Engidaw Ambelu

1. CKD
BY MERSHA MAMO (MD)
February 2018 Gondar
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2. CONTENT
Definition & Staging
Etiology
Pathogenesis
Management (general
principles)
2

3. DEFINITION
CKD is defined by the presence of
kidney damage or decreased
kidney function for three or
more months , irrespective of the
cause
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4. DEFINITION…
 Persistence of the damage or decreased function
for at least 3 months is necessary to distinguish
CKD from AKI.
 Kidney damage - refers to pathologic
abnormalities, whether established via renal
biopsy or imaging studies, or inferred from
markers( urinary sediment abnormalities or
Albuminuria)
 Decreased kidney function- refers to a
decreased glomerular filtration rate (GFR )
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5. A. DURATION
Duration ≥3 months, based on
documentation or inference
Clinical evaluation can often suggest
duration
Documentation of duration is usually
not available in epidemiologic studies
5

6. KIDNEY DAMAGE…
Pathologic(biopsy)- glomerular, vascular, or
tubulointerstitial disease
Imaging - PCKD, hydronephrosis, and small kidneys
Markers
 Albuminuria- ACR >30 mg/g
 Urinary sediment abnormalities- RBC and WBC casts
Kidney transplantation − all assumed to have kidney
damage
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7. ACR, PCR- clinical decision AER, PER- confirmatory
High urine ACR, positive dipsticks- confirm by urine
albumin excretion in a timed urine collection(24hrs)
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8. B. ALBUMINURIA
Urine ACR >30 mg/g(or equivalent)
have a significantly increased risk for
 All-cause and cardiovascular
mortality
 ESRD, AKI and CKD progression
compared with those who have a
lower ACR , even when eGFR is
normal
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9. C. DECREASED GFR
GFR is less than 60 mL/min per 1.73
m 2 defines CKD
kidney failure (ESRD) is defined as a
GFR <15 mL/min per 1.73 m 2 or
treatment by dialysis
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10. NORMAL GFR
 GFR is equal to the sum of the
filtration rates in all of the functioning
nephrons
Glomeruli filter approximately 180
liters per day (125mL/min) of plasma
Normal GFR ̃ 120ml/min/1.73m2
GFR =(140-age)weight(Kg)/72(Sct )
0.85(if female)
10

11. GFR…
 Normal annual mean decline in GFR with age from the
peak GFR (120 mL/min per 1.73 m2) attained during the
third decade of life is
1 mL/min per year per 1.73 m2,
 Percent of sclerosed glomeruli =
(age ÷ 2) +10
e.g. 40 year old will have 30% sclerosed glomeruli
 Relation b/n kidney mass(nephron mass) and GFR
11

12. GFR…
 The best index of overall kidney function
 Declining GFR is the hallmark of progressive KD
 Measured GFR(mGFR)- using exogenous filtration
markers such as inulin or iothalamate
 Estimated GFR(eGFR)- from the serum concentration of
creatinine, an endogenous filtration marker
 In clinical practice, GFR is typically estimated
12

13. STAGING
aWith risk factors for CKD bWith demonstrated kidney damage (e.g., persistent
proteinuria, abnormal urine sediment)KDOQI
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14. KDOQI guidelines and modified by NICE in 2008.
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15. REVISED CKD CLASSIFICATION BASED
UPON GFR AND ALBUMINURIA
Albuminuria staging
A1 − ACR <30 mg/g
A2 − ACR 30 to 299 mg/g
A3 − ACR ≥300 mg/g
KDIGO. Summary of recommendation statements. Kidney Int 2013
E.G- A person with an eGFR of 25
and an ACR of 35 mg/g has CKD
G4A2.
15

16. PATHOPHYSIOLOGY OF CKD
Two broad sets of mechanisms of damage:
(1) initiating mechanisms - (e.g., genetic, IC deposition
and inflammation or toxin exposure )
(2) Progressive mechanisms- Compensatory
hyperfiltration and hypertrophy of viable nephrons
- Eventually, these short-term adaptations of hypertrophy
and hyperfiltration become maladaptive
- Increased intrarenal activity of the renin-angiotensin
axis appears to contribute both mechanisms
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17. PATHOPHYSIOLOGY
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• Renal injury
• Reduction in renal mass
• Glomerular capillary hypertension
• ↑glomerular permeability to
macromolecules•↑filtration of
plasmaproteins(proteinuria)
• Excessive tubular protein reabsorption
• Tubulointerstitial inflammation
• Renal scarring
RAAS
is
respon
sible
for
most of
these
process
es

18. ETIOLOGY AND EPIDEMIOLOGY
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19. PATHOPHYSIOLOGY OF UREMIA
Uremia is constellation of symptoms in advanced
renal failure resulting from
 Accumulations of toxins that normally undergo renal
excretion
 Loss of renal function: fluid and electrolyte
homeostasis and hormonal regulation
 Progressive systemic inflammation with its nutritional
and vascular consequence
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20. CLINICAL MANIFESTATIONS
 Manifestations depend on severity of renal
impairment and underlying disease
 Most patients with early(Stage 1&2) CKD
asymptomatic.
 CKD is silent kiler.
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21. EVALUATION OF THE PATIENTS: HX
 Symptoms are subtle or absent until renal failure
supervenes
 Look for underlying causes
 Hx of hypertension, DM, abnormal U/A, problems with
pregnancy
 Drug history
 Family history
 Evidence of autoimmune diseases
 Look for uremic symptoms
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22. CLINICAL MANIFESTATION …
 In late CKD uremic manifestations like
easy fatigability,
anorexia,
vomiting,
deficits in cognitive function
Hiccups
peripheral edema,
muscle cramps,
Pruritis
restless leg syndro
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23. PHYSICAL EXAMINATION
 Focus on
 Hypertension and target organ damage from
hypertension
 volume status, Edema
 Sensory polyneuropathy
 Astrexis and pericardial friction rub
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24. LAB.
 Focus on clues to causes and degree of renal
impairment
 Serial serum creatinine
 Calculate GFR,
 Serum and urine protein electrophoresis
 24hr urine protein,
 ANA, anti DsDNA, HIV, Hep B and C
 Serum electrolyte, calcium, phosphorus, Vit D, PTH
 Renal biopsy only if indicated
 Abdominal U/S
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25. CKD: SCREENING
 All individuals during routine health encounters.
 Targeted evaluation of those at increased risk :
 those with DM, hypertension, CVD, family hx of
DM/HTN or CKD, etc
 Urinary exam for protein/albumin, creatinine
assessment ± additional tests
 Once Dx is made identify and treat cause &
potentially reversible factors and classify Sta
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26. EVALUATION OF THE PATIENT:
ESTABLISHING THE DIAGNOSIS AND
ETOIOLOGY
 Distinguish CKD from acute or subacute kidney
disease
 Previous Creatinine record
 Metabolic bone disease
 Small kidney
 Anemia
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27. EVALUATION OF THE PATIENT:
ESTABLISHING THE DIAGNOSIS AND
ETOIOLOGY
 R/o acute on CKD
 Common causes include:
 ECFV depletion
 UTI
 Obstruction
 Nephrotoxins
 reactivation or flare of original disesase eg lupus or vasculitis
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28. MANAGEMENT OF CKD
Principles of CKD Mx :
Establish the cause of CKD and treat (if
possible)
Identify and manage unexpected (acute)
deterioration in kidney function
Preventing or slowing ds progression
Treatment of the complications
Identification and adequate preparation
for RRT 28

29. Decreased renal perfusion
 Fluid loss , AMI, sepsis, ACEIs
Administration of nephrotoxic drugs
 Aminoglycoside
 Radiographic contrast material
 NSAIDs
Urinary tract obstruction
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30. Will Slow secondary factors (not
initiating)
The major factors are :
Intraglomerular hypertension
Glomerular hypertrophy
Additional causes
 Hyperlipidemia
Metabolic acidosis
Tubulointerstitial disease
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31. MEASURES TO SLOW CKD PROGRESSION
Control HTN
Control proteinuria
Control blood sugar
Dietary protein restriction?
Statin therapy
Antiplatelet therapy
Smoking cessation
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32. CONTROL OF HTN AND PROTEINURIA
 Control of systemic and glomerular HTN
 Lowering proteinuria – renoprotective
Target BP
 CKD alone < 140/90mmHg
 CKD and DM < 130/80mmHG
 CKD and proteinuria <130/80 (125/75 mmHg )
NICE 2014
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33. PROTEINURIA GOAL
 Less than 1000mg/day
 In patients who are nephrotic
(above goal is unobtainable) - reduction
at least 50 to 60 % from baseline
values plus protein excretion less than
3.5 g/day
K/DOQI recommendation 33

34. .
ACE inhibitors and ARBs – first line in patients with
proteinuria(DM, glomerular Ds)
 ACE plus ARB therapy - Not recommended
Non- Dihydropyridine CCBs - diltiazem & verapamil
 Second line agents
Other antihypertensive- no proteinuria
Salt restriction - proteinuria
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35. CONTROL OF BLOOD GLUCOSE
Excellent glycemic control in DM
patients reduces the risk of kidney
disease and its progression
Preprandial glucose b/n 90–130 mg/dl
and hemoglobin A1C should be < 7%
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36. DIETARY PROTEIN RESTRICTION
 Approximately 0.6 to 0.8 g/kg per day
 Benefit on the progression of CKD remain
controversial
 KDOQI guidelines- daily protein intake of between
0.60 and 0.75 g/kg per day
 Risk of protein-energy malnutrition in advanced
CKD
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37. CKD AND CVD
 CKD is an independent & important risk factor for CVD.
 Traditional CV risk factors :
 HTN usually with LVH, DM, dyslipidemia, smoking, old age
are more prevalent in CKD populations.
 Non-traditional risk factors unique to CKD
include:
 uremic toxins, abnormal bone mineral metabolism, anemia,
proteinuria, hyperhomocysteinemia and an increased
inflammatory-poor nutrition state
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38. STATIN THERAPY RECOMMENDATION…
For all individuals aged ≥50 years with
stages 3–5 CKD, if not receiving
dialysis or transplanted
 For those aged < 50 years, if another
cardiovascular risk factor is present, or
if 10-year risk of a coronary heart
disease event exceeds 10%.
KDIGO guideline 201338

39. OTHER SECONDARY FACTORS
Smoking cessation - is
associated with a slower rate of
progression of CKD
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40. TREATMENT OF THE COMPLICATIONS
CXns of renal
dysfunction
 Volume overload
 Hyperkalemia
 Metabolic acidosis
 Hyperphosphatemia
 Renal osteodystrophy
 Hypertension
 Anemia
 Dyslipidemia
 Sexual dysfunction
complications of ESRD
 Malnutrition
 Uremic bleeding
 Pericarditis
 Uremic neuropathy
 Thyroid dysfunction
 Infection →
vaccination
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41. ANEMIA
NCNC anemia
Can result in deterioration in cardiac
function, decreased cognition and
mental acuity
 Increased risk of morbidity and
mortality
Ventricular dilation, and ventricular
hypertrophy
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42. 42

43. ANEMIA - TREATMENT
 Target Hgb = 10.5-12g/dl (most guidelines)
 Treatment options- RBC transfusions,
androgens, and ESA
 Initiate ESAs when the Hb level is <10 g/dL
 Dose of EPO is usually 10,000 units
subcutaneously once weekly
 With EPO- maintenance supplemental iron( to
maintain a transferrin saturation between 20 to 50
%) and a serum ferritin level between 100 and
500 ng/mL.
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44. THE COMPONENTS OF MINERAL AND BONE
METABOLISM
 Complications mainly
manifest on skeletal
system and vascular
beds
 Are usually the
consequence of
hyperphosphatemia
and hypocalcemia with
secondary
hyperparathyroidism
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45. ALTERED MINERAL METABOLISM IN
CKD-MBD
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46. RENAL REPLACEMENT THERAPY
 Early identification of those with CKD and referral to
a specialists
 Clear indications to initiate RRT
 Uremic pericarditis,
 Encephalopathy,
 Intractable muscle cramping
 Anorexia, and nausea not attributable to reversible
causes such as peptic ulcer disease
 Evidence of malnutrition
 Fluid and electrolyte abnormalities, principally
hyperkalemia or ECF volume overload, that are
refractory to other measures 46

47. RRT…
 Choice of RRT: Counsel patient about
Hemodialysis, Peritoneal Dialysis and renal
transplantation
 Transplantation is the treatment of choice for most
patients with ESRD
 Prepare for the chosen RRT modality.
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