Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three children, two of whom were siblings, had pseudohypoaldosteronism. The features of this condition include failure to thrive, hyperkalemia, metabolic acidosis, salt wasting, elevated peripheral renin activity, and increased plasma aldosterone concentration. Hyperplasia of juxtaglomerular apparatus was seen in a renal biopsy specimen from one of these patients. Administration of large quantities of salt normalized the serum electrolyte abnormalities and permitted normal growth. Furthermore, the serum electrolyte abnormalities were prevented by administration of increased amounts of salt to one of these children from birth.
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PMID:Pseudohypoaldosteronism. 47 44

Renal tissue was obtained from 36 patients with renal cell carcinoma, some of whom received renal arterial embolization. The removed specimens was examined histopathologically and the concentration of some vasoactive substances in these patients was measured. Nephrectomy alone produced no discernible changes in blood pressure, vasoactive substances determined or histopathological findings of the kidney. Renal arterial embolization raised the blood pressure in association with the elevation of plasma renin activity (PRA) and urinary prostaglandin (PG) E2 excretion. A linear relationship was found to exist between PRA and mean blood pressure (r = 0.70, p less than 0.001). Hyperplasia of the juxtaglomerular (JG) apparatus, and high granularity of sudan black B granules in renomedullary interstitial cells were confirmed in removed kidneys of patients who had received embolization alone. Subsequently high renin production would be anticipated to influence overproduction of renal PG E2 in acute ischemic kidney in patients with renal cell carcinoma, and hypertension following renal arterial embolization appears to be caused by the hyperplasia of the JG apparatus.
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PMID:Hyperplasia of juxtaglomerular cells and renomedullary interstitial cells after renal arterial embolization in patients with renal cell carcinoma. 306 3

Nine white leghorn chickens were injected i.m. with furosemide (10 to 60 mg/kg body weight) twice daily for 18 days. The birds were then anesthetized with a combination of equithesin and diazepam and the kidneys perfused via the heart. Kidney tissue was sectioned serially and the granular epithelioid cells were counted in the juxtaglomerular apparatuses of the furosemide treated birds and in 3 normal chickens. Hyperplasia and hypergranulation of the epithelioid cells was found to occur in the juxtaglomerular apparatuses of both mammalian and reptilian type nephrons (with and without Henles loop) in the furosemide treated group. This finding was interpreted as an effect of hypovolaemia on the juxtaglomerular apparatuses. Furosemide caused an immediate stop in weight gain, an increase in the erythrocyte volume fraction and a sudden drop in blood pressure. The blood pressure later rose to subnormal levels. The heart rate was not altered. Plasma sodium and chloride fell significantly one day after furosemide administration and remained low throughout the experiment. Potassium fell during the second part of the experimental period. Captopril was injected after 18 days of furosemide treatment and lowered the blood pressure significantly. This was interpreted as indirect evidence for the presence of renin in the granular epithelioid cells and indicates the importance of the renin angiotensin system in maintaining the blood pressure in hypovolaemic conditions.
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PMID:Effect of volume depletion on the afferent arterioles in the avian kidney. 311 Oct 78

The most pronounced hyperplasia of the juxtaglomerular apparatus (JGA) with the appearance of numerous rhombus-like protogranules in the epithelioid cell cytoplasm is found electronmicroscopically in the mesangioproliferative glomerulonephritis (GM) with hypertension while in the membranous FN the hyperplasia was the least pronounced. Hyperplasia of JGA in the fibroplastic GN was observed in the preserved glomeruli only. Morphometric evaluation in mesangioproliferative GN has shown that there is an inverse relationship between the volume of the interstitium and the renin activity in the blood plasma, the positive correlation between the volume of the interstitium and blood pressure and the negative correlation between the elliptical shape of the granules in the JGA epithelioid cells and the surface of the interstitium. Atrophic changes in the interstitial cells are found.
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PMID:[Juxtaglomerular apparatus and interstitial cells of the kidney medulla in glomerulonephritis]. 671 13

Essential hypertension is fundamentally a genetic disease which emerges because of environmental impact. The genetic factors involve intracellular abnormalities which affect calcium metabolism within smooth muscle cells and possibly within the heart and sympathetic nervous system. These abnormalities are influenced by one or more proteins of which calmodulin is a candidate. Sodium pump abnormalities may be primary but may be secondary feedback effects. Homeostasis keeps the blood pressure and cardiac function normal, but eventually becomes less effective. Such homeostasis is produced by negative feedback, but positive external factors also influence the eventual results. Gross homeostasis is provided by the baroreceptors, the renin-angiotensin-aldosterone system, etc. The malfunction of any one or any combination of these systems may produce or accelerate hypertension. Hyperplasia and hypertrophy of arteriolar smooth muscle play their role but also multiply the genetic cellular defects. It is possible that in the early history of man essential hypertension had an advantage which now has become obsolete because normotensive man's potential lifespan has been increased by modern civilization.
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PMID:The relation of genetics to essential hypertension: a review. 713 17

We had a 20-year-old male patient of secondary aldosteronism similar to Bartter's syndrome, which had proved to be evident after the remission of nephrotic syndrome. In the patient, hypokalemic alkalosis and hyperreninemic hyperaldosteronemia were observed, although the blood pressure was normal. Hyperplasia of juxtaglomerular cells was observed and no abnormalities indicating either glomerulonephritis or renal artery stenosis were found; the pressor response to intravenously infused angiotensin (ang) II was markedly decreased; urinary prostaglandin (PG) E2, kallikrein and kinin excretion were elevated. The inhibition of PG synthesis with indomethacin decreased renal PG production and partially corrected both hypokalemia and pressor responsiveness to ang II. Thus, this case is considered to be a case of Bartter's syndrome. Contrary to the previously reported observations, the effective fractional chloride reabsorption rate in the renal distal tubules was normal (> 80%) and not changed by PG inhibition. Plasma atrial natriuretic peptide level was normal. An interaction between renin-angiotensin and PG systems appears to play a prior role in this case. To explain the pathophysiology, we have hypothesized an abnormal function of ang II receptor signal transduction which excessively stimulates PLA2, resulting in overproduction of PG synthesis in tissues.
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PMID:A case of secondary aldosteronism similar to Bartter's syndrome with no abnormality in renal chloride reabsorption. 769 92

Primary hyperaldosteronism (adrenal adenoma and idiopathic hyperplasia) is a disorder with hypertension, hypokalemia, elevated serum aldosterone and suppressed plasma renin activity. Hyperplasia is managed medically whereas adenomas are treated surgically. Selective adrenal venous catheterization and aldosterone measurement is a useful tool in making the distinction in 95% of cases. We report a case of bilateral idiopathic hyperplasia of the adrenal glands adequately treated with medications for 6 years followed by worsening. Selective catheterization was consistent with a right sided adenoma. Surgical removal of the right adrenal gland alleviated her symptoms. Pathological examination showed focal nodular hyperplasia. We propose that in the course of the disease the focal hyperplastic nodule became autonomous and behaved like an adenoma. Monitoring of patients with adrenal hyperplasia for recurrence of symptoms is prudent as surgery is beneficial in patients who develop an autonomous nodule.
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PMID:Idiopathic hyperplasia of the adrenal gland behaving like an aldosterone producing adenoma. 907 69