Renal osteodystrophy describes the bony changes accompanying end-stage renal disease.

Children in whom renal disease develops in infancy or early childhood are more likely to have osteodystrophy than those who are older when the renal disease develops.

Chronic renal insufficiency in childhood – Renal hypoplasia, polycystic disease of the kidney, hydronephrosis, chronic pyelonephritis, and giomerulonephriitis

Renal osteodystrophy is more common in renal disease secondary to the congenital or hereditary conditions than in acquired renal failure.

Damaged glomerulus inability to excrete phosphorus => Hyperphosphatemia => Shut down the production of dihydroxy Vitamin D => Calcium absorption from small intestine is diminished => Hypocalcemia => Increased release of PTH => Demineralization of bone (Bone resorption) => RENAL OSTEODYSTROPHY

The early signs are of failure to grow at the normal rate and development of deformities, particularly of genu valgum.

Skeletal changes are rarely seen sooner than 2 years after kidney insufficiency has become apparent and usually in much older children than in vitamin D deficiency rickets.

Typical case – Child is small, dwarfism affecting the limbs, the complexion is sallow and unhealthy, Skin is dry and hair is sparse, Epiphysis enlarged, and severe asymmetrical knock knee deformity.

Renal symptoms are associated with anemia, general debility, abnormal thirst, albuminuria, and polyuria.

Serum phosphate, serum alkaline phosphatase, and parathyroid hormone assay – Elevated

Serum calcium and albumin – Decreased

25(OH) vitamin D – Normal

1,25(OH)₂ vitamin D – Decreased

Acidosis – Present

Anaemia – Present

Blood urea nitrogen and serum creatinine – Elevated

Radiological finding –

Milder case, rickets changes may predominate with widening and irregularity of the epiphyseal line, broadening of the metaphysis but without cupping and deformity particularly at the knee

Severe cases, hyperparathyroidism changes may be added with osteoporosis, wooliness, and stippling of the metaphyseal region and appearance of subperiosteal bone resorption (femoral neck and digits), and Rugger jersey spine.

Medical treatment –

Medical treatment of renal osteodystrophy is best managed by a pediatric nephrologist with expertise in metabolic bone disease.

The usual treatment consists of the dietary phosphate restriction, vitamin D particularly calcitriol, sodium bicarbonate (treatment of acidosis), phosphate-binding agent (treatment of hyperphosphatemia), and administration of recombinant human growth hormone to restore growth.

Dialysis and transplantation of the kidney

Parathyroidectomy may play a role in the control of bony disease in recalcitrant renal osteodystrophy.

Orthopedic treatment –

Angular deformity – may need guided growth or corrective osteotomies

Slipped capital femoral epiphysis – vigilant observation and at the appropriate time, stabilization of the physis is done with in-situ fixation.

Avascular necrosis of femoral head – due to prolonged steroid use and treatment is symptomatic.

Needs long term treatment for renal disease and it sequelae