Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of NC in VLBW infants appears to be multifactorial. The vulnerability of extreme immaturity and the underdevelopment of renal function may be the most important variables. In some ways, we view this problem as similar to that of retinopathy of prematurity. (Clearly the exposure of the retina to high partial pressures of oxygen contributes to the development of retinopathy of prematurity but other variables--some known, such as an immature retina, and others not yet defined--must be present.) Hypercalciuria is common in the VLBW infant, yet not all develop NC. Decreased glomerular filtration rate, low citrate excretion, and frequently an alkaline urine are in part due to the immaturity of renal function of these infants. The need for prolonged hyperalimentation resulting in increased oxalate excretion and the development of BPD frequently requiring diuretics that may cause phosphaturia and magnesium depletion and that may increase calcium excretion are more common in the smallest and sickest of premature infants. Even transient insults to the kidneys, such as hypoxia or hypotension or the use of nephrotoxic drugs that provoke tubular injury and cell death with the probability of crystal formation and growth by way of heterogeneous nucleation, are likely to occur more frequently in this vulnerable population.
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PMID:Nephrocalcinosis. 157 67

Metabolic studies were performed in streptozotocin-induced diabetic (D) rats and normal control (C) rats to assess the role of hyperphagia in the hypercalciuria of diabetes. Urinary calcium excretion (UCaV) was significantly higher in D v C rats fed ad libitum. When D rats were pair-fed (calorie and mineral restriction) with C rats, UCaV declined but remained significantly higher than in C rats. When D rats were allowed their usual increased calorie intake but restricted to C rat mineral consumption, UCaV remained elevated. These findings suggested a tubular reabsorptive defect. In vivo microinjection studies were then performed to identify the site(s) of the tubular reabsorptive defect. Using 1.0 mmol/L Ca in the injectate, 45Ca recovery in the urine (CaR%) was significantly higher in D rats after intratubular injections into early and late proximal tubules and late distal but not early distal tubules. An additional load-dependent defect was revealed in the terminal nephron when the Ca concentration of the injectate was increased to 1.8 mmol/L. After early distal injection, CaR% was significantly increased in D v C rats. Infusion of PTH into thyroparathyroidectomized C and D rats enhanced Ca absorption to a similar degree but did not correct the reabsorptive defect in D rats. These results argue against a lack of end-organ responsiveness to PTH in diabetes or a low serum PTH level as the cause of the hypercalciuria. We conclude that hyperphagia contributes to the hypercalciuria of diabetes in the absence of increased Ca intake. Also, two tubular reabsorptive defects exist: one in the loop of Henle; the other, load-dependent in the terminal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of hypercalciuria in streptozotocin-induced diabetic rats. 335 15

Urolithiasis is a multifactorial recurrent disease of world-wide distribution in rural, urban, industrial and non-industrial regions. Changes in urinary pH is a risk factor especially with hyperuricosuria, hypercalciuria or hyperoxaluria. With recurrence, hypercalcuria and higher urinary oxalate levels are more frequent. Hypercalciuria and hyperuricosuria showed correlation with family history of stones. The ionic relations between various stone forming salts in urine of patients are opposite to that in controls and are well represented in stone composition. Obesity is a risk factor in both genders. Over eating a diet rich in all nutrients was associated with hyperuricosuria while a diet high only in fat was associated with other urinary disturbances. High protein and fat intake are risk factors. High or low calcium diet was associated with urolithiasis and supplemental calcium is not a risk factor. Potassium and magnesium citrate are potent in inhibiting the growth of stone fragments after extracorporeal shock wave lithotripsy. Whether in patients or normal subjects, drinking hard water should be avoided; tap water or low calcium content water is preferable. Seasonal variations in temperature affected urinary volume, pH and relative saturation of uric acid. To prevent recurrence, patients should maintain high fluid intake achieving a urine volume of 2 liters per day.
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PMID:Urolithiasis in adults. Clinical and biochemical aspects. 1595 54