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Subsequently, we attempted to analyse the causes of RTA. While evaluating the aetiology of MBD, they were diagnosed with RTA. We describe five cases who presented with MBD in varied forms. Most of these patients may, in fact, undergo orthopaedic interventions without primary correction of acidosis. Recognizing the disease in its early course is important to prevent permanent sequelae of skeletal involvement. In distal RTA, hypercalciuria and secondary hyperparathyroidism may play a key role for bone involvement. Other contributory factors include abnormal renal handling of phosphate leading to hypophosphataemia in proximal RTA, and impaired vitamin D metabolism and action. The postulated mechanism for bone involvement includes acidosis-mediated exaggerated osteoclastic bone resorption. In addition, there can be a myriad of other skeletal manifestations like fractures, pseudofractures, secondary osteoporosis and even sclerotic bone disease. Rickets and osteomalacia remain the commonest manifestations of uncorrected RTA. Long-standing uncorrected acidosis can lead to metabolic bone disease (MBD). Type 1 and type 2 RTA are the most common, and are caused by defective secretion of hydrogen ions and impaired absorption of bicarbonate, respectively.
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Renal tubular acidosis (RTA) is a condition characterized by normal anion gap metabolic acidosis.