Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.16 (calcineurin)
 17,112 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transplantation is an established therapy for end-stage diseases of the kidney, endocrine pancreas, heart, liver, lung, intestines and for many hematological disorders. Current immunosuppressive regimens with glucocorticoids and calcineurin inhibitors produce excellent patient and graft survival rates. This has resulted in both increases in transplant numbers and an increased recognition of previously neglected long-term complications of transplantation such as fractures and osteoporosis. Both pretransplantation bone disease and immunosuppressive therapy result in rapid bone loss and increased fracture rates. Patients are particularly at risk early after transplantation. The bone health of candidates for organ transplantation should be assessed with bone densitometry of the hip and spine. Spinal x-rays should be performed to diagnose prevalent fractures. Any secondary causes of osteoporosis should be identified and treated. Vitamin D deficiency should be corrected with vitamin D doses selected to achieve a serum 25-hydroxyvitamin D concentration of at least 20 ng/ml. All patients should receive calcium. Patients with kidney failure should be evaluated and treated for chronic kidney disease-mineral and bone disorder, including renal osteodystrophy. Secondary hyperparathyroidism, in particular, should be treated. Treatment is indicated in the immediate posttransplantation period irrespective of bone mineral density because further rapid bone loss will occur in the first several months after transplantation. Long-term organ transplant recipients should also have bone mass measurement and treatment of osteoporosis. Oral and iv bisphosphonates are the most promising approach for the management of transplantation osteoporosis. Active vitamin D metabolites may have additional benefits in reducing hyperparathyroidism, particularly after kidney transplantation.
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PMID:Approach to the patient with transplantation-related bone loss. 1942 Feb 72

Hyperchloremic metabolic acidosis of renal origin results from a defect in renal tubular acidification mechanism, and this tubular dysfunction can consist of an altered tubular proton secretion or bicarbonate reabsorption capability. Studies have documented that all forms of renal tubular acidosis (RTA), type I to IV, are documented in kidney transplant patients. Among RTA pathophysiologic mechanisms have been described the renal mass reduction, hyperkalemia, hyperparathyroidism, graft rejection, immunologic diseases, and some drugs such as renin-angiotensin-aldosterone blockers, and calcineurin inhibitors. RTA can lead to serious complications as is the case of muscle protein catabolism, muscle protein synthesis inhibition, renal osteodystrophy, renal damage progression, and anemia promotion. RTA should be treated by suppressing its etiologic factor (if it is possible), avoiding hyperkalemia, and/or supplying bicarbonate or a precursor (citrate). In conclusion: Hyperchloremic metabolic acidosis of renal origin is a relatively frequent complication in kidney transplantation patients, which can be harmful, and should be adequately treated in order to avoid its renal and systemic adverse effects.
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PMID:Hyperchloremic metabolic acidosis in the kidney transplant patient. 3092 3