1. CKD-PRE DIALYSIS
MANAGEMENT
Shruthi K

2. Chronic kidney disease
 Global health problem
 Rising incidence – doubled in last 15 years
 In India – 0nly 10% of patients with ESRD have
access to RRT

3. CKD-definition
 GFR ≤ 60ml/min/1.73m that is present for ≥ 3months
with or without evidence of kidney damage
OR
 Evidence of kidney damage with or without decreased
GFR that is present for ≥ 3months as evidenced by
 Microalbuminuria
 Proteinuria
 Glomerular haematuria
 Pathological abnormalities (e.g. abnormal biopsy)
 Anatomical abnormalities (e.g. scarring seen on imaging or
polycystic kidneys)

6. Pre dialysis management – Why?
 Optimal pre-dialysis care improve
 Morbidity
 Mortality
 Dialysis and transplantation outcome

7. CKD Predicts CVD
40
36.6
Age-Standardized Rate of Cardiovascular
35
30
Events (per 100 person-yr)
25
21.8
20
15
11.29
10
5 3.65
2.11
0
≥ 60 45-59 30-44 15-29 < 15
Estimated GFR (mL/min/1.73 m2)

8. Early Treatment Makes a Difference
Brenner, et al., 2001

9. Goal
 To establish diagnosis
 Rule out reversible causes
 Slow down progression
 Evaluate and treat complications
 Treat co-morbidities
 Reduce cardiovascular risk
 Prepare for replacement therapy
 Select & start renal replacement therapy at
appropriate time

10. Management
 Treatment of reversible causes
 Preventing or slowing the progression of disease
 Treatment of the complications
 Identification and adequate preparation of the
patient in whom renal replacement therapy will be
required

11. Treatment of reversible causes
 Decreased renal perfusion
 Hypovolemia (such as vomiting, diarrhea, diuretic use,
bleeding)
 Hypotension (due to myocardial dysfunction or
pericardial disease)
 Infection /sepsis
 Drugs which lower the GFR
 Urinary tract obstruction

12. Slowing the rate of progression
 Proteinuria
< 1 gm/day or at least 60% of baseline values
 Optimal level of protein intake
 Not been determined
 0.8 to 1.0 g/kg/day
 ACEI/ARB
 Smoking cessation

13.  Blood pressure
 <130/80mmHg
 <125/75mmHg if proteinuria >1g/day
 Salt restriction
 Antihypertensives
 ACE,diuretics,CCB
 Exercise

15. Treatment of complications
 Volume overload
 Salt restriction
 Loop diuretics

16.  Hyperkalemia
 Developsin the patient who is oliguric or who has an
additional problem such as a high potassium diet,
increased tissue breakdown, or hypoaldosteronism
 Low K+ diet – 40 to 70meq / day
 Avoid NSAIDs

17.  Metabolic acidosis
 Due to
 Decreased ability to regenerate bicarbonate
 Reduced ammonia production
 Decreased hydrogen ion secretion
 Decreased filtration of titrable acids – sulphate,
phosphate, urate, hippurates
 Decreased proximal tubular re-absorption of
bicarbonate

18.  Treatment of academia is desirable
 Bicarbonate supplementation may slow the progression
of CKD
 Bone buffering of the some of the excess hydrogen ion
is associated with the release of calcium and phosphate
from bone, contributing to worsening of renal
osteodystrophy
 Uremia acidosis can increase skeletal muscle
breakdown and diminish albumin synthesis leading to
loss of lean body mass and muscles weakness-
contributing to malnutrition

19.  Therapy is targeted to maintain serum bicarbonate
concentration above 23 mEq/Lit
 Drug of choice : sodium bicarbonate < 0.5-1.0
mEq/kg/day

20.  Hyperphosphatemia
 Dietrestriction : 800mg/day
 GFR<25 to 30 ml/min: oral phosphate binders
 Stage 3 & 4 : between 2.7 and 4.6 mg/dL
 Stage 5 : between 3.5 and 5.5 mg/dL

21.  Renal osteodystrophy
 High phosphate load and hypocalcemia stimulate
PTH secretion
 Leads to sec hyper parathyroidism which increases
bone resorption

22. Treatment
 Control serum phosphate
 CKD stage-specific target levels of intact PTH
 CKD stage 3: treat elevated PTH to target
35-70pg/ml
 CKD stage 4 to target 70-110 pg/ml
 CKD stage 5 to target 150-300 pg/ml
 Next step is assessment of 25-(OH)D levels and
replacement with vitamin D (ergocalciferol) if levels
are lower than 30 ng/mL.

23.  If the intact PTH level is elevated and the serum 25-
(OH)D level is higher than 30 ng/mL, treatment with
an active form of vitamin D is indicated
 Available options
 Calcitriol
 Alfacalcidol
 Doxecalciferol

24.  Cinacalcet
 Calcimimetic
 Used if elevated phosphorus/Ca limit use of vit D

25. Hypertension
 Cause and complication of CKD
 Target
 <130/80 or <125 /75 mmHg if proteinuria is >1
gm /day or diabetes is +
 Non pharmacological
 Lifestyle modification
 Salt restriction
 Exercise,weight reduction
 Diet
 Smoking cessation etc….

26.  Pharmacological
 May require 3 or more drugs
 Diabetes & proteinuria : treat with ACEI /ARB as 1st line
therapy
 Monitor Creatinine & K+ on day 3 ,7 &weekly
 Loop and thiazide diuretics as an adjunct therapy
 CVD: beta blockers
 CCBs
 Alpha blockers : prazosin,doxazosin followed by direct
vascular smooth muscle relaxant minoxidil is considered

27. Anemia
 Caused by insufficient erythropoietin production
,short life span of RBCs , iron deficiency
 Target Hb: 10 to 12gm%
 Correct iron deficiency
 EPO : 80 to 120units/kg/wk
 Alternative : darbepoietin alfa
 Longer acting agent
 Dose: 0.45µg/kg s/c once a week

28. Preparation for RRT
 Counselling
 HD,peritoneal dialysis / renal transplant
 If not for transplant : vascular access should be
created in preferably native AV fistula in CKD
stage 4
 Venous preservation should start from stage 2 or 3
 Vaccinate against hep B, pneumococcal and H
influenza infection
 Drug dosage according to eGFR, avoid contrast