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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uroliths composed predominantly of calcium phosphates have been infrequently identified in dogs. Factors incriminated in the etiopathogenesis of calcium phosphate urolithiasis include an alkaline urine pH, hypercalciuria, decreased urine concentrations of crystallization inhibitors, and increased urine concentrations of crystallization promoters. Disorders associated with calcium phosphate urolith formation in dogs include primary hyperparathyroidism, hyperadrenocorticism, and idiopathic hypercalciuria. Medical therapy of patients with recurring calcium phosphate uroliths should be directed at removing or minimizing factors contributing to urine supersaturation with calcium phosphate.
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PMID:Canine calcium phosphate uroliths. Etiopathogenesis, diagnosis, and management. 1002 56

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.
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PMID:Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure. 1272 57

The frequency of hypercalciuria is increasing in western countries with an incidence of nephrolithiasis which can reach 13%. Hypercalciuria appears as an alteration of the calcium transport system (kidney, bowel, bone) which is regulated by calcitriol and parathormone. The aim of this review was to screen etiologies of hypercalciuria taking into account recent genetic advances (calcium epithelial channel and calcium sensing receptor). Hypercalciuria may be favored by nutritional causes (diet rich in calcium, sodium, carbohydrates, proteins, poor in phosphates and potassium). It may also be related to an increase in calcium absorption (vitamin D excess, primary hyperparathyroidism, sarcoidosis, lymphoma, estrogens, and certain genetic causes), an increase in osteoresorption (bone metastasis, myeloma, Paget, hyperthyroidism, immobilization, hypercortisolism and corticosteroid therapy), or a decrease of kidney tubular resorption (diuretics, Cacci and Ricci, acromegally, Bartter, familial dominant hypocalcemia, Fanconi, Dent, familial hypomagnesemia-hypercalciuria syndrome, type 1 distal tubular acidosis, pseudohypoaldosteronism, diabetes). If no cause is identified, persistence of hypercalciuria after instituting a correct diet is defined as idiopathic hypercalciuria. Treatment of the cause is essential in secondary hypercalciuria, in addition to diet (low sodium intake, normocalcic diet, hydration), associated with thiazide diuretics and biphosphonates if necessary.
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PMID:[Hypercalciuria]. 1635 16

The negative effect on bone due to the glucocorticoid excess is mediated by the direct action of cortisol in reducing bone apposition and increasing bone resorption, and by indirect mechanisms such as the calcium malabsorption, hypercalciuria and hypogonadism. The condition of overt hypercortisolism, also called Cushing's syndrome, leads to osteoporosis and fractures in up to the 70% of cases, even in the presence of normal gonadal status and in males. The recovery from Cushing's syndrome leads to a normalization of bone mineral density only after several years, even if some data show that the risk of fractures normalizes after one year from the cure. Alendronate has been demonstrated to be useful to accelerate the restoration of normal bone mass after the cure of Cushing's syndrome Several studies, even not all, have been demonstrated that also the condition of asymptomatic or "subclinical" hypercortisolism (often associated to adrenal adenoma) is associated to a reduction of bone mineral density and increased prevalence of fracture even in the presence of eugonadal status and in males. Unfortunately, data regarding the effect of the normalization of cortisol secretion on bone mass and risk of fractures are lacking. On the other hand, it is known that osteoporotic fractures may be the clinical presentation of an otherwise asymptomatic hypercortisolism. In a recent study we have demonstrated that in a population of outpatients with established osteoporosis and without known or clinically evident secondary causes, the prevalence of subclinical hypercortisolism is about 10%. This finding suggests that the presence of subclinical hypercortisolism has to be taken in to account when evaluating patients with unexplainable established osteoporosis.
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PMID:[Role of cortisol hypersecretion in the pathogenesis of osteoporosis]. 1871 63

Glucocorticoids (GCs) affect renal development and function in fetal and mature kidneys both indirectly, by influencing the cardiovascular system, and directly, by their effects on glomerular and tubular function. Excess GCs due to endogenous GC overproduction in Cushing's syndrome or exogenous GC administration plays a pivotal role in hypertension and causes increased cardiac output, total peripheral resistance and renal blood flow. Glucocorticoids increase renal vascular resistance (RVR) in some species and experimental settings and decrease RVR in others. Short term administration of adrenocorticotrophic hormone or GCs causes an increased glomerular filtration rate (GFR) in humans, rats, sheep and dogs. Interestingly, chronic exposure may cause a decreased GFR in combination with a higher cardiovascular risk in human patients with Cushing's syndrome. Glomerular dysfunction leads to proteinuria and albuminuria in canine and human Cushing's patients, and some cases also show histological evidence of glomerulosclerosis. Tubular dysfunction is reflected by an impaired urinary concentrating ability and disturbed electrolyte handling, which can potentially result in increased sodium reabsorption, hypercalciuria and urolithiasis. Conversely, chronic kidney disease can also alter GC metabolism. More research needs to be performed to further evaluate the renal consequences of Cushing's syndrome because of its implications for therapeutic aspects as well as the general well-being of the patient. Because there is a high incidence of Cushing's syndrome in canines, which is similar to the syndrome in humans, dogs are an interesting animal model to investigate the link between hypercortisolism and renal function.
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PMID:Cushing's syndrome, glucocorticoids and the kidney. 2065 18