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Query: UMLS:C0451641 (urolithiasis)
 3,973 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

In patients with hypercortisolism, who are frequently obese, the prevalence of elevated urinary excretion rates of the potential lithogenic factors (calcium, oxalate, and uric acid) is increased. We examined whether the 24-hour urinary excretion rates of calcium, oxalate, and uric acid are already associated with body fat and endogenous glucocorticoids in healthy free-living children, taking relevant nutritional and acid-base factors into account. Urinary analyte excretions were determined in 24-hour urine samples of 300 healthy children aged 4 to 14 years. Potentially bioactive free glucocorticoids were assessed as urinary free cortisol + urinary free cortisone. Associations of glucocorticoids and percentage body fat with the outcome variables were examined in regression models adjusted for sex, height, growth velocity, urinary volume, net acid excretion, and relevant nutritional factors. Percentage body fat and urinary free cortisol + urinary free cortisone explained most of the growth-independent variation of urinary uric acid and also a relevant part of oxalate, but none of calcium. Net acid excretion, an indicator of endogenous acid production, and dietary protein, salt, and fiber intakes were also variably associated with the outcomes urinary calcium, oxalate, and uric acid. In conclusion, body fatness and potentially bioactive free glucocorticoids (even in the physiologic range) appear to affect urinary excretion rates of oxalate and uric acid, whereas urinary calcium output is more strongly related to dietary factors in healthy children. Our data provide the first in vivo-based evidence that the obesity- or hypercortisolism-associated urolithiasis may be a pathophysiologic continuation of the corresponding endocrine metabolic variations in healthy children.
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PMID:Glucocorticoids and body fat associated with renal uric acid and oxalate, but not calcium excretion, in healthy children. 1976 65

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

The number of exotic companion pet rodents seen in veterinary practices is growing very rapidly. According to the American Veterinary Medical Association's surveys, more than 2,093,000 pet rodents were kept in US households in 2007 and in 2012 it was more than 2,349,000 animals. This article summarizes the most important evidence-based knowledge in exotic pet rodents (diagnostics of the hyperadrenocorticism in guinea pigs, pituitary tumors in rats, urolithiasis in guinea pigs, use of itopride as prokinetics, use of deslorelin acetate in rodents, cause of dental disease, and prevention of mammary gland tumors in rats).
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PMID:Evidence-Based Advances in Rodent Medicine. 2878 Oct 34

Cushing syndrome (CS) occurs rarely in children. The clinical presentation of CS varies according to the extent and duration of glucocorticoid excess, and urolithiasis is one of the common complications of CS. We report the first case of a patient with CS associated with acute kidney injury (AKI) due to urolithiasis. A 6-year-old boy came to the emergency room with seizure. On physical examination, he had clinical features of CS and high blood pressure. Brain computerized tomography (CT) suggested posterior reversible encephalopathy syndrome due to hypertension. On the evaluation of hypertension, the laboratory tests suggested adrenocortical tumor, but the abdominal CT suggested pheochromocytoma. During further evaluation, his condition deteriorated with AKI due to bilateral ureteral stones, therefore he underwent continuous renal replacement therapy in the intensive care unit. After controlling hypercortisolism with etomidate and performing ureteral stent indwelling, resection of an adrenal mass was performed, and the mass was histologically confirmed as an adrenocortical adenoma. We review the clinical manifestations and diagnosis, and management of CS associated with urolithiasis and AKI. Early recognition and careful monitoring of urolithiasis in CS are important to avoid severe complications of urolithiasis.
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PMID:Cushing syndrome with acute kidney injury due to ureteral stones in a 6-year-old boy. 3287 46