibrosis)
 Bladder (e.g., BPH, neuropathic bladder)
 Urethra (e.g., stricture)
Acute Renal Failure
Diagnostic Tools
 Urinary sediment
 Urinary indices
 Urine volume
 Urine electrolytes
 Radiologic studies
Urinary Sediment (1)
 Bland
 Pre-renal azotaemia
 Urinary outlet obstruction
Urinary Sediment (2)
 RBC casts or dysmorphic RBCs
 Acute glomerulonephritis
 Small vessel vasculitis
Red Blood Cell Cast
Red Blood Cells
Monomorphic Dysmorphic
Dysmorphic Red Blood Cells
Urinary Sediment (3)
 WBC Cells and WBC Casts
 Acute interstitial nephritis
 Acute pyelonephritis
White Blood Cells
Urinary Sediment (4)
 Renal Tubular Epithelial (RTE) cells, RTE cell casts,
pigmented granular (“muddy brown”) casts
 Acute tubular necrosis
Renal Tubular Epithelial Cell Cast
Pigmented Granular Casts
Acute Renal Failure
Urine Volume (1)
 Anuria (< 100 ml/24h)
 Acute bilateral arterial or venous occlusion
 Bilateral cortical necrosis
 Acute necrotizing glomerulonephritis
 Obstruction (complete)
 ATN (very rare)
Acute Renal Failure
Urine Volume (2)
 Oliguria (<100 ml/24h)
 Pre-renal azotemia
 ATN
 Non-Oliguria (> 500 ml/24h)
 ATN
 Obstruction (partial)
ARF-Signs and Symptoms
 Weight gain
 Peripheral oedema
 Hypertension
ARF Signs and Symptoms
 Hyperkalemia
 Nausea/Vomiting
 Pulmonary edema
 Ascites
 Asterixis
 Encephalopathy
Lab findings
 Rising creatinine and urea
 Rising potassium
 Decreasing Hb
 Acidosis
 Hyponatraemia
 Hypocalcaemia
Mx ARF
 Immediate treatment of pulmonary edema and hyperkalaemia
 Remove offending cause or treat offending cause
 Dialysis as needed to control hyperkalaemia, pulmonary edema,
metabolic acidosis, and uremic symptoms
 Adjustment of drug regimen
 Usually restriction of water, Na, and K intake, but provision of
adequate protein
 Possibly phosphate binders and Na polystyrene sulfonate
Recognise the at-risk patient
 Reduced renal reserve:
Pre-existing CRF, age > 60, hypertension, diabetes
 Reduced intra-vascular volume:
Diuretics, sepsis, cirrhosis, nephrosis
 Reduced renal compensation:
ACE-I’s (ATII), NSAID’s (PG’s), CyA
Indications for acute dialysis
AEIOU
 Acidosis (metabolic)
 Electrolytes (hyperkalemia)
 Ingestion of drugs/Ischemia
 Overload (fluid)
 Uremia
Objectives
• RF
CKD
death
Stages in Progression of Chronic Kidney Disease and
Therapeutic Strategies
Complications
Screening
for CKD
risk factors
CKD risk
reduction;
Screening for
CKD
Diagnosis
& treatment;
Treat
comorbid
conditions;
Slow
progression
Estimate
progression;
Treat
complications;
Prepare for
replacement
Replacement
by dialysis
& transplant
Normal
Increased
risk
Kidney
failure
Damage  GFR
Definition of CKD
Structural or functional abnormalities of the kidneys
for >3 months, as manifested by either:
1. Kidney damage, with or without decreased
GFR, as defined by
 pathologic abnormalities
 markers of kidney damage, including abnormalities in
the composition of the blood or urine or abnormalities
in imaging tests
2. GFR <60 ml/min/1.73 m2, with or without
kidney damage
Clinical Practice Guidelines for the Detection,
Evaluation and Management of CKD
Stage Description GFR Evaluation Management
At increased
risk
Test for CKD Risk factor management
1
Kidney
damage with
normal or 
GFR
>90
Diagnosis
Comorbid
conditions
CVD and CVD
risk factors
Specific therapy, based on diagnosis
Management of comorbid conditions
Treatment of CVD and CVD risk factors
2
Kidney
damage with
mild  GFR
60-89
Rate of
progression
Slowing rate of loss of kidney function 1
3
Moderate 
GFR
30-59 Complications Prevention and treatment of complications
4 Severe  GFR 15-29
Preparation for kidney replacement therapy
Referral to Nephrologist
5 Kidney Failure <15 Kidney replacement therapy
1
Target blood pressure less than 130/80 mm Hg. Angiotension converting enzyme inhibitors
(ACEI) or angiotension receptor blocker (ARB) for diabetic or non-diabetic kidney disease with spot
urine total protein-to-creatinine ratio of greater than 200 mg/g.
Classification of CKD by Diagnosis
 Diabetic Kidney Disease
 Glomerular diseases (autoimmune diseases, systemic
infections, drugs, neoplasia)
 Vascular diseases (renal artery disease, hypertension,
microangiopathy)
 Tubulointerstitial diseases (urinary tract infection,
stones, obstruction, drug toxicity)
 Cystic diseases (polycystic kidney disease)
 Diseases in the transplant (Allograft nephropathy, drug
toxicity, recurrent diseases, transplant glomerulopathy)
Objectives
 CKD
 Dialysis
 Access
 Eckel pearls
 Scenarios
 Kidney Failure
 Stages of Chronic Kidney Disease
 Definition and Classification of CKD
• GFR
• Proteinuria
• Etiology
 Current use of ICD-9-CM codes for CKD
 Proposed changes to ICD-9-CM
Chronic Kidney Disease
Types of dialysis
1. Hemodialysis (HD)
2. Ultrafiltration (UF)
3. Continuous Veno-Venous hemofiltration (CVVH)
4. Peritoneal Dialysis
Hemodialysis
 Semipermeable membrane
 Solute removal via passive diffusion
 Inversely proportional to the size (ie effective
removal of K, urea, C; not of PO4)
Ultrafiltration
 use of hydrostatic pressure gradient to induce
convection (filtration of water)
 solvent drag (pulls dissolved solutes) across
 removal of excess fluid
CVVH
 highly permeable membrane
 fluid and solute removal via ultrafiltration
 filtrate is discarded
 replacement fluid is infused similar to plasma (but no
K, urea, Cr, PO4)
 used in ICU, runs 12-24h, through double lumen
catheter
 less drastic fluid shifts
Peritoneal Dialysis
 peritoneal
membrane =
partially permeable
membrane
 dextrose dialysate
 diffusion and
osmosis until
equilibrium
 3-10 dwells per
night with 2-2.5 L
per dwell
Indications for Dialysis
 Acidosis
 Electrolytes
 Ingestions
 Overload
 Uremia
Access
 Arteriovenous fistula (AVF)
 Graft
 Tunneled catheter
Arteriovenous Fistula
 Highest patency
 Lowest risk of infection
 Low risk of thrombus
 Maturation time (3-4mo)
 Steal syndrome (poor blood
supply to the rest of the
limb)
 Aneurysm formation
Arteriovenous Graft
 Easier to create
 Maturation time 3-6 weeks
 Poor patency (often
requires thrombectomy or
angioplasty)
 Infection
 Aneurysms
 Steal syndrome
Tunneled Catheter
 Immediate use
 Bridge to AVF/AVG
 Poor flow (decreased HD
efficiency)
 High infection risk
 Venous stenosis
 Thrombosis
Dialysis Rx:
 Time: 2-5 hours
 Bath
 Blood flow rate: 400-450cc/min
 Dialysate flow rate: 500-800cc/min
 Anticoagulant
 Additives:
◦ Anemia (EPO, blood)
◦ Bone metabolism (vit D, calcitriol, etc)
◦ Meds (antibiotics)
Dialysate Bath
Calciphylaxis
Calcinosis cutis
Imaging in CKD
 Avoid contrast in CKD patients
 If you have to, prep
◦ volume expansion: isotonic IVFs
 3 cc/kg x 1h before
 1cc/kg x 6h after
◦ ? alkalinization: sodium bicarbonate
◦ ? acetylcysteine
◦ radiology can give you the protocol
 (treat empirically)

Acute renal failure by Pandian M.

  • 1.
  • 2.
    Overview  Definitions  Classificationand causes  Presentation  Treatment
  • 3.
    Definition Acute Renalfailure (ARF)  Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes  Different to renal insufficiency where kidney function is deranged but can still support life  Exact biochemical/clinical definition not clear – 26 studies – no 2 used the same definition
  • 4.
    ARF  Occurs overhours/days  Lab definition  Increase in baseline creatinine of more than 50%  Decrease in creatinine clearance of more than 50%  Deterioration in renal function requiring dialysis
  • 5.
    ARF definitions  Anuria– no urine output or less than 100mls/24 hours  Oliguria - <500mls urine output/24 hours or <20mls/hour  Polyuria - >2.5L/24 hours
  • 6.
    ARF  Pre renal(functional)  Renal-intrinsic (structural)  Post renal (obstruction)
  • 7.
    ARF Pirouz Daeihagh,M.D.Internal medicine/Nephrology Wake Forest University School of Medicine. Downloaded 4.6.09
  • 8.
    Causes of ARF Pre-renal: Inadequate perfusion  check volume status  Renal: ARF despite perfusion & excretion  check urinalysis, FBC & autoimmune screen  Post-renal: Blocked outflow  check bladder, catheter & ultrasound
  • 9.
    Causes of ARF Pre-renalRenal Post-renal Absolute hypovolaemia Glomerular (RPGN) Pelvi-calyceal Relative hypovolaemia Tubular (ATN) Ureteric Reduced cardiac output Interstitial (AIN) VUJ-bladder Reno-vascular occlusion Vascular (atheroemboli) Bladder neck- urethra
  • 10.
    ARF Pre renal Decreased renal perfusion without cellular injury  70% of community acquired cases  40% hospital acquired cases
  • 11.
    ARF Intrinsic  Acutetubular necrosis (ATN)  Ischaemia  Toxin  Tubular factors  Acute interstitial Necrosis (AIN)  Inflammation  oedema  Glomerulonephritis (GN)  Damage to filtering mechanisms  Multiple causes as per previous presentation
  • 12.
    ARF Post renal Post renal obstruction  Obstruction to the urinary outflow tract  Prostatic hypertrophy  Blocked catheter  Malignancy
  • 13.
    Prerenal Failure 1 •Oftenrapidly reversible if we can identify this early. •The elderly at high risk because of their predisposition to hypovolemia and renal atherosclerotic disease. •This is by definition rapidly reversible upon the restoration of renal blood flow and glomerular perfusion pressure. •THE KIDNEYS ARE NORMAL. •This will accompany any disease that involves hypovolemia, low cardiac output, systemic dilation, or selective intrarenal vasoconstriction. ARF Anthony Mato MD Downloaded 5.8.09
  • 14.
    Differential Diagnosis 2 Hypovolemia  GI loss: Nausea, vomiting, diarrhea (hyponatraemia)  Renal loss: diuresis, hypo adrenalism, osmotic diuresis (DM)  Sequestration: pancreatitis, peritonitis,trauma, low albumin (third spacing).  Hemorrhage, burns, dehydration (intravascular loss). ARF Anthony Mato MD Downloaded 5.8.09
  • 15.
    Differential Diagnosis 3 Renal vasoconstriction: hypercalcaemia, adrenaline/noradrenaline, cyclosporin, tacrolimus, amphotericin B.  Systemic vasodilation: sepsis, medications, anesthesia, anaphylaxis.  Cirrhosis with ascites  Hepato-renal syndrome  Impairment of autoregulation: NSAIDs, ACE, ARBs.  Hyperviscosity syndromes: Multiple Myeloma, Polycyaemia rubra vera
  • 16.
    Differential Diagnosis 4 Low CO  Myocardial diseases  Valvular heart disease  Pericardial disease  Tamponade  Pulmonary artery hypertension  Pulmonary Embolus  Positive pressure mechanical ventilation
  • 17.
    The only organwith entry and exit arteries
  • 18.
    Glomerular blood flow Afferentarteriole Efferent art Glomerular Capillaries & Mesangium Constrictors: endothelin, catecholamines, thromboxane Compensatory Constrictor: Angiotensin II Blocker: ACE-I Compensatory Dilators: Prostacyclin, NO Blocker: NSAID
  • 19.
    Pre-Renal Azotemia Pathophysiology 7 Renal hypoperfusion  Decreased renal blood flow and GFR  Increased filtration fraction (GFR/RBF)  Increased Na and H2O reabsorption  Oliguria, high Uosm, low UNa  Elevated BUN/Cr ratio Malcolm Cox
  • 20.
    Acute Tubular Necrosis(ATN) Classification  Ischemic  Nephrotoxic
  • 21.
    Acute Renal Failure NephrotoxicATN  Endogenous Toxins  Heme pigments (myoglobin, hemoglobin)  Myeloma light chains  Exogenous Toxins  Antibiotics (e.g., aminoglycosides, amphotericin B)  Radiocontrast agents  Heavy metals (e.g., cis-platinum, mercury)  Poisons (e.g., ethylene glycol)
  • 22.
    Acute Interstitial Nephritis Causes Allergic interstitial nephritis  Drugs  Infections  Bacterial  Viral  Sarcoidosis
  • 23.
    Allergic Interstitial Nephritis(AIN) ClinicalCharacteristics  Fever  Rash  Arthralgias  Eosinophilia  Urinalysis  Microscopic hematuria  Sterile pyuria  Eosinophiluria
  • 24.
    Contrast-Induced ARF Risk Factors Renal insufficiency  Diabetes mellitus  Multiple myeloma  High osmolar (ionic) contrast media  Contrast medium volume
  • 25.
    Contrast-induced ARF Clinical Characteristics Onset - 24 to 48 hrs after exposure  Duration - 5 to 7 days  Non-oliguric (majority)  Dialysis - rarely needed  Urinary sediment - variable  Low fractional excretion of Na
  • 26.
    Pre-Procedure Prophylaxis 1. IVFluid (N/S) 1-1.5 ml/kg/hour x12 hours prior to procedure and 6-12 hours after 2. Mucomyst (N-acetylcysteine) Free radical scavenger; prevents oxidative tissue damage 600mg po bd x 4 doses (2 before procedure, 2 after) 3. Bicarbonate (JAMA 2004) Alkalinizing urine should reduce renal medullary damage 5% dextrose with 3 amps HCO3; bolus 3.5 mL/kg 1 hour preprocedure, then 1mL/kg/hour for 6 hours postprocedure 4. Possibly helpful? Fenoldopam, Dopamine 5. Not helpful! Diuretics, Mannitol
  • 27.
    ARF Post-renal Causes1  Intra-renal Obstruction  Acute uric acid nephropathy  Drugs (e.g., acyclovir)  Extra-renal Obstruction  Renal pelvis or ureter (e.g., stones, clots, tumors, papillary necrosis, retroperitoneal fibrosis)  Bladder (e.g., BPH, neuropathic bladder)  Urethra (e.g., stricture)
  • 28.
    Acute Renal Failure DiagnosticTools  Urinary sediment  Urinary indices  Urine volume  Urine electrolytes  Radiologic studies
  • 29.
    Urinary Sediment (1) Bland  Pre-renal azotaemia  Urinary outlet obstruction
  • 30.
    Urinary Sediment (2) RBC casts or dysmorphic RBCs  Acute glomerulonephritis  Small vessel vasculitis
  • 31.
  • 32.
  • 33.
  • 34.
    Urinary Sediment (3) WBC Cells and WBC Casts  Acute interstitial nephritis  Acute pyelonephritis
  • 35.
  • 36.
    Urinary Sediment (4) Renal Tubular Epithelial (RTE) cells, RTE cell casts, pigmented granular (“muddy brown”) casts  Acute tubular necrosis
  • 37.
  • 38.
  • 39.
    Acute Renal Failure UrineVolume (1)  Anuria (< 100 ml/24h)  Acute bilateral arterial or venous occlusion  Bilateral cortical necrosis  Acute necrotizing glomerulonephritis  Obstruction (complete)  ATN (very rare)
  • 40.
    Acute Renal Failure UrineVolume (2)  Oliguria (<100 ml/24h)  Pre-renal azotemia  ATN  Non-Oliguria (> 500 ml/24h)  ATN  Obstruction (partial)
  • 41.
    ARF-Signs and Symptoms Weight gain  Peripheral oedema  Hypertension
  • 42.
    ARF Signs andSymptoms  Hyperkalemia  Nausea/Vomiting  Pulmonary edema  Ascites  Asterixis  Encephalopathy
  • 43.
    Lab findings  Risingcreatinine and urea  Rising potassium  Decreasing Hb  Acidosis  Hyponatraemia  Hypocalcaemia
  • 44.
    Mx ARF  Immediatetreatment of pulmonary edema and hyperkalaemia  Remove offending cause or treat offending cause  Dialysis as needed to control hyperkalaemia, pulmonary edema, metabolic acidosis, and uremic symptoms  Adjustment of drug regimen  Usually restriction of water, Na, and K intake, but provision of adequate protein  Possibly phosphate binders and Na polystyrene sulfonate
  • 45.
    Recognise the at-riskpatient  Reduced renal reserve: Pre-existing CRF, age > 60, hypertension, diabetes  Reduced intra-vascular volume: Diuretics, sepsis, cirrhosis, nephrosis  Reduced renal compensation: ACE-I’s (ATII), NSAID’s (PG’s), CyA
  • 46.
    Indications for acutedialysis AEIOU  Acidosis (metabolic)  Electrolytes (hyperkalemia)  Ingestion of drugs/Ischemia  Overload (fluid)  Uremia
  • 47.
  • 48.
    CKD death Stages in Progressionof Chronic Kidney Disease and Therapeutic Strategies Complications Screening for CKD risk factors CKD risk reduction; Screening for CKD Diagnosis & treatment; Treat comorbid conditions; Slow progression Estimate progression; Treat complications; Prepare for replacement Replacement by dialysis & transplant Normal Increased risk Kidney failure Damage  GFR
  • 49.
    Definition of CKD Structuralor functional abnormalities of the kidneys for >3 months, as manifested by either: 1. Kidney damage, with or without decreased GFR, as defined by  pathologic abnormalities  markers of kidney damage, including abnormalities in the composition of the blood or urine or abnormalities in imaging tests 2. GFR <60 ml/min/1.73 m2, with or without kidney damage
  • 50.
    Clinical Practice Guidelinesfor the Detection, Evaluation and Management of CKD Stage Description GFR Evaluation Management At increased risk Test for CKD Risk factor management 1 Kidney damage with normal or  GFR >90 Diagnosis Comorbid conditions CVD and CVD risk factors Specific therapy, based on diagnosis Management of comorbid conditions Treatment of CVD and CVD risk factors 2 Kidney damage with mild  GFR 60-89 Rate of progression Slowing rate of loss of kidney function 1 3 Moderate  GFR 30-59 Complications Prevention and treatment of complications 4 Severe  GFR 15-29 Preparation for kidney replacement therapy Referral to Nephrologist 5 Kidney Failure <15 Kidney replacement therapy 1 Target blood pressure less than 130/80 mm Hg. Angiotension converting enzyme inhibitors (ACEI) or angiotension receptor blocker (ARB) for diabetic or non-diabetic kidney disease with spot urine total protein-to-creatinine ratio of greater than 200 mg/g.
  • 51.
    Classification of CKDby Diagnosis  Diabetic Kidney Disease  Glomerular diseases (autoimmune diseases, systemic infections, drugs, neoplasia)  Vascular diseases (renal artery disease, hypertension, microangiopathy)  Tubulointerstitial diseases (urinary tract infection, stones, obstruction, drug toxicity)  Cystic diseases (polycystic kidney disease)  Diseases in the transplant (Allograft nephropathy, drug toxicity, recurrent diseases, transplant glomerulopathy)
  • 52.
    Objectives  CKD  Dialysis Access  Eckel pearls  Scenarios  Kidney Failure  Stages of Chronic Kidney Disease  Definition and Classification of CKD • GFR • Proteinuria • Etiology  Current use of ICD-9-CM codes for CKD  Proposed changes to ICD-9-CM
  • 53.
  • 54.
    Types of dialysis 1.Hemodialysis (HD) 2. Ultrafiltration (UF) 3. Continuous Veno-Venous hemofiltration (CVVH) 4. Peritoneal Dialysis
  • 55.
    Hemodialysis  Semipermeable membrane Solute removal via passive diffusion  Inversely proportional to the size (ie effective removal of K, urea, C; not of PO4)
  • 57.
    Ultrafiltration  use ofhydrostatic pressure gradient to induce convection (filtration of water)  solvent drag (pulls dissolved solutes) across  removal of excess fluid
  • 58.
    CVVH  highly permeablemembrane  fluid and solute removal via ultrafiltration  filtrate is discarded  replacement fluid is infused similar to plasma (but no K, urea, Cr, PO4)  used in ICU, runs 12-24h, through double lumen catheter  less drastic fluid shifts
  • 59.
    Peritoneal Dialysis  peritoneal membrane= partially permeable membrane  dextrose dialysate  diffusion and osmosis until equilibrium  3-10 dwells per night with 2-2.5 L per dwell
  • 60.
    Indications for Dialysis Acidosis  Electrolytes  Ingestions  Overload  Uremia
  • 61.
    Access  Arteriovenous fistula(AVF)  Graft  Tunneled catheter
  • 62.
    Arteriovenous Fistula  Highestpatency  Lowest risk of infection  Low risk of thrombus  Maturation time (3-4mo)  Steal syndrome (poor blood supply to the rest of the limb)  Aneurysm formation
  • 63.
    Arteriovenous Graft  Easierto create  Maturation time 3-6 weeks  Poor patency (often requires thrombectomy or angioplasty)  Infection  Aneurysms  Steal syndrome
  • 64.
    Tunneled Catheter  Immediateuse  Bridge to AVF/AVG  Poor flow (decreased HD efficiency)  High infection risk  Venous stenosis  Thrombosis
  • 65.
    Dialysis Rx:  Time:2-5 hours  Bath  Blood flow rate: 400-450cc/min  Dialysate flow rate: 500-800cc/min  Anticoagulant  Additives: ◦ Anemia (EPO, blood) ◦ Bone metabolism (vit D, calcitriol, etc) ◦ Meds (antibiotics)
  • 66.
  • 67.
  • 68.
    Imaging in CKD Avoid contrast in CKD patients  If you have to, prep ◦ volume expansion: isotonic IVFs  3 cc/kg x 1h before  1cc/kg x 6h after ◦ ? alkalinization: sodium bicarbonate ◦ ? acetylcysteine ◦ radiology can give you the protocol  (treat empirically)