This document discusses chronic kidney disease (CKD). It defines CKD and outlines its stages based on glomerular filtration rate. Later stages present with complications like metabolic bone disease, anemia, growth failure, and others. Major complications include disturbances in calcium, phosphate, and acid-base metabolism resulting in renal osteodystrophy and rickets. Lack of erythropoietin production leads to anemia. Insulin resistance and other endocrine dysfunctions also complicate CKD.

1. Dr. Galgallo
Chronic Kidney Disease

2. Learning objectives
⚫ Define Chronic Kidney disease
⚫ Explain the pathogenesis and treatment of
complications of chronic kidney disease.
⚫ Delineate a plan to help the family with the
outcome of renal failure.

3. Defination
⚫ Irrecoverable , bilateral abnormalities fo
the renal parenchyma that results in
glomerular filtration rate below the normal
range
⚫ GFR in childhood is calculated by schwartz
formula
⚫ GFR(ml/min/1.73m3
= Height in cm x 40
Creatinine(umol/L

4. Gradation of GFR
GFR
(ml/min/1.73m
3
Features
Grade 1 >90 Renal parenchymal disease present
Grade 2 60-89 Usually no symptoms but may
develop biochemical abnormalities
at the lower end of the GFR range
Grade 3 30-59 Biochemical abnormalities and in
addition may develop poor growth
and appetite
Grade 4 15-29 Symptoms more severe
Grade 5 <15 Renal replacement therapy required

5. Clinical presentation
⚫ The first stage of chronic renal disease coincides with
a GFR of 50% to 75% of normal for age. Usually
asymptomatic
⚫ When GFR fall below 50% normal there is increases in
serum urea nitrogen, creatinine, and parathyroid
hormone ensue
⚫ At GFR of 25% to 50% of normal for age there is heavy,
asymptomatic proteinuria of more than 1,000 mg/d
often is present.
⚫ GFR of 15% to 25% of normal is characterized by the
clinical features of anemia, acidosis,
hyperphosphatemia, and hypocalcemia as well as
renal osteodystrophy and rickets.
⚫ end-stage renal disease, coincides with the GFR of less

6. ⚫ The first two stages of CRF (vide supra)
often are asymptomatic
⚫ Functional impairment is accelerated by
various reversible causes
⚫ (eg, dehydration, hypertension, congestive
heart failure, hypercalcemia, hyperuricemia,
hypokalemia, alkalosis, and nephrotoxic
agents including certain antibiotics,
cyclooxygenase inhibitors, converting
enzyme inhibitors, and nonsteroidal
anti-inflammatory agents).

7. Major complications of CKD
⚫ disturbances in calcium, phosphate, and
acid-base metabolism develop, resulting in
renal rickets and growth retardation.
⚫ lack of erythropoietin production
associated with kidney failure results in
anemia
⚫ Insulin resistance, thyroid, and other
endocrine dysfunctions complicate CRF.
⚫ Anorexia frequently complicates the late
stages, resulting in nutritional deficiency

8. ⚫ Renal Osteodystropy
⚫ Growth failure
⚫ Anaemia

9. Renal osteodystropy
⚫ Impaired phosphate excretion result in
reciprocal decrease in calcium resulting
secondary hyperparathyroidism and renal
osteodystropy
⚫ Impaired formation of active form of vitamin
D resulting into impaired instestinal Ca
absorption
⚫ Ureamia cause skeletal PTH resistance with
subsequent development of secondary
hyperparathyroidism
⚫ Metabolic acidosis and uremia result in

12. Growth failure
⚫ Growth hormone stimulate formation of Insulin
like Growth Factor-1 (IGF-1)
⚫ Tissue resistance to endogenous and exogenous
growth hormone has been documented carefully
in recent studies showing that the expression of
IGF-1 in uremia is significantly blunted
⚫ Growth hormone receptor mRNA also is
inhibited by the uremic condition
⚫ The increased IGF-binding proteins encountered
in CRF also interfere with growth hormone action
⚫ Recombinant growth hormone used to treat

13. Anaemia
⚫ Erythropoeitin deficiency
⚫ Nutritional Folate and Iron deficiency

15. Metabolic acidosis and Growth
failure
⚫ Increased proteolysis occurs in response to
a relatively small decrease in serum
bicarbonate from 20 mEq/L to 17 mEq/L.
⚫ Metabolic acidosis inhibits growth
hormone pulsatile secretion and
expression has led to the recommendation
by the Kidney Foundation (K/DOQ1 2000)
that serum bicarbonate be maintained at
22 mEq/L with bicarbonate therapy

16. Carbohydrate, lipid and nitrogenous
disorder
⚫ The glucose intolerance in uremia is
associated with peripheral insulin resistance.
⚫ Elevated serum cholesterol and triglyceride
and reduced high-density lipoprotein
cholesterol levels may be related to this
dysfunction in carbohydrate metabolism.
⚫ The retention of nitrogenous products results
in anorexia, nausea, vomiting, and uremic
stomatitis, but no specific agent or single
“uremic toxin” has been identified to account

17. Other systemic disorders
⚫ Impaired immunologic defences and delayed
wound healing give rise to a higher incidence
of infection in uremic patients.
⚫ A progressive encephalopathy, developmental
delay, seizures, myoclonus, hypotonia, ataxia,
and chorea
⚫ Duodenal ulcers is increased in those who
have uremia, which may be related to a rise in
serum gastrin concentration
⚫ Pericardial effusion