Renal Bone disease (Renal Osteodystrophy)
- What is Renal Bone disease?
- Who gets Renal Bone disease?
- Predisposing Factors
- Progression
- Probable Outcomes
- How is Renal Bone disease Diagnosed?
- How is Renal Bone disease treated?
- Renal Bone disease References
What is Renal Bone disease?
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.Who gets Renal Bone disease?
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.Predisposing Factors
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:1. Congenital and inherited disease - Polycystic kidney disease, Alport's syndrome and congenital hypoplasia.
2. Glomerular Disease
a. Primary glomerulonephritides
b. Secondary glomerular disease - SLE, diabetic glomerulosclerosis, vasculitides
3. Vascular Disease - Arteriosclerosis, systemic sclerosis with renal involvement
4. Tubulointerstitial disease - Tubulointerstitial nephritis (idiopathic, drug-induced, or immunological), reflux nephropathy, Tuberculosis , Schistosomiasis, Nephrocalcinosis.
5. Urinary Tract Obstruction - Calculous disease, prostatic disease, pelvic tumours and retroperitoneal fibrosis.
Progression
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.
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