Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of 10,159 normal spontaneous vaginal deliveries was performed to examine racial differences in mean birth weight of infants whose mothers were without antepartum or intrapartum medical complications of pregnancy. The study was limited to black and white infants of low-income mothers who were inborn, singleton, and weighed greater than or equal to 500 gm at birth. High-risk maternal transfer patients and patients with hypertension, toxemia, bacteriuria, pyelonephritis, renal failure, diabetes, anemia, polyhydramnios, oligohydramnios, prolapsed cord, vaginal bleeding, placenta previa, abruptio placentae, prolonged rupture of membranes, maternal fever on admission, amnionitis, sexually transmitted diseases, or fewer than five prenatal care visits were excluded. When statistically significant differences in demographic characteristics were controlled, black infants had an average birth weight 181 gm less than that of white infants.
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PMID:Birth weights of infants of black and white mothers without pregnancy complications. 203 72

Renal tubular dysgenesis (RTD), with hypoplasia especially of renal proximal convoluted tubules and clinical neonatal anuria or oliguria, has been reported as a congenital familial (autosomal recessive) disease, variably with features of oligohydramnios, Potter syndrome, or pulmonary hypoplasia. A similar tubular lesion due to antenatal tubular atrophy has been reported for conjoined twins with twin-twin transfusion syndrome or acardia and in infants of mothers given antihypertensive agents, including angiotensin-converting enzyme (ACE) inhibitors, during pregnancy, and it has been seen as a unilateral lesion in young infants with renal artery stenosis due to arteritis or medial arterial calcinosis. The renal tubular changes in RTD are very like those of the "endocrine kidney" in experimental animals and resemble those of the renal tubular atrophy of end-stage kidney diseases such as glomerulonephritis, tubulointerstitial kidney disease, obstructive uropathy/pyelonephritis, graft rejection of transplanted kidneys, or the renal parenchymal changes seen with protracted dialysis therapy. Labeled lectins that differentially mark proximal convoluted, distal convoluted and connecting, and collecting tubules showed no distinctive differences in staining patterns of the hypoplastic renal tubules of infants and children with RTD, postnatal renal artery obstruction, or the various types of end-stage renal disease with the lectins used (PNA, GSLI, UEA, and LTA). The findings suggest that the renal tubular changes in some if not all the conditions studied are the result of renal ischemia. The reported familial RTD with hypernephronic nephromegaly may be a specific disorder, but other forms could reflect renal ischemia acquired in utero or in early or later postnatal life.
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PMID:Labeled lectin studies of renal tubular dysgenesis and renal tubular atrophy of postnatal renal ischemia and end-stage kidney disease. 815 24