CHRONIC KIDNEY DISEASE ( CKD) &

CHRONIC KIDNEY FAILURE ( CKF)

Mihaela Balgradean MD. PhD

Professor of Pediatrics
CHRONIC KIDNEY DISEASE (CKD)

 CKD is the result of reducing the number of functional

nephron and the glomerular filtration rate (RFG↓), due to
bilateral renal parenchima damage

 The progressive decreasing of renal function to end stage

renal disease ( ESRD) it is found in all cases of moderate and
severe CKD

 The decline of renal function is usually announced by

worsening proteinuria
CKD STAGES
(conforming Kidney Disease Outcome Quality Initiative – 2002)

STAGE GFR (mL /min/1,73 m2)

I ≥90

II 60-89

III 30-59

IV 15-29

V < 15
 CKD ETIOLOGY IN CHILDREN

CAKUT – congenital anomalies of the kidney and urinary tract

CHRONIC KIDNEY FAILURE (CKF)

 CKD / CKF does not appear if only one kidney is affected

 Almost half of the CKD cases are caused by congenital

malformations of the kidney and urinary tract are detected today
by fetal US ( screening US). More may be omitted if US is
not done in the third trimester of pregnancy

 There are CKD cases diagnosed late in children : creatinine

level increases along with the size and muscle mass, but
CKD child is small and weak. In these conditions serum
creatinine does not decrease until the kidney function does
not decline to half of its normal value
 CHRONIC KIDNEY DISEASE (KDOQI;K/ KDIGO) / National
Kidney Foundation Kidney Disease Outcomes Quality Initiative ; Kidney
Disease Improving Global Outcome
CKD STAGES
GFR ( ml/min/1,73 m²) CLINICAL SIGNES

 Stage 1 > 90 Known renal parenchima disease

 Stage 2 60 – 90 No clinical signs , Laboratory is upper limit
of normal GFR
 Stage 3 30 – 6 Laboratory tests are modified , growth is slow, the
appetite is low
 Stage 4 15 – 30 More severe symptomatology and
laboratory
 Stage 5 < 15 ( ESRD) The renal substitutive treatment is
necessary
( Kidney failure cf KDIGO/ K/KDOQI
Tubulointerstitial fibrosis)
CHRONIC KIDNEY DISEASE (CKD)

ELEMENTS OF SUSPICION FOR CKD

 Plasma creatinine > normal for the age

 Bilateral renal defects on fetal US
 Bilateral renourinary disorders on imaging ( in UTI context often )
 Familial history of renal disease (ADPKD- polycystic kidney disease - ,
Alport syndrome)
 Persistent proteinuria
 AKI/ARF in history disease
 Hypertension
CHRONIC KIDNEY DISEASE (CKD)

NORMAL VALUES OF PLASMA CREATININE IN CHILDREN

µmol/L mg/dL

< 2 years 35 – 40 0,4 – 05

2 – 8 years 40 – 60 0,5 – 0,7
9 – 18 years 50 – 80 0,6 – 0,9
 CHRONIC KIDNEY DISEASE (CKD )
SUGGESTIVE CLINICAL / LABORATORY / IMAGING
SIGNES
1. GROWTH FAILURE : in > 50% of CKD cases.
 Impaired growth is worse if CKD is instaled before 2 years of
age.
 Anorexia,nausea,vomiting, gastroesophageal refux cause caloric
loss
 Untreatedmetabolicacidosis,anemia,hypertension,osteodistrophy,
all of them are implicated in CKD growth failure.
 Growth disturbances in CKD exhibit resistance to growth
hormone (GH),and Insulin – like growth factor I factor (IGF- I)
2. CHRONIC ANEMIA : It occurs when RFG < 30 – 35 ml/1,73 m²
 CKD anemia is normochromic, normocytic ,not only responds to
treatment with iron. (Iron deficit could be implicated:
gastrointestinal loss, decreased nutrient intake)
 Anemia of CKD occurs due to deficiency of erythropoietin,
the hormone produced by the kidney that promotes the
maturation of the red blood precursors
CHRONIC KIDNEY DISEASE (CKD )
SUGGESTIVE CLINICAL / LABORATORY / IMAGING SIGNES

 3. Frequent / Unexplained vomiting : gastrointestinal persistent

symptomatology (vomiting,anorexia,nausea,weight loss–in the absence of
diarrhea ) ex: morning vomiting →indicative for severe CKD. Is due to
intestinal motility disorders ( caused by metabolic disturbances) and to
polypeptide decreased clearence
 4. Urologic pathology : nocturnal and diurnal urine incontinence,
rare/frequent micturations + urgency, chronic constipation/encopresis UTI
associated, instable bladder, Hinman syndrome, neurogenic bladder,
posterior urethral valves, etc. All of them represent renourinary disorders
accompanied by progressive renal lesions and CKD
 5. Hypertension : In 70% of cases, hypertension in children has specified
etiology, and, in 50 – 80% of cases hypertension has kidney related
cause. It is due by exccesive production of renin, fluid retention and
systemic vasoconstriction.
CHRONIC KIDNEY DISEASE (CKD)
SUGGESTIVE CLINICAL / LABORATORY / IMAGING SIGNES

 6. Rare bone disorders . Rachitism ,valgue legs deformations,

fractures after minime traumatic injury, could represents clinical signs
of CKD. Renal osteodystrophy affects 60 – 80% of children suffering
of CKD. It occurs when renal function reach < 50%. It is the result of
chronic hyperphosphatemia, secondary hyperparathiroidism and
inadequate production of 1,25 – vitamin D.

 7. Poor unexplained scholar performance. Attention disorders,

fatigue, headache, withdrawal of the various activities . There are the
consequences of the uremic toxins accumulation, of the chronic
metabolic acidosis and anemia
CHRONIC KIDNEY DISEASE (CKD)
CLINICAL & LABORATORY EVALUATION (1)

 Blood pressure measurement, urinalisis, evaluation of growth

parameters (including serum creatinine), familial history ( Alport
syndrome, polichistic renal disease)

 Azotemia, hyperphosphatemya and metabolic acidosis, they are

always present in CKD

 Renal Clearance (GFR), measured by creatinine clearance, or by renal

scan (99m Tc DTPA scintigraphy), appreciates CKD progression and
severity
CHRONIC KIDNEY DISEASE (CKD)
LABORATORY EVALUATION ( 2)

 Hyperphosphatemia, hypocalcemia, & high level of alkaline

phosphatasis , are frequent associated with CKD
Hyperphosphatemia is the consequence of phosphorus decreased
excretion and calcium reduced absorption, due to secondary increased
secretion of parathormon which promotes bone calcium resorption starting
renal osteodistrophy

 Acidosis increases calcium resorption

 Relative resistance to vitamin D binds to decreased renal hydroxilation of

25-vitamin D, which in turn lowers calcium absorption in the intestin.

¤ Hypocalcemia is not symptomatic , due to metabolic acidosis which

increases ionic calcium
 CHRONIC KIDNEY DISEASE
LABORATORY EVALUATION (3)

Estimating GFR based on serum creatinine

(Schwartz Formula)

e RFG = k x /Waist T(cm) / serum creatinine ( µmol/L)

K = 0,33 premature K = 0.45 term newborn

K= 0,55 1-12 years
Conversion factors

 Serum creatinine : µmol/L x 0,0113 = mg/dL mg/dLx 88,5 =

µmol/L

 Urea : mmol/L x 6 = mg/dL si mg/dL x 0,167 =

mmol/L
 Serum albumin : g/L x 0,1 = g/dL si g/dL x 10 = g/L
CHRONIC KIDNEY DISEASE (CKD)
LABORATORY EVALUATION (4)

 Normochromic , normocytic anemia is due to decreasing of

erytrocytes production, and life-shortening erytrocyte.
- Iron deficiency & acid folic deficiency is the result of nutrient
intake.
- Erythropoietin level is low in CKD

 High level of uric acid could aggravate CKD by uric

nephropathy

 Triglycerides and cholesterol levels are increased

CHRONIC KIDNEY DISEASE (CKD)
IMAGING / RENAL BIOPSY

 Renovesical ultrasonography, IV urography , micturation cistography

, different types of renal-scan ( Tc -99m DTPA, DMSA , MAG3) are used
in establishing etiology and the stage in CKD.
 Radiographs of the knee and hand , RMN, sates the injuries of renal
osteodistrophy.
 Renal biopsy is useful in defining pathology of glomerular lesions in
glomerular nephropaties
BOALA RENALA CRONICA ( BRC)
CONSERVATIVE TREATMENT

 Multidisciplinary team + child + familly

 Treatment is adressed to prevention of CKD progression ,hypertension,

anemia, cardiovascular disease, osteopathy , failure to thrive

 For minimising symptomatology : metabolic disorders correction could

ameliorate vomiting, fatigue, malaise

 Renal osteodistrophy become symptomatic when GFR <50-80

mL/min/1,73 m² (bone pain and fractures )→ nutrient intake poor in
phosphor , phosphorus chelatin agents orally administrated, active vitamin D
( calcitriol & alfacalcidol, 15 µg/kg/zi). Calcium carbonate ,100mg/kg/daily

 Anemia : Ferum & de Acid folic supplements orally, IV – administrated

ferrum, precocius used of eriytropoietin

 Hypertension + proteinuria:conversion ensyme inhibitors, angiotensin

receptor antagonists ( sartans). Severe hypertension crises need IV-
therapy, diuretics ,ß-blockers , selective channel of calcium blockers (
nifedipine) !
 CHRONIC KIDNEY DISEASE (CKD)
CONSERVATIVE TREATMENT
 Cardiovascular disease
- CKD is a proatherogenic entity; influences hypertrophy and left ventricular
disfunction.
- Hyperlypidemia, hypoalbuminemia, increasing calcium phosphorus products ,
hypoalbuminemia and hypertension , there are known risk factors.
- Needs hypertension correction, hidric and electrolyte balance disorders
treatment, monitoring hyperlipidemia and calcium phosphorus product
 Acidobasic disorders:- Acidosis is the consequence of bicarbonate
disturbance resorption in proximal tube, and of acids excretion disturbance in
the distal tube . Therapy will be with bicarbonate.
 Medication ( antibiotics & other medi.) will be adjusted beginning with GFR<
50mL/min/1,73 m²
 Energy and protein in CKD:
- Child nutrition should promote growth and development
Especially in infant, longitudinal growth is primary dependent by an adequate
proteic intake ( eng 115-150 kcal/kg, proteins 2,1-3 g/kg).
In child , until puberty 1460-2755 kcal/daily , proteins 2-2,5 g/kg (postpubertal
1-1,5g/kg/zi).
- Phosphor intake should be limited in infant. Will give supplements : ex.
Locasol a nutritional complet powdered feed, etc
CHRONIC KIDNEY DISEASE( CKD/CRF/ESRD)
SUBSTITUTIVE RENAL TREATMENT

 Peritoneal Dialysis (ambulatory & continuous ) in little child

 Hemodialysis → in elder child & adolescent
 Renal transplantation is the elective treatment in ESRD
CHRONIC KIDNEY DISEASE (CKD)
PSICHOSOCIAL ASPECTS. SCHOLARITY

 Children suffering of CKD have depressive traits , but does not suffer from
a special psychiatric pathology
 They require constant , efficient and stimulatory psychological support for
their compliance in respect of diet and medication . Also, they need
support in many cases of phobia of needles (caused by fistula, catheters,
venous access, frequents blood tests)
 Social workers / professors are included in the multidisciplinary team
 Progression to ESRD is not unavoidable, in some situations adequate
diagnosis and treatment are directed to prevent and temporize this stage