Information
about kidney and it’s
problems
Dr Lalit Agarwal
Consultant Nephrologist
Woodlands Hospital
The Urinary System
The Urinary System
Structure of the Kidney
A Typical Nephron
Each kidney contains about 1 million nephrons
A Renal Corpuscle
Renal Corpuscles
FUNCTION OF KIDNEYS
• Produce urine by filtering blood and excretes waste products
• Balance fluid content in the body.
• Adjust levels of minerals and other chemicals to keep the body
working properly.
• Produce the enzyme Renin that helps control Blood Pressure.
• Produce hormone Erythropoietin to help make Red Blood
Cells.
• Activate Vitamin D to maintain healthy bone.
Types of kidney disease
•Acute kidney Injury (AKI)
or acute rise in creatine
•Chronic kidney Disease (CKD)
or chronic rise in creatine
• AKI on CKD
•Kidney Failure or CKD Stage 5
What is AKI?
An abrupt (within 7 days) &
sustained (>6 hours)
decrease in renal function/GFR
(usually reversible)
resulting in accumulation of
waste products.
Key causes of AKI
• Prerenal AKI
Functional or minimal cellular damage with
treatment rapid recovery
• Intrinsic AKI
Glomerular, Tubular , Interestitial and
Vascular
• Postrenal AKI
OR ACUTE KIDNEY INJURY
Definition of AKI - KDIGO
• Increase in S.cr by ≥ 0.3 mg/dl within 48
hrs or
• Increase in S.cr to ≥ 1.5 times of baseline,
which is known or presumed to have
occurred within prior 7 days or
• Urine volume < 0.5 ml/kg/hr for 6 hours.
ADQI(RIFLE) -- AKIN-- KDIGO GROUP
Staging of AKI(KDIGO)
Stage Serum Creatinine Urine output
1 1.5-1.9 times baseline within 1 wk or
≥ 0.3 mg/dl increase within 48 hrs
<0.5ml/kg/h for
6-12 hrs
2 2.0-2.9 times baseline <0.5ml/kg/h for
≥ 12 hrs
3 3.0 times baseline or
increase in serum creat to ≥ 4.0 mg/dl or
initiation of RRT or
in patients < 18 yrs, decrease in eGFR to
<35ml/min per 1.73 m²)
<0.3ml/kg/h for
≥ 24 hrs or
Anuria for ≥ 12
hrs
MAJOR COMPLICATIONS OF AKI
• Volume overload
• Hyperkalemia
• Metabolic acidosis
• Hypocalcemia
• Hyperphosphatemia
• Hyperuricemia and hypermagnesemia
• Signs of uremia
Distinguishing AKI from CKD
• Review h/o kidney disease and old
records
• Ultrasonography
• Anemia (GFR < 30ml/min , absence of
anemia suggests AKI( exception
HUS/TTP)
Prevention of AKI
• Identify patients at increased risks
advanced age,low eGFR,proteinuria,low
albumin, DM,previous AKI,
• Avoidance of renal insults
Volume depletion, nephrotoxic drugs
(NSAIDS, ACEI/ARB, contrast,TLS,
amphotericin, aminoglycosides etc.)
• Prophylactic treatments
Good hydration,?NAC,IV Sodabicarbonate
TREATMENT OF AKI
• Determine cause of AKI with special
attention to reversible causes
• Stage severity of AKI according to
creatinine and urine output
• Manage as per AKI stage and specific
cause
• Management of complications of AKI
RRT in AKI-1
• Conservative vs RRT?
• When to start RRT?
• Early vs late?
• What modality (IHD vs CRRT) of RRT to
use
• What dose of RRT to give?
RRT in AKI-2
• What type of temporary dialysis access to
use?
• What type of dialysis membranes to use?
• What choice of anticoagulation?
• When to stop RRT in AKI? ( CRRT to IHD,
recovery of kidney function)
Initiation of RRT in AKI
• Extremely variable on clinical situation,
empirical and if no improvement to
medical/supportive interventions.
• RRT indicated in severe (stage 3) kidney
injury.
• Absolute/urgent (objective) and
relative/elective (subjective) indications
• ICU:(early/low threshold to start in MOF)
• Renal ward:(single organ AKI)
Modality of dialysis in ITU
• IHD (rapid removal of solute & water)
• SLED
• Hemofiltration
• Hemodiafiltration
• UF (Aquapharesis)
• Approx. 10% pts with AKI cannot be treated with
IHD because of hemodynamic instability
• SLED and CRRT meta-analysis: no difference in
outcome (Zhang et al AJKD Aug 2015)
Outcomes of AKI
• Recovery
• Predialysis-CKD
• ESRD (10-30%)
• Death
25
SIRS inducing MODS
Sepsis , Trauma ,Major Surgery
Pancreatitis, CPB .
Host Defenses
Tissue damage and hypotension
Cellular activation & release of IM
CKD usually means
fewer functioning
nephrons
CKD is reduced kidney function
and/or kidney damage
• Chronic kidney disease
– Kidney function
• Glomerular filtration rate (GFR)< 60mL/min/1.73m2 for
≥ 3 with or without kidney damage
– Kidney damage
• ≥ 3 months with or without decreased GFR, manifested
by either
– Pathological abnormalities
– Markers of kidney damage, e.g., albuminuria
– Urine albumin-to-creatinine ratio (UACR)> 30mg/g
This definition does not account for age related GFR
decline
Causes of CKD
• Diabetes - rapid loss of renal function
• Hypertension - both cause and effect
• Glomerulonephritis
• Cystic Disease
• Drug toxicity
• Interstitial disease
• Chronic infections
Zone of “Compensation”
(Adequate Renal Reserve)
Cr
K
Na
Normal Range
Serum
creatinine
G F R percent of Normal
Renal
Failure
0 25% 50% 75% 100%
1.4mg/dl
4 Sr. Cr 1.4 mg/dl
Sr. creatinine > 1.4
indicates G F R is
down by 50 %
Relationship between serum creatinine and GFR
Creatinine as a marker of KIDNEY FUNCTION(GFR)
Formula based GFR measurements
• MDRD formula (6 variable)
• Modified MDRD formula (4 variable)
• CKD-EPI formula
• Cystatin C (independent of muscle mass)
• Cockcroft -Gault formula
• Creatinine clearance test (measured GFR)
Creatinine GFR
1 100
2 50
3 25
4 12.5
5 6.125
6 3.06125
GFR which is related directly to urine creatinine excretion and
inversely to plasma creatinine. on the basis of this
relationship GFR will fall in roughly inverse proportion or
reciprocal to the rise in plasma creatinine. Creatinine is used
as a surrogate to eGFR. Direct GFR measurement is not
feasible.
Rough GFR
Note: further refined by KDIGO 2012 CKD work group
Albuminuria categories
Category
AER
(mg/24hr)
ACR
(Approximate equivalent)
(mg/mmol) (mg/g)
Terms
A1 < 30 < 3 < 30
Normal to mildly
increased
A2 30 - 300 3 - 30 30 - 300
Moderately
increased
A3 > 300 > 30 > 300
Severely
increased
No longer uses prefixes “normo”, “micro”, or “macro” when referring to
albuminuria because these terms are antiquated, non-descriptive
definations
Classification of CKD
• It is recommended that CKD be classified
by:
– Cause
– GFR category
– Albuminuria category
• This is collectively referred to as “CGA
staging”
• Represents a revision of the previous
KDOQI CKD guidelines, which included
staging only by level of GFR
Each kidney has about 1 million nephrons;
slow loss may not be noticeable
• We have a large physiological reserve
• Slow, progressive loss of functioning
nephrons may not be noticeable
• The person with CKD may not feel
different up to ckd stage 4
Early referral to nephrologist
• Identify reversible/treatable factors
• Avoid nephrotoxic drugs
• Retardation of progression of renal
disease
• Prevent cardiovascular mortality
• Better planning of RRT
Early Treatment Makes a Difference
Slow CKD progression
Optimal Care in CKD-prevent CVD
The incidence rate of new ESRD declined for the first
time in 2011 after been stable since 2000.(USRDS 2013)
Timely initiation
of dialysis/Txp
Timely access
placement
Informed choice
of RRT
Education
Modification of
comorbidity
Preparation for
RRT
Early detection
Protein restriction
Blood sugar control
BP control
ACE inhibitors/ARB
Secondary
hyperparathyroidism
Anemia
Malnutrition
Interventions that
delay progression
Management of
complications
Retinopathy
(diabetics)
Neuropathy
(diabetics)
Vascular disease
Cardiac disease
Acidosis/
dyslipidemia
Kidney Failure is an eGFR < 15
• Kidneys cannot maintain homeostasis
• Kidney failure is associated with fluid,
electrolytes and hormonal imbalances and
metabolic abnormalities
• ESRD means the patient is on dialysis or
has a kidney transplant
Symptoms of kidney failure that can be caused by a build-
up of wastes in the body include:
• A metallic taste in the mouth or ammonia breath
• Nausea and vomiting
• Loss of appetite
• Difficulty in concentrating
• Itchiness (pruritis)
• Weight Loss
Symptoms of kidney failure that can be caused by a build-
up of fluid in the body include:
• Swelling in the face, feet or hands
• Shortness of breath (from fluid in the lungs)
SYMPTOMS OF KIDNEY FAILURE
Symptoms of kidney failure that can be caused by
damage to the kidneys include:
• Making more or less urine than usual
• Urine that is foamy or bubbly (may be seen when protein is in
the urine)
• Blood in the urine (typically only seen through a microscope)
Symptoms of kidney failure that can be caused by anemia (a
shortage of red blood cells) include:
• Fatigue
• Weakness
• Feeling cold all the time
• Shortness of breath
• Mental confusion
CKD
ESRD
GLOBAL CKD-ESRD: Prevalence/Incidence
500 MILLION ADULTS WITH CKD
2.5 MILLION
Many CKD patients die
prematurely from CVD
CKD
ESRD
CKD-ESRD: INDIA Prevalence/Incidence
17% of ADULTS WITH CKD
25,000/yr get RRT
Many CKD patients die
prematurely from CVD
IN INDIA ONLY 25,000 (10% NEW ESRD GET RRT) AND 90% (2,50,000) UNABLE TO
AFFORD RRT AND SIMPLY DIE.
50,000 patients undergoing regular MHD in 5500 machines in 800 dialysis centers
5000 patients on PD and 5000 transplant done annually.
In India dialysis population is growing at a rate of 10%
46
What are CKD patients Dying From?
Stroke Myocardial
Infarction
Heart
Failure
Sudden
Death
TREATMENT OPTIONS
INTRODUCTION
It is not the end of the world for a person with
impaired,non-functional kidneys.
"QUALITY OF LIFE" can be improved by proper
and timely medical intervention.
The four options for treating
kidney failure
• Renal replacement therapy (RRT)
1. Hemodialysis
- In-centre or home
2. Peritoneal dialysis
3. Kidney transplantation
• Conservative management
4. Active medical management without RRT
Indications to begin dialysis
depend on objective and subjective criteria
• Absolute indications :
• Traditional indications/uremic symptoms
• Relative indications:
• anorexic, sleepiness, loss of energy,
malnutrition, decrease in cognition
• Diabetics need to initiate dialysis earlier
than non diabetics.
Main Goals of Dialysis
• Remove
– Fluid
– Waste Products
• Urea
• Creatinine
• Potassium
• Phosphorous
• Sodium
• Maintain
– Fluid
– Electrolyte
– Acid-base balance
BENEFITS OF DIALYSIS
improve quality and
quantity of life
HEMODIALYSIS
DIALYSER
Vascular access
Temporary Permanent
Femoral
cannulation
Central
Venous
Cannulation
AV Fistula AV Graft
Permanent
Venous
Catheter
Internal Jugular Subclavian
Arteriovenous Fistula/Graft
Central Venous Catheter
Peritoneal
Dialysis
International Variation in PD
Peritoneal Dialysis
• Blood is cleaned inside the
body, through the Peritoneum
• The peritoneum allows waste
products to pass through it .
• Dialysis Fluid pass through
Tenckhoff Catheter.
The two aspects of peritoneal
transport
1. Solute clearance.
• Diffusive
• Convective.
2. Fluid removal
(Ultrafiltration)
Getting Ready for PD
Peritoneal Dialysis Options
CAPD
–Continuous
–Ambulatory
–Peritoneal
–Dialysis
APD
–Automated
–Peritoneal
–Dialysis
Chronic Peritoneal Dialysis:
Continuous
Ambulatory PD
Automated PD
• 2.0-2.5 L dwells
• 4-8 hours
• 4 times/day
• 3-10 dwells nightly
• CCPD:Continuous
Cycling PD– 1 dwell
during the day
• NIPD:Nocturnal
Intermittment PD- dry
during day
CAPD
• Perform 4-5 exchanges
per day
– Treatment can be done
almost anywhere
– No machine needed
– Exchange takes about 30
to 40 minutes
– Ultra BagTM
Fluid Bags- contain fluid Blue Clamps-Control Flow
Transfer Set-barrier to infection
Minicap-prevent germs entry
CAPD Components
Peritoneal dialysis: There are three phases of PD
Fill- New Fluid enters the peritoneal cavity
Dwell-The fluid stays inside your body for
4-6 hours.
Drain-The fluid plus waste is drained out and
replaced with new fluid.
Drain
How does PD work?
Automated Peritoneal
Dialysis
CCPD
• Dialysate solution
is changed by a
machine, at night.
• 8-12 liters over 8-
10 hours
• Leave 1-2 liters to
dwell during the
day.
Complications of PD
• Infectious
• Non-infectious
Infectious complications
• Exit – site infection
• Tunnel infection
• Peritonitis: remains significant cause of
– Hospitalization
– PD failure
– Damage to peritoneal membrane
– Morbidity and mortality
A Normal Exit Site
The Problem with
ONE GERM
is that
it becomes a lot of germs!!
A
single germ
can turn
into over
a million
in just
5 hours!!
In 15 minutes 1 germ divides into 2
In 30 minutes 2 germs divide into 4
In 45 minutes 4 germs divide into 8
In 60 minutes 8 germs divide into 16
In 75 minutes 16 germs divide into 32
In 90 minutes 32 germs divide into 64
In 105 minutes 64 germs divide into 128
In 120 minutes 128 germs divide into 256
In 135 minutes 256 germs divide into 512
In 150 minutes 512 germs divide into 1024
In 165 minutes 1024 germs divide into 2048
In 180 minutes 2048 germs divide into 4096
In 195 minutes 4096 germs divide into 8192
In 210 minutes 8192 germs divide into 16384
In 225 minutes 16384 germs divide into 32768
In 240 minutes 32768 germs divide into 65536
In 255 minutes 65536 germs divide into 131072
In 270 minutes 131072 germs divide into 262144
In 285 minutes 262144 germs divide into 524288
In 300 minutes 524,288 germ divides into 1,048,576!!
Non-infectious complications
Non infectious
complications
Catheter related Catheter unrelated
•Outflow failure
•Pericatheter leak
•Abdominal wall herniation
•Catheter cuff extrusion
•Intestinal perforation
GERD Hemoperitoneum
Back/abdominal pain UF failure
Abdominal wall herniation Peritoneal sclerosis
Pleural effusion Metabolic
Acute peritoneal dialysis
KIDNEY
TRANSPLANTATION
Benefits of Transplantion
 Improve life expectancy
 Cardio-vascular benefits
 Improve Quality-of-life
 Socio-economic benefits
The Transplantation Process
 Pre-transplant evaluation
 Legal compliance
 The operation
 Immunosuppression
 Complications
 Short and long term follow up
Kidney Donor
Living related.
Living unrelated (altruistic).
Deceased/Cadaveric (Brain-dead).
Beating and non-beating heart.
The Final Look
Surgical Complications
 Vascular Complications: arterial, venous
 Ureteric complications : urine leak/obstruction
 Perigraft Fluid Collections:
Seroma & Hematoma
Abscess
Urinoma
Lymphocele
 Wound infection
 Delayed graft function
Medical Complications
 Acute rejection
- Acute cellular rejection
- Antibody-mediated rejection-C4d
 NODAT/PTDM
 Infectious complications
- Cytomegalovirus
- BK virus
- Post op infections
 Malignancy-PTLD and Skin Carcinoma
common
 Chronic allograft dysfunction(r/o reversible
factors)
India – Legal Aspects
Transplantation of Human Organs Act,
1994
Aims
• Regulate removal, storage and
transplantation of human organs for
therapeutic purposes
• To prevent commercial dealings in
organs
• Recognise Brain Death
WHAT IS REJECTION?
• Rejection is a normal reaction of the body to a foreign object.
When a new kidney is placed in a person's body, the body sees
the transplanted organ as a threat and tries to attack it
What is done to prevent rejection?
Medications is given for the rest of the life to fight rejection.
The anti-rejection medications most commonly used includes:
Immunosuppressive Medications
 Induction:
–Corticosteroids
–Anti-thymocyte globulin (ATG)
–IL-2 receptor antagonists - Basiliximab
 Maintenance:
–Corticosteroids
–Calcineurin inhibitors (CNIs)
–mTOR inhibitors
–Antimetabolites
Immunosuppressive Medications
• Treatment of rejection (Rescue) :
– Corticosteroids
– Anti-thymocyte globulin
– Intravenous Immunoglobulin (IVIG)
– Rituximab
– Plasmapheresis
T-10
Risks and possible side
effects
Lowered resistance to illness
• Immunosuppressive
medications lower your
resistance to infection
• To stay healthy, you must
protect yourself from coming
in contact with infections
• Take the correct dosage of
medication and see your
doctor regularly
In conclusion, renal transplantation should be
recommended as the preferred mode of RRT for
most patients with ESRD in whom surgery and
subsequent immuno-suppression is safe and
feasible.
Chronic Allograft Dysfunction:
Why Do Grafts Fail?
• Chronic low-grade immune injury
• Long-standing hypertension
• Recurrent disease (diabetic nephropathy
or glomerulonephritis)
• Repeated episodes of acute rejection
• Donor disease
• Calcineurin inhibitor nephrotoxicity
USRDS 1999.
Expected
Years
Remaining*
0
35
10
20
30
Prostate
Ca
21.6
13
8
4.5
2.5
* Based on adult, age 59 years
Survival in ESRD
Kidney Disease Cycle
Dialysis
At-risk  Chronic  Kidney Failure 
Kidney Disease (Stage 5)
(Stage 1 – 4)
Transplant
Continuum of kidney disease
care
• Prevent kidney disease (awareness of
risk)
• Identify kidney disease (awareness of
diagnosis)
• Manage kidney disease (knowledge to
achieve management goals)
• Renal replacement or conservative care
for renal failure
Any Questions?
Woodlands.world kidney day 2020

Woodlands.world kidney day 2020

  • 1.
    Information about kidney andit’s problems Dr Lalit Agarwal Consultant Nephrologist Woodlands Hospital
  • 2.
  • 3.
  • 4.
  • 5.
    A Typical Nephron Eachkidney contains about 1 million nephrons
  • 6.
  • 7.
  • 8.
    FUNCTION OF KIDNEYS •Produce urine by filtering blood and excretes waste products • Balance fluid content in the body. • Adjust levels of minerals and other chemicals to keep the body working properly. • Produce the enzyme Renin that helps control Blood Pressure. • Produce hormone Erythropoietin to help make Red Blood Cells. • Activate Vitamin D to maintain healthy bone.
  • 9.
    Types of kidneydisease •Acute kidney Injury (AKI) or acute rise in creatine •Chronic kidney Disease (CKD) or chronic rise in creatine • AKI on CKD •Kidney Failure or CKD Stage 5
  • 10.
    What is AKI? Anabrupt (within 7 days) & sustained (>6 hours) decrease in renal function/GFR (usually reversible) resulting in accumulation of waste products.
  • 11.
    Key causes ofAKI • Prerenal AKI Functional or minimal cellular damage with treatment rapid recovery • Intrinsic AKI Glomerular, Tubular , Interestitial and Vascular • Postrenal AKI
  • 12.
  • 13.
    Definition of AKI- KDIGO • Increase in S.cr by ≥ 0.3 mg/dl within 48 hrs or • Increase in S.cr to ≥ 1.5 times of baseline, which is known or presumed to have occurred within prior 7 days or • Urine volume < 0.5 ml/kg/hr for 6 hours. ADQI(RIFLE) -- AKIN-- KDIGO GROUP
  • 14.
    Staging of AKI(KDIGO) StageSerum Creatinine Urine output 1 1.5-1.9 times baseline within 1 wk or ≥ 0.3 mg/dl increase within 48 hrs <0.5ml/kg/h for 6-12 hrs 2 2.0-2.9 times baseline <0.5ml/kg/h for ≥ 12 hrs 3 3.0 times baseline or increase in serum creat to ≥ 4.0 mg/dl or initiation of RRT or in patients < 18 yrs, decrease in eGFR to <35ml/min per 1.73 m²) <0.3ml/kg/h for ≥ 24 hrs or Anuria for ≥ 12 hrs
  • 16.
    MAJOR COMPLICATIONS OFAKI • Volume overload • Hyperkalemia • Metabolic acidosis • Hypocalcemia • Hyperphosphatemia • Hyperuricemia and hypermagnesemia • Signs of uremia
  • 17.
    Distinguishing AKI fromCKD • Review h/o kidney disease and old records • Ultrasonography • Anemia (GFR < 30ml/min , absence of anemia suggests AKI( exception HUS/TTP)
  • 18.
    Prevention of AKI •Identify patients at increased risks advanced age,low eGFR,proteinuria,low albumin, DM,previous AKI, • Avoidance of renal insults Volume depletion, nephrotoxic drugs (NSAIDS, ACEI/ARB, contrast,TLS, amphotericin, aminoglycosides etc.) • Prophylactic treatments Good hydration,?NAC,IV Sodabicarbonate
  • 19.
    TREATMENT OF AKI •Determine cause of AKI with special attention to reversible causes • Stage severity of AKI according to creatinine and urine output • Manage as per AKI stage and specific cause • Management of complications of AKI
  • 20.
    RRT in AKI-1 •Conservative vs RRT? • When to start RRT? • Early vs late? • What modality (IHD vs CRRT) of RRT to use • What dose of RRT to give?
  • 21.
    RRT in AKI-2 •What type of temporary dialysis access to use? • What type of dialysis membranes to use? • What choice of anticoagulation? • When to stop RRT in AKI? ( CRRT to IHD, recovery of kidney function)
  • 22.
    Initiation of RRTin AKI • Extremely variable on clinical situation, empirical and if no improvement to medical/supportive interventions. • RRT indicated in severe (stage 3) kidney injury. • Absolute/urgent (objective) and relative/elective (subjective) indications • ICU:(early/low threshold to start in MOF) • Renal ward:(single organ AKI)
  • 23.
    Modality of dialysisin ITU • IHD (rapid removal of solute & water) • SLED • Hemofiltration • Hemodiafiltration • UF (Aquapharesis) • Approx. 10% pts with AKI cannot be treated with IHD because of hemodynamic instability • SLED and CRRT meta-analysis: no difference in outcome (Zhang et al AJKD Aug 2015)
  • 24.
    Outcomes of AKI •Recovery • Predialysis-CKD • ESRD (10-30%) • Death
  • 25.
    25 SIRS inducing MODS Sepsis, Trauma ,Major Surgery Pancreatitis, CPB . Host Defenses Tissue damage and hypotension Cellular activation & release of IM
  • 26.
    CKD usually means fewerfunctioning nephrons
  • 27.
    CKD is reducedkidney function and/or kidney damage • Chronic kidney disease – Kidney function • Glomerular filtration rate (GFR)< 60mL/min/1.73m2 for ≥ 3 with or without kidney damage – Kidney damage • ≥ 3 months with or without decreased GFR, manifested by either – Pathological abnormalities – Markers of kidney damage, e.g., albuminuria – Urine albumin-to-creatinine ratio (UACR)> 30mg/g This definition does not account for age related GFR decline
  • 28.
    Causes of CKD •Diabetes - rapid loss of renal function • Hypertension - both cause and effect • Glomerulonephritis • Cystic Disease • Drug toxicity • Interstitial disease • Chronic infections
  • 29.
    Zone of “Compensation” (AdequateRenal Reserve) Cr K Na Normal Range Serum creatinine G F R percent of Normal Renal Failure 0 25% 50% 75% 100% 1.4mg/dl 4 Sr. Cr 1.4 mg/dl Sr. creatinine > 1.4 indicates G F R is down by 50 % Relationship between serum creatinine and GFR
  • 30.
    Creatinine as amarker of KIDNEY FUNCTION(GFR) Formula based GFR measurements • MDRD formula (6 variable) • Modified MDRD formula (4 variable) • CKD-EPI formula • Cystatin C (independent of muscle mass) • Cockcroft -Gault formula • Creatinine clearance test (measured GFR)
  • 31.
    Creatinine GFR 1 100 250 3 25 4 12.5 5 6.125 6 3.06125 GFR which is related directly to urine creatinine excretion and inversely to plasma creatinine. on the basis of this relationship GFR will fall in roughly inverse proportion or reciprocal to the rise in plasma creatinine. Creatinine is used as a surrogate to eGFR. Direct GFR measurement is not feasible. Rough GFR
  • 32.
    Note: further refinedby KDIGO 2012 CKD work group
  • 33.
    Albuminuria categories Category AER (mg/24hr) ACR (Approximate equivalent) (mg/mmol)(mg/g) Terms A1 < 30 < 3 < 30 Normal to mildly increased A2 30 - 300 3 - 30 30 - 300 Moderately increased A3 > 300 > 30 > 300 Severely increased No longer uses prefixes “normo”, “micro”, or “macro” when referring to albuminuria because these terms are antiquated, non-descriptive definations
  • 34.
    Classification of CKD •It is recommended that CKD be classified by: – Cause – GFR category – Albuminuria category • This is collectively referred to as “CGA staging” • Represents a revision of the previous KDOQI CKD guidelines, which included staging only by level of GFR
  • 35.
    Each kidney hasabout 1 million nephrons; slow loss may not be noticeable • We have a large physiological reserve • Slow, progressive loss of functioning nephrons may not be noticeable • The person with CKD may not feel different up to ckd stage 4
  • 36.
    Early referral tonephrologist • Identify reversible/treatable factors • Avoid nephrotoxic drugs • Retardation of progression of renal disease • Prevent cardiovascular mortality • Better planning of RRT
  • 37.
    Early Treatment Makesa Difference Slow CKD progression
  • 38.
    Optimal Care inCKD-prevent CVD The incidence rate of new ESRD declined for the first time in 2011 after been stable since 2000.(USRDS 2013) Timely initiation of dialysis/Txp Timely access placement Informed choice of RRT Education Modification of comorbidity Preparation for RRT Early detection Protein restriction Blood sugar control BP control ACE inhibitors/ARB Secondary hyperparathyroidism Anemia Malnutrition Interventions that delay progression Management of complications Retinopathy (diabetics) Neuropathy (diabetics) Vascular disease Cardiac disease Acidosis/ dyslipidemia
  • 39.
    Kidney Failure isan eGFR < 15 • Kidneys cannot maintain homeostasis • Kidney failure is associated with fluid, electrolytes and hormonal imbalances and metabolic abnormalities • ESRD means the patient is on dialysis or has a kidney transplant
  • 40.
    Symptoms of kidneyfailure that can be caused by a build- up of wastes in the body include: • A metallic taste in the mouth or ammonia breath • Nausea and vomiting • Loss of appetite • Difficulty in concentrating • Itchiness (pruritis) • Weight Loss Symptoms of kidney failure that can be caused by a build- up of fluid in the body include: • Swelling in the face, feet or hands • Shortness of breath (from fluid in the lungs) SYMPTOMS OF KIDNEY FAILURE
  • 41.
    Symptoms of kidneyfailure that can be caused by damage to the kidneys include: • Making more or less urine than usual • Urine that is foamy or bubbly (may be seen when protein is in the urine) • Blood in the urine (typically only seen through a microscope) Symptoms of kidney failure that can be caused by anemia (a shortage of red blood cells) include: • Fatigue • Weakness • Feeling cold all the time • Shortness of breath • Mental confusion
  • 43.
    CKD ESRD GLOBAL CKD-ESRD: Prevalence/Incidence 500MILLION ADULTS WITH CKD 2.5 MILLION Many CKD patients die prematurely from CVD
  • 44.
    CKD ESRD CKD-ESRD: INDIA Prevalence/Incidence 17%of ADULTS WITH CKD 25,000/yr get RRT Many CKD patients die prematurely from CVD IN INDIA ONLY 25,000 (10% NEW ESRD GET RRT) AND 90% (2,50,000) UNABLE TO AFFORD RRT AND SIMPLY DIE. 50,000 patients undergoing regular MHD in 5500 machines in 800 dialysis centers 5000 patients on PD and 5000 transplant done annually. In India dialysis population is growing at a rate of 10%
  • 45.
    46 What are CKDpatients Dying From? Stroke Myocardial Infarction Heart Failure Sudden Death
  • 46.
    TREATMENT OPTIONS INTRODUCTION It isnot the end of the world for a person with impaired,non-functional kidneys. "QUALITY OF LIFE" can be improved by proper and timely medical intervention.
  • 47.
    The four optionsfor treating kidney failure • Renal replacement therapy (RRT) 1. Hemodialysis - In-centre or home 2. Peritoneal dialysis 3. Kidney transplantation • Conservative management 4. Active medical management without RRT
  • 48.
    Indications to begindialysis depend on objective and subjective criteria • Absolute indications : • Traditional indications/uremic symptoms • Relative indications: • anorexic, sleepiness, loss of energy, malnutrition, decrease in cognition • Diabetics need to initiate dialysis earlier than non diabetics.
  • 49.
    Main Goals ofDialysis • Remove – Fluid – Waste Products • Urea • Creatinine • Potassium • Phosphorous • Sodium • Maintain – Fluid – Electrolyte – Acid-base balance BENEFITS OF DIALYSIS improve quality and quantity of life
  • 50.
  • 51.
  • 53.
    Vascular access Temporary Permanent Femoral cannulation Central Venous Cannulation AVFistula AV Graft Permanent Venous Catheter Internal Jugular Subclavian
  • 54.
  • 55.
  • 56.
  • 57.
  • 58.
    Peritoneal Dialysis • Bloodis cleaned inside the body, through the Peritoneum • The peritoneum allows waste products to pass through it . • Dialysis Fluid pass through Tenckhoff Catheter.
  • 59.
    The two aspectsof peritoneal transport 1. Solute clearance. • Diffusive • Convective. 2. Fluid removal (Ultrafiltration)
  • 60.
  • 61.
  • 62.
    Chronic Peritoneal Dialysis: Continuous AmbulatoryPD Automated PD • 2.0-2.5 L dwells • 4-8 hours • 4 times/day • 3-10 dwells nightly • CCPD:Continuous Cycling PD– 1 dwell during the day • NIPD:Nocturnal Intermittment PD- dry during day
  • 63.
    CAPD • Perform 4-5exchanges per day – Treatment can be done almost anywhere – No machine needed – Exchange takes about 30 to 40 minutes – Ultra BagTM
  • 64.
    Fluid Bags- containfluid Blue Clamps-Control Flow Transfer Set-barrier to infection Minicap-prevent germs entry CAPD Components
  • 65.
    Peritoneal dialysis: Thereare three phases of PD Fill- New Fluid enters the peritoneal cavity Dwell-The fluid stays inside your body for 4-6 hours. Drain-The fluid plus waste is drained out and replaced with new fluid. Drain How does PD work?
  • 66.
    Automated Peritoneal Dialysis CCPD • Dialysatesolution is changed by a machine, at night. • 8-12 liters over 8- 10 hours • Leave 1-2 liters to dwell during the day.
  • 68.
    Complications of PD •Infectious • Non-infectious
  • 69.
    Infectious complications • Exit– site infection • Tunnel infection • Peritonitis: remains significant cause of – Hospitalization – PD failure – Damage to peritoneal membrane – Morbidity and mortality
  • 71.
  • 73.
    The Problem with ONEGERM is that it becomes a lot of germs!!
  • 74.
    A single germ can turn intoover a million in just 5 hours!! In 15 minutes 1 germ divides into 2 In 30 minutes 2 germs divide into 4 In 45 minutes 4 germs divide into 8 In 60 minutes 8 germs divide into 16 In 75 minutes 16 germs divide into 32 In 90 minutes 32 germs divide into 64 In 105 minutes 64 germs divide into 128 In 120 minutes 128 germs divide into 256 In 135 minutes 256 germs divide into 512 In 150 minutes 512 germs divide into 1024 In 165 minutes 1024 germs divide into 2048 In 180 minutes 2048 germs divide into 4096 In 195 minutes 4096 germs divide into 8192 In 210 minutes 8192 germs divide into 16384 In 225 minutes 16384 germs divide into 32768 In 240 minutes 32768 germs divide into 65536 In 255 minutes 65536 germs divide into 131072 In 270 minutes 131072 germs divide into 262144 In 285 minutes 262144 germs divide into 524288 In 300 minutes 524,288 germ divides into 1,048,576!!
  • 75.
    Non-infectious complications Non infectious complications Catheterrelated Catheter unrelated •Outflow failure •Pericatheter leak •Abdominal wall herniation •Catheter cuff extrusion •Intestinal perforation GERD Hemoperitoneum Back/abdominal pain UF failure Abdominal wall herniation Peritoneal sclerosis Pleural effusion Metabolic
  • 77.
  • 80.
  • 81.
    Benefits of Transplantion Improve life expectancy  Cardio-vascular benefits  Improve Quality-of-life  Socio-economic benefits
  • 82.
    The Transplantation Process Pre-transplant evaluation  Legal compliance  The operation  Immunosuppression  Complications  Short and long term follow up
  • 83.
    Kidney Donor Living related. Livingunrelated (altruistic). Deceased/Cadaveric (Brain-dead). Beating and non-beating heart.
  • 86.
  • 87.
    Surgical Complications  VascularComplications: arterial, venous  Ureteric complications : urine leak/obstruction  Perigraft Fluid Collections: Seroma & Hematoma Abscess Urinoma Lymphocele  Wound infection  Delayed graft function
  • 88.
    Medical Complications  Acuterejection - Acute cellular rejection - Antibody-mediated rejection-C4d  NODAT/PTDM  Infectious complications - Cytomegalovirus - BK virus - Post op infections  Malignancy-PTLD and Skin Carcinoma common  Chronic allograft dysfunction(r/o reversible factors)
  • 89.
    India – LegalAspects Transplantation of Human Organs Act, 1994 Aims • Regulate removal, storage and transplantation of human organs for therapeutic purposes • To prevent commercial dealings in organs • Recognise Brain Death
  • 90.
    WHAT IS REJECTION? •Rejection is a normal reaction of the body to a foreign object. When a new kidney is placed in a person's body, the body sees the transplanted organ as a threat and tries to attack it What is done to prevent rejection? Medications is given for the rest of the life to fight rejection. The anti-rejection medications most commonly used includes:
  • 91.
    Immunosuppressive Medications  Induction: –Corticosteroids –Anti-thymocyteglobulin (ATG) –IL-2 receptor antagonists - Basiliximab  Maintenance: –Corticosteroids –Calcineurin inhibitors (CNIs) –mTOR inhibitors –Antimetabolites
  • 92.
    Immunosuppressive Medications • Treatmentof rejection (Rescue) : – Corticosteroids – Anti-thymocyte globulin – Intravenous Immunoglobulin (IVIG) – Rituximab – Plasmapheresis
  • 93.
    T-10 Risks and possibleside effects Lowered resistance to illness • Immunosuppressive medications lower your resistance to infection • To stay healthy, you must protect yourself from coming in contact with infections • Take the correct dosage of medication and see your doctor regularly
  • 96.
    In conclusion, renaltransplantation should be recommended as the preferred mode of RRT for most patients with ESRD in whom surgery and subsequent immuno-suppression is safe and feasible.
  • 97.
    Chronic Allograft Dysfunction: WhyDo Grafts Fail? • Chronic low-grade immune injury • Long-standing hypertension • Recurrent disease (diabetic nephropathy or glomerulonephritis) • Repeated episodes of acute rejection • Donor disease • Calcineurin inhibitor nephrotoxicity
  • 98.
  • 99.
    Kidney Disease Cycle Dialysis At-risk Chronic  Kidney Failure  Kidney Disease (Stage 5) (Stage 1 – 4) Transplant
  • 100.
    Continuum of kidneydisease care • Prevent kidney disease (awareness of risk) • Identify kidney disease (awareness of diagnosis) • Manage kidney disease (knowledge to achieve management goals) • Renal replacement or conservative care for renal failure
  • 101.