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)

We report the results of clinicopathological and histochemical studies on 64 renal adenomas found in 22 patients. We selected typical renal adenomas for these studies, discarding borderline lesions. The ages of the patients ranged from 42 to 84 years, with an average of 61 years. Male to female sex ratio was 6.3:1. The background conditions included renal cell carcinoma, long-term dialysis, chronic glomerulonephritis, pyelonephritis, hydronephrosis and polycystic kidney. The sizes of the tumors ranged from 0.1 to 2.3 mm in maximum diameter, with an average of 0.9 mm. All the tumors were located in the cortex, especially in the superficial one-third. The cytoplasm of the tumor cells was predominantly eosinophilic, and the tumor structure was predominantly papillary. Histochemical study of 19 adenomas from 13 patients demonstrated that all of the adenomas from 13 patients demonstrated that all of the adenomas were positive for EMA, and for at least one marker of the distal tubulus, i.e., DBA, PNA, SBA and PKK1, and that 9 adenomas were positive for at least one marker of the proximal tubulus, i.e., LM1 and LTA. Renal adenomas had predominant histochemical features of the distal tubulus, suggesting differentiation to a distal tubulus-like histology.
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PMID:Renal adenoma. Clinicopathological and histochemical studies. 261 60

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