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8-2. Management of chronic renal failure. Isidro Salusky (eng)
1. Isidro B. Salusky, M.D.
Distinguished Professor of Pediatrics
Chief, Division of Pediatric Nephrology
Director, Clinical Translational Research Center
Associate Dean of Clinical Research
David Geffen School of Medicine at UCLA
5. % Annual mortality
100
Dialysis Population
10
1
GP Male
GP Female
GP Black
GP White
Dialysis Male
Dialysis Female
Dialysis Black
Dialysis White
0.1
0.01
0
25-34
35-44
45-54
55-64
65-74
75-84
>85
Age (yr)
NKF Task Force on Cardiovascular Disease. Am J Kidney Dis. 1998;32(suppl 3):S115.Sarnak MJ,
Levey AS. Am J Kidney Dis. 2000;35(suppl 1):S117-S131.
7. –Protein and Calorie Malnutrition
–Acidosis/Electrolyte Abnormalities
–Primary kidney disease
–Anemia
–Renal bone diseases
–Hormonal Factors
–Immunosuppressive Medications
8. GFR
Description
(mL/min/1.73 m2)
1
Kidney damage with
normal or GFR
90
2
Kidney damage with
mild GFR
60-89
3
Moderate
30-59
4
Severe
5
Kidney failure
Stage
GFR
GFR
15-29
15 or dialysis
K/DOQI: Evaluation, classification and stratification. AJKD 39: 2001
10. SAs
s of Anemia in CKD Patients (1 of 3)
• Renal insufficiency = EPO deficient state
Kidney
ency
Decreased
erythropoietin
production
production
etin
n of uremic
Erythroid
progenitor cells
Inhibition of
erythropoiesis
Bone
Bone
marrow
11. • EPO resistance
– Iron deficiency
– Hyperparathyroidism
– High dose ACE
inhibition
– Aluminum toxicity
– Antibodies to ESA
–
–
–
–
–
–
Inflammation
Folate/B12 deficiency
Hemoglobinopathies
Hemolysis
Chronic Blood Loss
Chronic infection
15. • Loss of appetite-may manifest early in the
course of kidney disease
• Spontaneous food intake decreases with
worsening kidney failure
• Calorie Malnutrition-seen during the first
years of life
• Protein Malnutrition-not frequently seen in
children with kidney failure
16. • Adequate caloric intake
– Infants-growth rates during this period are
correlated with calorie intake
• Nasogastric (NG) or Gastrostomy (G) Tube Feeding
– Older children- intake should not be less than 80%
of the Recommended Daily Allowance (RDA)
• Therapy with recombinant human growth
hormone
20. • North America: Oligo-anuric, high glucose exposure and
treatment with RhGH
• Europe: Biocompatible PD fluids
• Turkish: Lower serum albumin levels, higher serum P levels and use of
amino-acids containing solutions
• Latin America: Persistent residual renal function, higher use of
phosphate binders and lowest rate of NaCl supplementation
Rees L et al. JASN 22:2302, 2011
21. • Many congenital kidney diseases lead to
loss of electrolytes and decreased ability of
the kidneys to concentrate urine
• Infants with kidney failure due to renal
dysplasia-high urinary losses of sodium
• Metabolic acidosis- kidney function below
50%
• The specific effect of bicarbonate therapy
on growth in CKD remains to be defined
• Correction prior to treatment with rhGH
22. • Effects on bone remodeling and modeling
– Skeletal fracture and microfracture repair
– Bone deformities
– Growth retardation
• Relationship to:
– Osteopenia / osteoporosis
– Changes in bone mass over time during long-term dialysis
– Vascular calcifications
• Bone loss after renal transplantation and
cardiovascular disease
23. 100
Bone turnover
% of Subjects
80
PTH
60
40
20
0
2
3
CKD Stage
4
Wesseling-Perry K CJASN (2012) 7:146
29. A systemic disorder of mineral and bone metabolism due to
CKD manifested by either one or a combination of the
following:
– Abnormalities of calcium, phosphorus, PTH, or vitamin D
metabolism
– Abnormalities in bone
turnover, mineralization, volume, linear growth, or strength
– Vascular or other soft tissue calcification
Moe et al Kidney International 2006
30. • Patients with Stage 5 CKD are at high risk for vascular
calcification
• Vascular calcifications are present in almost 50% of
patients with stage 4 CKD and new dialysis patients
• Vascular calcification can be quantified
• Vascular calcification is associated with modifiable risk
factors
– Ca intake from calcium-based binders
– S-P, S-Ca and Ca P product
• Vascular calcification results in arterial stiffening and
increased pulse pressure and adynamic bone disease
31. Therapeutic Options for the Treatment of
CKD-MBD
Phosphate Binders
Calcitriol
Paricalcitol
D2-D3
1,25(OH)D
Doxercalciferol
Ca-Salts
Sevelamer:
Ca free – Metal Free
Lanthanum Ca:
Ca free - Metal +
Ergocalciferol
Calcimimetic
Drugs
Cinacalcet
32. Treatment
Stage
Treatment Target Range
3
KDIGO: Upper Limit of Normal* (2C)
KDOQI: 35-70 pg/mL
4
KDIGO: Upper Limit of Normal* (2C)
KDOQI: 70-110 pg/mL
5
KDIGO: Upper Limit of Normal* (2C)
KDOQI: 150-300 pg/mL
5D
KDIGO: 2 to 9 times Upper Limit of Normal (2C)
KDOQI: 150-300 pg/mL
Europe Children: 2 to 3 x upper Limit of Normal
*In patients with CKD stages 3-5 not on dialysis, in whom serum PTH is progressively rising and remains
persistently above the upper limit of normal for the assay despite correction of modifiable factors, treatment with
calcitriol or vitamin D analogs is suggested. (2C)
1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline
for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD)
Kidney Int. 2009;76(suppl 113):S1-S130.
2. Adapted from National Kidney Foundation (NKF). KDOQI clinical practice guidelines for bone metabolism and disease in
chronic kidney disease. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.
