Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal function in the newborn infant varies with conceptual age and should be evaluated in this context. Very preterm infants less than 34 weeks' conceptual age have reduced GFR and tubular immaturity in the handling of filtered solutes when compared to term infants. Premature infants between 34 and 37 weeks' conceptual age undergo rapid maturation of renal function similar to term infants, with establishment of glomerulotubular balance early in the postnatal period. ARF in neonates differs from that seen in older children and adults in that ischemic (e.g., hypoxic) insults and congenital malformations constitute the major pathophysiologic mechanisms responsible for clinically observed oliguria and azotemia. Principles of conservative management are similar to those used in older children except for the greatly increased insensible water loss requirements of the very preterm and premature infant. Technical advances have added peritoneal dialysis and CAVH to the therapeutic regimen for persistent ARF or life-threatening complications of reduced renal function.
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PMID:Renal function and renal failure in the newborn. 265 61

Chronic renal failure was diagnosed in 6 young Standard Poodles from 2 related litters. Clinically, the disease was characterized by polydipsia, polyuria, anorexia, lethargy, vomiting, and bony deformities suggestive of fibrous osteodystrophy. Laboratory evaluation revealed azotemia and hypercholesterolemia in all 6 dogs and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia and another 2 were hypercalcemic. Isosthenuria and proteinuria were found in both dogs for which urinalyses were available. The kidneys were characterized pathologically by interstitial fibrosis, variable interstitial infiltrates of lymphocytes and plasma cells, tubular atrophy, tubular dilatation, tubular basement membrane mineralization, cystic glomerular atrophy, and immaturity of glomeruli, with inconspicuous capillary lumens.
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PMID:Juvenile renal disease in related Standard Poodles. 662 80

Kaspareit-Rittinghausen described a rodent model of inherited polycystic kidney disease (PKD), the Han:SPRD rat [1, 2], in which heterozygotes develop renal cysts and renal failure (in males) over several months, whereas homozygous animals develop rapidly progressive renal enlargement that leads to death in a few weeks. In this study, we examined selected elements of the pathogenesis of this disease in heterozygotes and homozygotes from birth to advanced disease. Heterozygous male rats developed slowly progressive renal cystic disease with interstitial fibrosis and azotemia seen by six months of age. Female heterozygotes developed slowly progressive renal cystic disease, but did not develop interstitial fibrosis or azotemia. Epithelial cells lining cyst cavities showed various degrees of morphologic immaturity. Cyst walls also developed basement membrane thickening, especially in areas of cellular immaturity, suggesting an interrelationship between this basement membrane thickening and cellular dedifferentiation. Thickened basement membranes were associated with increased immunoreactivity for type IV collagen, laminin, and fibronectin. Homozygous rats developed massive renal enlargement, marked azotemia, and died near three weeks of age. Renal c-myc proto-oncogene expression was elevated in homozygous cystic infants and in adult heterozygotes. In situ hybridization showed high levels of c-myc mRNA in cyst epithelia, suggesting abnormal regulation of cellular proliferation in the cells lining cysts, as seen in other models of PKD. The Han:SPRD rat is the only well-documented animal model of inherited PKD with an autosomal-dominant inheritance pattern and appears to have several features which resemble human ADPKD.
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PMID:Autosomal-dominant polycystic kidney disease in the rat. 845 52