Renal Disease In Rats Research Articles

The role of prolactin in the development of chronic progressive nephropathy in the rat.

Prolactin as a factor in the etiology of chronic progressive nephropathy in rats has been studied by exogenous administration and by endogenous inhibition with bromocriptin. Exogenous prolactin caused a significant increase in frequency and severity of the lesions, with accompanying sodium retention. Conversely endogenous inhibition significantly decreased the frequency and severity of the lesions and increased urine volume, pH and sodium excretion. Thus prolactin is important in the etiology of this renal disease in rats.

Acute and chronic effects of chemically induced unilateral renal disease in rats.

Chemically induced unilateral renal disease was associated with a high incidence of proteinuria, diuresis, a morphological spectrum ranging from perinephritis to acute tubular or cortical necrosis, and unilateral or bilateral glomerular fibrinogen deposition during the first 2 wk after induction. Later, a decrease in proteinuria and return to normal urine output was not infrequently followed by recurrent proteinuria, hypergammaglobulinemia, morphological alterations, and deposition of IgG and beta1C on the glomerular basement membranes and mesangium of the contralateral kidney and the treated kidney. Intercapillary deposition of fibrinogen in association with IgG and beta1C was occasionally observed in one or both kidneys. The morphologic, immunohistologic, serologic, and chemical findings suggest that this model may be useful for further defining the course and prognosis of unilateral renal disease produced by vascular insufficiency.

PHENACETIN-INDUCED RENAL DISEASE IN RATS.

Excerpt There is a growing body of clinical evidence suggesting a relationship between the excessive ingestion of analgesic medication and the development of chronic renal disease. The evidence is ...

Nephropathy of potassium depletion: report of a fatal case.

Case Reports1 October 1960NEPHROPATHY OF POTASSIUM DEPLETION: REPORT OF A FATAL CASEWU-HAO TU, M.D., CARROLL C. JONES, M.D., MAX S. ALLEN, M.D., F.A.C.P.WU-HAO TU, M.D.Search for more papers by this author, CARROLL C. JONES, M.D.Search for more papers by this author, MAX S. ALLEN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-53-4-796 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe effects of potassium depletion on the structure and function of the kidneys have probably been observed for at least 40 years. In 1919 Jaffé and Sternberg1described vacuolar degeneration of the renal tubules in patients who died of dysentery. These observers suggested that the lesion was a distinct pathologic entity, perhaps associated with intestinal disease. Deficiency of potassium as a cause of such renal lesions was suggested by Perkins et al.2and by Luft et al.3The subject has recently been well reviewed by Relman and Schwartz,4, 5, 6who confirmed the etiology and pathogenesis of the lesion by...Bibliography1. JafféSternberg RHH: Ueber die vakuolare Nierendegeneration bei chronischer Ruhr, Virchows Arch. f. path. Anat. 227: 313, 1920. CrossrefGoogle Scholar2. PerkinsPetersonRiley JPABJA: Renal and cardiac lesions in potassium deficiency due to chronic diarrhea, Am. J. Med. 8: 115, 1950. CrossrefMedlineGoogle Scholar3. LuftRingertzSjögren RNB: Two cases of cryptogenetic hypokalemia with pathological anatomical findings, Acta endocrinol. 7: 196, 1951. CrossrefMedlineGoogle Scholar4. RelmanSchwartz ASWB: The kidney in potassium depletion, Am. J. Med. 24: 764, 1958. CrossrefMedlineGoogle Scholar5. RelmanSchwartz ASWB: The nephropathy of potassium depletion. A clinical and pathological entity, New England J. Med. 255: 195, 1956. CrossrefMedlineGoogle Scholar6. SchwartzRelman WBAS: Metabolic and renal studies in chronic potassium depletion resulting from overuse of laxatives, J. Clin. Investigation 32: 258, 1953. CrossrefMedlineGoogle Scholar7. SchribnerBurnell BHJM: Interpretation of the serum potassium concentration, Metabolism 5: 468, 1956. MedlineGoogle Scholar8. SimmonsAvedon DHM: Acid-base alterations and plasma potassium concentration, Am. J. Physiol. 197: 319, 1959. CrossrefMedlineGoogle Scholar9. WellerLownHoigneWyattCriscitielloMerrillLevine JMBRVNFMJPSA: Effect of acute removal of potassium from dogs. Changes in the electrocardiogram, Circulation 11: 44, 1955. CrossrefMedlineGoogle Scholar10. BrownCurrensMarchand MRJHJF: Muscular paralysis and electrocardiographic abnormalities resulting from potassium loss in chronic nephritis, J. A. M. A. 124: 545, 1944. CrossrefGoogle Scholar11. Conn JW: Primary aldosteronism, a new clinical syndrome, J. Lab. and Clin. Med. 45: 661, 1955. MedlineGoogle Scholar12. Siebenmann RE: Ueber eine toedliche verlaufende Anorexia nervosa, Schweiz. med. Wchnschr. 20: 469, 1955. Google Scholar13. RossierStaehelinBuehlmanLabhart PHDAA: Alkalose und Hypokalaemie bei Anorexia mentalis, Schweiz. med. Wchnschr. 85: 466, 1955. Google Scholar14. SquiresRuth RDEJ: Experimental potassium depletion in normal human subjects. I. Relation of ionic intakes to the renal conservation of potassium, J. Clin. Investigation 38: 1134, 1959. CrossrefMedlineGoogle Scholar15. KulkaPearsonRobbins JPCMSL: A distinctive vacuolar nephropathy associated with intestinal disease, Am. J. Path. 26: 349, 1950. MedlineGoogle Scholar16. Keye JD: Death in potassium deficiency. Report of a case including morphologic findings, Circulation 5: 766, 1952. CrossrefMedlineGoogle Scholar17. Case Records of the Massachusetts General Hospital (Case 40081), New England J. Med. 250: 334, 1954. CrossrefGoogle Scholar18. MahlerStanbury RFSW: Potassium-losing renal disease, Quart. J. Med. 25: 21, 1956. MedlineGoogle Scholar19. FinkenstedtRuiz-QuinazuMoreauMorrisonMerrill JTALRSJP: Experimental acute potassium depletion in dogs, Clin. Sc. 16: 171, 1957. MedlineGoogle Scholar20. FourmanMcCanceParker PRARA: Chronic renal disease in rats following a temporary deficiency of potassium, Brit. J. Exper. Path. 37: 40, 1956. MedlineGoogle Scholar21. AlbrightReifenstein FEC: The parathyroid glands and metabolic bone disease, 1948, The Williams & Wilkins Company, Baltimore. Google Scholar22. WrongDavies DHE: The excretion of acid in renal disease, Quart. J. Med. 28: 259, 1959. MedlineGoogle Scholar23. WallisEngle LARL: The adult Fanconi syndrome. II. Review of eighteen cases, Am. J. Med. 22: 13, 1957. CrossrefMedlineGoogle Scholar24. WilliamsMacMaron RHHE: Gastroenterocolitis; carcinoma of pancreas; "clear-cell" nephrosis, Bull. New England M. Center 9: 274, 1947. MedlineGoogle Scholar25. Conway EJ: The blood ammonia, with observations on normal human blood, Biochem. J. 29: 2755, 1935. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Kansas City, Kansas*Received for publication April 19, 1960.From the Department of Medicine, University of Kansas School of Medicine, Kansas City, Kansas.†Research Fellow, Kansas Heart Association.‡Trainee of the National Cancer Institute.Requests for reprints should be addressed to Max S. Allen, M.D., Professor of Medicine, University of Kansas Medical Center, Rainbow Boulevard at Thirty-ninth Street, Kansas City 12, Kansas. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byWork-Up of the Patient with Suspected Renal DiseaseThe role of sodium, potassium and water in the hypo-osmotic states of heart failure 1 October 1960Volume 53, Issue 4Page: 796-807KeywordsDysenteryDyspneaEtiologyHeartHypotensionKidneysLesionsPathogenesisPotassiumUrea ePublished: 1 December 2008 Issue Published: 1 October 1960 PDF downloadLoading ...

Electron and light microscopic study of the pathologic course of experimental renal disease in rats

Electron and light microscopic study of the pathologic course of experimental renal disease in rats

Antigenic Property of Renal Cortex.

Summary1. Ten rabbits were treated with extracts of bloodfree rat kidneys. Eight of the sera obtained from these rabbits induced severe renal disease in rats, weighing 50-70 g, when injected in a dose of 0.19 to 1.2 cc.2. Nine rabbits were treated with extracts of renal cortex obtained from rats. Eight of the sera obtained from these rabbits induced severe renal disease in rats, weighing 50-70 g, when injected in a dose of 0.2-1.15 cc.3. Seven rabbits were treated with extracts of renal medulla obtained from rats. Only one of the sera obtained from these rabbits induced severe renal disease in rats weighing from 50-70 g when injected in a dose of 1.5-2.1 cc.4. It is concluded that the antigen of renal tissue is localised in the renal cortex.