Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone involvement in idiopathic calcium nephrolithiasis is characterized by the following abnormalities: a) the bone density is decreased, the severity of bone loss being dependent upon the existence of hypercalciuria and upon the pathophysiology of this latter: it is inconsistent in the absence of hypercalciuria or when hypercalciuria is of the absorptive type I or II, whereas it is almost constant in fasting hypercalciuria without secondary hyperparathyroidism and constant and severe in the rare true renal hypercalciuria. b) The bone histology (which has been evaluated only in idiopathic hypercalciuric patients) mainly shows a defect in bone formation at the exception of the rare renal hypercalciuria. Osteoclastic hyperresorption is only seen in this latter type of hypercalciuria whereas in the other types of hypercalciuria only an increase of the total or inactive resorption surface is observed. This phenomenon is possibly explained only by a delayed refilling of the resorption lacunae secondary to the decreased bone formation. The osteoid thickness is either normal or decreased despite decrease in mineralization apposition rate which seems therefore to be secondary to the decreased bone formation. c) Symptomatic bone disease in hypercalciuric stone formers is exceptional and always related to a severe long term calcium restriction. d) The biochemical markers of bone resorption tend to be increased in idiopathic hypercalciuria. Hydroxyprolinuria is more often elevated than pyridinolinuria. However pyridinolinuria is negatively correlated to bone density. The contrast between the increase of these bone resorption markers and the usual normality of plasma PTH and of the osteoclastic resorptive surfaces, suggest the role of meat induced acid load which may favor inactive resorption by dissolution of bone buffers. A disturbed profile synthesis of cytokines which induce differentiation and proliferation of the osteoclasts and which modulate the osteoblastic proliferation and function (IL-1, IL-6, TNF-alpha, GM-CSF...) may play a role in the bone loss of calcium stone formers but further studies are necessary to precise its transient or permanent involvement in their bone disease. e) The decrease of bone formation may be explained by the suppressed PTH secretion which may be explained by hypercalcitriolemia. This excess of calcitriol synthesis may be secondary either to monocyte increased synthesis of IL-1 which stimulates the renal 1 alpha-hydroxylase by the mean of an increased PGE2 synthesis or to the relative hypophosphatemia of the calcium stone formers comparatively to healthy controls. Hypercalcitriolemia may originate from the activated monocyte itself. The decrease in bone formation may also be secondary to the action of monokines on the osteoblast differentiation and/or function.
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PMID:[Bone involvement in idiopathic calcium lithiasis]. 756 25

Sarcoidosis is a multisystem granulomatous disease of unknown aetiology characterized by the presence of noncaseating granulomas. It may affect any organ including the kidney. A disordered calcium metabolism is most often responsible for the development of renal failure. Granulomatous interstitial nephritis is the most typical histological finding, but it rarely leads to renal insufficiency. Since development of renal insufficiency in sarcoidosis is uncommon, we lack large (randomized) trials concerning the treatment of this disorder. We gather most information from case reports and small series. Our knowledge of pulmonary sarcoidosis is more comprehensive. It is, however, impossible to treat renal manifestations identically because some of the drugs used in pulmonary sarcoidosis are nephrotoxic. Moreover, renal sarcoidosis is a specific entity with its own characteristics and response to therapy. A guideline for treatment is currently missing. Based on a review of the literature, we present an overview of the different treatment options to promote a more uniform and scrutinized approach of this disease. Hypercalcaemia and hypercalciuria can be treated with corticosteroids, (hydroxy)chloroquine or ketoconazole. Preventive measures play a supportive role. In granulomatous interstitial nephritis, glucocorticoids are the standard of care. In patients with failure of or a contraindication to corticosteroids or in those patients who need a high maintenance dose of corticosteroids, azathioprine or mycophenolate mofetil can be used. TNF-alpha inhibitors are useful in case of steroid-resistant sarcoidosis or in patients who develop severe steroid toxicity. With increasing insight in the pathogenesis of sarcoidosis, other immunosuppressive drugs have been proposed, but more research is necessary before their routine use can be advocated.
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PMID:Treatment of renal sarcoidosis: is there a guideline? Overview of the different treatment options. 2423 78