How to manage your orthopaedic patient who has chronic renal failure: Renal Osteo Dystrophy

Chronic renal failure: Renal Osteo Dystrophy



Non-primary causes of hyperparathyroidism

Secondary hyperparathyroidism Hypocalcaemia

•Vitamin D Deficiency (renal insufficiency)
•Decreased calcium intake

Tertiary hyperparathyroidism

•Accelerated response to chronic Hypocalcaemia
• PTH overproduced -> Hyercalcaemia

Secondary hyperparathyroidism is a response to hypocalcaemia brought on by Vitamin D shortage (No active - 1 Alpha stage due to the kidney disease).

Eventually the parathyroid glands become autonomous and are not inhibited by the high calcium levels – this is known as tertiary hypoparathyroidism.  There is hypercalcaemia and phosphatemia in this stage.

Bone Biopsy

Is indicated in all chronic renal patients. Almost all patients who have been dialyzed for > 1yr have abnormal bone histology.  Osteomalacia is a common pattern. Here osteoid production with increased bone width is seen. Tetracycline labelling demonstrated increased new bone formation.  All dialyzed patients need bone biopsy to determine hyper or hypo bone activity. Aluminium can also be stained for. 

If the GFR falls below 40%, woven osteoid appears on bone biopsy.

Bone Histology in CRF

The bone histology can be classified as follows:


1.Predominately hyperparathyroid:

Seen in 5 to 30% dialyzed patients. Irregular trabeculae, irregular remodelling sites. Numerous osteocytes. Thickened osteoid seam.

2.Low turnover (uraemic):

Profound decrease in the number of active remodelling sites.  "Adynamic bone disease" i.e. few osteoid seams.

3.Mixed uraemic osteodystrophy:

Caused by hyper parathyroid and defective mineralisation without decreased bone formation.

4.Aluminium related bone disease:

Not always adynamic - it can superimpose any of the above described groups. PTH seems to increase uptake of Al into bone. Aluminium interferes with the mineralisation process.

Aluminium Osteodystrophy

Al can cause Renal Osteodystrophy


•Al in dialysate
•Al containing P04 binders

Al can be stained for and is often in the dystrophic bone. Al can be chemically measured in the tissues. Al levels made worse by parathyroidectomy. Treatment by chelation – deferoxamine.



Histology of hyperparathyroidism in boneIf hyperparathyroidism predominates there is mostly bone resorption. In this slide many osteoclasts can be seen actively eating away the bone.

Prevention of Hyperparathyroidism

•Keep Phosphate down
• Diet (no meat or dairy products)
• Oral phosphate binders
•Aluminium free dialysate
•Avoid transfusion

The biggest challenge it to get the patient to stick to a low protein (no meat al all) diet. Dairy products, a possible source of Vitamin D are also banned!

Orthopaedic Referrals

The following are common reasons patients with CRF are referred to the Orthopaedic Surgeon:

•Joint sepsis / arthritis
•Avascular necrosis (Transplants)
•Entrapment neuropathy
•Bone Biopsy

There are also many doctor related reasons that we have to refer patients to the renal unit.

Iaterogenic causes of renal failure


•Arteriogram in shock
• NSAID over prescription
• Amino glycosides

Arteriogram after a knee dislocation

Contrast material is nephrotoxic. Avoid performing arteriogram while your patient is shocked or dehydrated. The reason is erythrocyte cerenation and vasoconstriction in the kidney causing decreased renal perfusion. Other factors that may cause adverse effects after an arteriogram are the presence of diabetes or multiple myeloma. Administration Acetyl Cystine (Parvolux) before the arteriogram may prevent some of the nephrotoxicity of the contrast medium.

Avoid NSAIDS in the elderly, patients on diuretics or ACE inhibitors.

Amyloglycosides are nephrotoxic and all patients on these antibiotics need the levels measured daily.

Tumoral calcinosis

X ray of tumoral calcinosis

In this condition calcium (as Pyrophosphate) is deposited in the soft tissues.

This can be congenital, but is often caused by the dystrophic calcification seen in tertiary hyperparathyroidism.

Pathylogical fracture in tumoral calcinosis

CT reconstruction showing  a pathological fracture of the proximal femur seen in a limb of a young  woman with with tumoral calcinosis and underlying secondary hyperparathyroidism.  Fractures do develop in ROD especially if “brown  tumours” are present from hyperparathyroidism. A high incidence of fractures is seen in Aluminium osteodystrophy. This condition is also known as known as “fracturing osteodystrophy”

Tertiary Hyperparathyroidism

Teriiary hyperparathyroidism
This patient on renal dialysis has tumoral calcinosis about the shoulder.. Note the scar (and the clips) from his parathyroidectomy.

Xray: Hyperparathyroidism of hands

Hand of a patient with R.O.D. and secondary hyperparathyroidism. Note the resorption of the terminal tufts of the phalanges

Other x ray findings in Hyperparathyridism


Pepperpot skull of hyperparathyroidism
Pepper pot skull
Ruggerjersey spine
Ruggerjersey spine




In hyperparathyroidism the skull takes on a mottled or "pepper pot" appearance. The spine shows sclerotic bends on plain x ray. This is known as a "rugger jersey" spine.

Indications for a parathyroidectomy

Are Osteitis fibrosa not responding to conservative treatment.

Conservative treatment of renal osteo dystrophy

Conservative treatment of tertiary hypoparathyroidism: Calcitrol to enhance gut absorption Ca++ Serum calcium should be maintained at high normal levels. Phosphate intake should be restricted. NB Patients on renal dialysis are never allowed dairy products.

When renal osteodystrophy gets worse, despite adequate conservative treatment, a hyperparathyriodectomy is indicated.

Nonsteroidal anti inflammatory drugs

•Prostaglandins beneficial – increase renal blood flow
• NSAIDS -  adverse in:
• Aged (N.B. 1 mm GFR lost /yr.)
•  Renal failure
• Dehydration
• Ace Inhibitors & diuretics
• Diabetics

Non steroidal antiinflammatory drugs. Are very nephrotoxic in the presence of dehydration and renal failure.

Prostaglandins play a major role in haemodynamic regulation in the kidney and in the excretion of water and electrolytes. All the NSAIDS inhibit PG synthesis.

Prostaglandins have an important role in conducting renal blood flow by counteracting the vasoconstrictive influence of compounds such as angiotensin II Under these circumstances, inhibition of PG synthesis could cause a marked decrease in renal blood flow by removing this compensatory  vasodilatation.

In CRF the use of "Clinoril" (sulindac) is the safest when an antiprostaglandin is needed. (it has less effect on renal function than the others.)

Operating on your renal patient

Preoperative considerations

Timing of surgery:

Time to operate on the day between dialyses.


Look for electrolyte abnormalities (mainly Na and K)

    •Hb- Function on a Hb of 6 to 7 get it up to 10 g % for major surgery. Give blood the day before surgery on dialysis.
    •Acid / Base:

    Acid base should be corrected on dialysis.

Vascular status:

May have limited veins for drips, or have vascular shunts in situ.


Do not work alone - a dialysis patient should not go to theatre unless supervised by a physician!

Operative considerations

Bleeding and platelet aggregation can lead to problems. Unstable blood pressures, myocardial ischemia, stroke: all are problems for the surgeon and anaesthetist.


Total joint arthroplasty in CRF

•Dialysis means higher risk

• Renal transplant have the same risk as non renal AVN:

J Lieberman, J Arthroplasty, Vol 10, 1995, P 191-195

“ The renal transplant patients exhibited generally satisfactory results. Their postoperative course was comparable to that of patients with avascular necrosis undergoing hip reconstruction without underlying renal disease. However, patients undergoing hip arthroplasty while on chronic renal dialysis hadpoor results (81 %), including a deep infection rate of 19%. It was concluded that total hip arthroplasty be reserved for patients who are expecting a renal transplant preferably for those who have already received a successful transplant.”

Postoperative considerations


Avoid non straddles. Morphine, and other narcotics in smaller dosages.


If aminoglycosydes must be used by culture – modify by dose and dosing interval – serum levels must be used. Same applies to Vancomycin.


Volume will depend volume of urine produced and when the next dialysis is scheduled. Avoid K containing fluids in general.

Next dialysis:

If possible, wait 48 hours before next dialysis.







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