Chronic Nephritis in Rats Fed High Protein Diets

Blatherwick, N. R.; Medlar, E. M.

doi:10.1001/archinte.1937.00170200014002

Cited by 68 publications

(22 citation statements)

References 6 publications

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“…This renal disease, which is a common feature in the aging rat, affects preferentially the male and has a higher incidence and severity for some strains such as the Sprague-Dawley (30)(31)(32)(33)(34)(35)(36).…”

Section: Long-term Conseguences Of the Nephrons' Adaptation To Their mentioning

confidence: 99%

Long-Term Effects of Mild Oligonephronia Induced In Utero by Gentamicin in the Rat

1991

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ABSTRACT. Renal clearance studies and morphologic observations were performed in rats aged 14, 21, and 28 d and 3, 6, 9, and 12 mo born with a 20% reduction in nephron number after administration of 75 mg/kg/d of gentamicin to their mothers during the second half of gestation. Gentamicin was still present in urine 3 mo after birth. Morphologic damage characteristic of gentamicin accumulation was observed in the kidney on d 14 and 21. Adequate compensatory adaptation to oligonephronia occurred for glomerular function within 14 d of birth, but tubular phosphate reabsorption was significantly low on d 21. On d 28, no evidence of histologic or functional damage to the kidney was observed. At 3 mo, mesangial lesions were observed in rats of the gentamicin group, whereas they were rarely present in 6-mo-old control rats. Furthermore, glomerular sclerotic lesions were already evident in about 5% of the juxtamedullary nephrons. The same percentage of injured nephrons was not observed before 12 mo in controls. Complementary morphologic data obtained in 24-mo-old rats showed that glomerulosclerosis involved 40% of the juxtamedullary nephron population at this age in animals of the gentamicin group versus 21% in controls.

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Section: Long-term Conseguences Of the Nephrons' Adaptation To Their mentioning

confidence: 99%

Long-Term Effects of Mild Oligonephronia Induced In Utero by Gentamicin in the Rat

1991

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“…The hepatic biosynthesis of this protein is under the control of androgens [4,5] and glucocorticoids [5], In the young male, the ot2u represents 25-30% of the total urinary pro tein (TUP) [6]. As the rat ages, the spontane ous degeneration of the kidney, called chronic or progressive glomerulonephrosis [7] leads to an increased excretion of TUP [8][9][10][11][12], In a study relating morphologic changes with age, Hirolcawa [13] demonstrated a fusion of podocytes and a glomerular thickening as early as 3 months of age. Since these changes are ac companied by an excretion of protein in the urine, it is thought that proteinuria is a con sequence of the renal changes.…”

Section: Introductionmentioning

confidence: 99%

Age-Dependent Changes in the Excretion of Urinary Proteins by the Rat

Neuhaus¹,

Flory²

1978

Nephron

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The excretion of total urinary proteins (TUP) of rats beginning at weaning and extending to 12 months of age was correlated with the output of the sex-dependent α2u-globulin and albumin. At puberty, 40 days of age, the excretion of TUP corresponded to the output of α2u-globulin. At this age, α2u represented 30% of the total while albumin less than 10%. From 100 to 200 days of age, TUP remained constant while the excretion of albumin steadily increased. After 150–180 days of age, the concentrations of α2u and albumin in TUP were approximately equal. Thereafter, the excretion of albumin and TUP increased markedly whereas α2u excretion remained constant. At 373 days of age, albumin represented over 50–60% of the TUP while α2u was only 6–7%. Female rats which excrete little or no α2u exhibited a much lower level of proteinuria than the male during the first year. We suggest the existence of two phases of proteinuria in the male rat, namely, an early physiologic or α2u-globulinuric phase and a later albuminuric phase during which increasing quantities of plasma proteins, especially albumin, are lost.

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“…Glomerular morphologic changes resembling those seen in diabetes have been associated with increases in capillary pressures and flows in other experimental forms of renal disease, including ablation ofrenal mass (11)(12)(13), high-protein diet (14), and some models of hypertension (15,16). Furthermore, the extent of glomerular lesions in diabetic rats can be enhanced by maneuvers known to increase glomerular capillary pressures and flows, such as contralateral renal arterial clipping (17), ablation of the contralateral kidney (18), or high-protein feeding (19).…”

mentioning

confidence: 99%

Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.

Zatz¹,

Meyer²,

Rennke³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

491

277

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Six groups of Munich-Wistar rats underwent micropuncture study 2-10 weeks and morphologic studies 11-13 months after induction of streptozotocin diabetes or after sham treatment. Diabetic rats received diets containing 6% (group D6), 12% (D12), or 50% protein (D50) and were maintained under similar conditions of moderate hyperglycemia by daily injections of ultralente insulin. Age-and weightmatched normal control rats were also given 6% (Group N6), 12% (N12), or 50% protein (N50 (9,10) to result from an augmentation of both glomerular plasma flow rate (QA) and local transcapillary hydraulic pressure difference (AlP). Glomerular morphologic changes resembling those seen in diabetes have been associated with increases in capillary pressures and flows in other experimental forms of renal disease, including ablation ofrenal mass (11-13), high-protein diet (14), and some models of hypertension (15, 16). Furthermore, the extent of glomerular lesions in diabetic rats can be enhanced by maneuvers known to increase glomerular capillary pressures and flows, such as contralateral renal arterial clipping (17), ablation of the contralateral kidney (18), or high-protein feeding (19).Studies to date have not dissociated the effects of glomerular hypertension and hyperperfusion from those of chronic hyperglycemia per se (20)(21)(22). In the present study, glomerular hemodynamic function was deliberately varied in rats with streptozotocin (STZ)-induced diabetes while stable moderate hyperglycemia was maintained by daily exogenous insulin. This approach made it possible to relate the early alterations in glomerular pressures and flows in experimental diabetes to the subsequent development of glomerular injury. METHODSNinety-three adult male Munich-Wistar rats (220-260 g each) were studied. Forty-three rats were made diabetic by a single intravenous injection of STZ (60 mg/kg). Morning blood glucose concentration was determined biweekly. Rats received daily evening injections of ultralente insulin (NOVO Industries, Copenhagen) (23) in doses to maintain blood glucose concentration (BG) between 200 and 400 mg/dl. Diabetic rats were maintained on diets containing 50% (group D50, n = 15), 12% (D12, n = 15), or 6% casein (D6, n = 13). Normal control rats matched for initial body weight received the same diets containing 50% (group N50, n = 18), 12% (N12, n = 16), or 6% casein (N6, n = 16). The composition of the diets was 82% (wt/wt) casein plus carbohydrate, 5% lipid, 1% phosphate, 1% calcium, and 11% other components.Twenty-five diabetic rats and 24 control rats underwent micropuncture study 2-10 weeks (mean 4.2) after STZ injection. Rats were anesthetized with Inactin (100 mg/kg) and prepared for mnicropuncture in standard fashion (24). Euvolemia was maintained by iso-oncotic plasma replacement (25). Inulin (10 g/dl in isotonic saline solution) was also infused at a rate of 1.2 ml/hr. Tubule fluid was collected from superficial proximal tubules for determinations of flow rate and inulin concentration (26). Blood samples fro...

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Chronic Nephritis in Rats Fed High Protein Diets

Cited by 68 publications

References 6 publications

Long-Term Effects of Mild Oligonephronia Induced In Utero by Gentamicin in the Rat

Long-Term Effects of Mild Oligonephronia Induced In Utero by Gentamicin in the Rat

Age-Dependent Changes in the Excretion of Urinary Proteins by the Rat

Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.

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