- What is Renal Bone disease (Renal Osteodystrophy)
- Statistics on Renal Bone disease (Renal Osteodystrophy)
- Risk Factors for Renal Bone disease (Renal Osteodystrophy)
- Progression of Renal Bone disease (Renal Osteodystrophy)
- Symptoms of Renal Bone disease (Renal Osteodystrophy)
- Clinical Examination of Renal Bone disease (Renal Osteodystrophy)
- How is Renal Bone disease (Renal Osteodystrophy) Diagnosed?
- Prognosis of Renal Bone disease (Renal Osteodystrophy)
- How is Renal Bone disease (Renal Osteodystrophy) Treated?
- Renal Bone disease (Renal Osteodystrophy) References
What is Renal Bone disease (Renal Osteodystrophy)
Renal Bone Disease occurs due to poor renal function. Poor renal function leads to low blood calcium as the kidney is responsible for both vitamin D metabolism and calcium reabsorption from the glomerular filtrate. The calcium harboured in bones must therefore liberated by increased parathyroid hormone levels to maintain blood calcium concentrations.
Statistics on Renal Bone disease (Renal Osteodystrophy)
Renal bone disease (AKA renal osteodystrophy) is present in many patients with moderate renal impairment and invariably in those patients with end-stage renal failure.
Risk Factors for Renal Bone disease (Renal Osteodystrophy)
Renal bone disease is a feature of chronic renal failure which represents the final pathway of many renal diseases. The predisposing factors leading to renal osteodystrophy are therefore the risk factors for chronic renal failure. These include:
- Congenital and inherited disease – Polycystic kidney disease, Alport’s syndrome and congenital hypoplasia.
- Glomerular Disease
- Primary glomerulonephritides
- Secondary glomerular disease – SLE, diabetic glomerulosclerosis, vasculitides
- Vascular Disease – Arteriosclerosis, systemic sclerosis with renal involvement
- Tubulointerstitial disease – Tubulointerstitial nephritis (idiopathic, drug-induced, or immunological), reflux nephropathy, Tuberculosis , Schistosomiasis, Nephrocalcinosis.
- Urinary Tract Obstruction – Calculous disease, prostatic disease, pelvic tumours and retroperitoneal fibrosis.
Progression of Renal Bone disease (Renal Osteodystrophy)
Most patients with chronic renal disease are found to have a mixture of the above renal osteodystrophy conditions. Bone disease will invariably deteriorate with further deterioration of renal function, as the activity of vitamin D within the circulation declines. If left untreated, secondary hyperparathyroidism may become tertiary hyperparathyroidism in which PTH becomes autonomously produced. In this setting, PTH will be over-produced despite the the artificial restoration of calcium and vitamin D levels to normal. Patients with osteitis fibrosa cystica and osteomalacia are prone to spontaneous fractures which heal slowly owing to the metabolic defect. The ribs are the most common site of fracture in osteitis fibrosa cystica. Consequently, patients will often complain of bone pain.
How is Renal Bone disease (Renal Osteodystrophy) Diagnosed?
Essentially, investigation of renal osteodystrophy requires an overall assessment of the patient’s renal function. If the aetiology of the renal failure remains unknown, then appropriate screening should be performed.
- Haematuria – may indicate glomerulonephritis or urinary tract obstruction.
- Proteinuria – strongly suggests glomerular disease
- Glycosuria – may indicate Diabetes Mellitus but remains a common feature to CRF
- Urine microscopy:
- White cells – indicates active bacterial urinary infection
- Eosinophils – suggests allergic tubulointerstitial nephritis
- Red cell casts – indicates glomerulonephritis
- Urine biochemistry:
- 24hr creatinine clearance – for best overall assessment of renal function
- Urine osmolarity – allows assessment of urinary concentrating ability and thus renal function
- Urine electrophoresis – detection of Ig light chains which are indicative of multiple myeloma
- Serum biochemistry
- Urea and creatinine
- Serum electrophoresis – for paraproteinaemia
- full blood count:
a. Eosinophilia suggests vasculitis, allergic tubuloinsterstitial nephritis or cholesterol embolism
b. Fragmented red cells indicates haemolytic uraemic syndrome or accelerated hypertension
c. Elevated ESR indicates multiple myeloma or vasculitis
- full blood count:
- Immunological screen:
- Complement – may be reduced in auto-immune disease
- Autoantibodies – SLE, scleroderma, granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis), PAN and Goodpastures syndrome.
- Urine culture
- Early morning urine culture for renal tuberculosis
- Antistreptococcal antibodies
- Hepatitis A, Hepatitis B and HIV screen
- Radiology: Renal ultrasound, intravenous pyelogram or CT or urinary system.
- Renal biopsy: Should be performed in patients when the cause of renal failure is unclear following the abovementioned investigations. If rapidly progressive glomerulonephirits is suspected, patient require an urgent biopsy to confirm the diagnosis and start immunosuppressive therapy as soon as possible.
Prognosis of Renal Bone disease (Renal Osteodystrophy)
The prognosis of renal bone disease is good, provided the condition is identified and treated accordingly. With calcium and/or vitamin D replacement therapy, bone mineral density and structure can be supported despite poor renal function.
How is Renal Bone disease (Renal Osteodystrophy) Treated?
Treatment of renal bone disease is usually administered by the renal specialist team. The disease can be managed with dietary or diasylate supplements, depending on the severity of renal bone disease. Agents commonly used in the management of renal osteodystrophy include calcium tablets such as caltrate, vitamin D supplements (in the form of calcitriol) and phosphate binders such as calcium carbonate or calcium acetate. As chronic renal failure is an irreversible process, (in the absence of renal transplantation) the duration of therapy with the above is life-long, in order to prevent further complications of renal bone disease.