Enhancement of Renal Compensatory Hypertrophy by Hyperadrenocorticism and its Modulation by Nutritional Factors

Reville, P; Laharpe, F. De; Köll-Back, M H; Roos, Marcel; Stephan, Friedrich K.

doi:10.1055/s-2007-1019054

Cited by 10 publications

(9 citation statements)

References 14 publications

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“…It has been reported recently that the hemodynamic and structural adaptation to injury is dissociated in the remnant kidney and the correlation between glomerular sclerosis and hy pertrophy is thus more evident than that between glomer ular sclerosis and glomerular hypertension [13,14]. Salt intake has been reported to influence compensatory renal 92 Nagashima/Okuda/Tamaki/Fujishima High Salt Diet and Glomerular Injury growth [1][2][3][4]. Dietary salt restriction inhibited the hyper trophic response to ablation and reduced glomerular inju ry in uninephrectomized spontaneously hypertensive rats [2], The effects of salt consumption on renal size and com position have also been studied in Dahl rats, in which renal growth due to hyperplasia accompanies the inges tion of a high salt diet in both salt-sensitive and resistant rats, but the growth rates differ between the strains [15].…”

Section: Discussionmentioning

confidence: 99%

“…Salt intake has been reported to influence compensato ry renal growth in rats [1][2][3][4]. A positive correlation between the solitary kidney weight and the daily urinary Na+ excretion was noticed in rats drinking a saline solu tion and treated with ACTH [1], In addition, the dietary salt restriction inhibited the hypertrophic responses to the Accepted: August 9.…”

Section: Introductionmentioning

confidence: 99%

“…A positive correlation between the solitary kidney weight and the daily urinary Na+ excretion was noticed in rats drinking a saline solu tion and treated with ACTH [1], In addition, the dietary salt restriction inhibited the hypertrophic responses to the Accepted: August 9. 1994 ablation of renal mass and markedly reduced the extent of glomerular injury in uninephrectomized spontaneously hypertensive rats [4], In that report, salt restriction did not have any effect on glomerular hemodynamics, and thus revealed the independent contribution of compensa tory growth to glomerular injury [2 ], Hypertrophy of the glomerulus is a phenomenon in variably associated with glomerular sclerosis.…”

Section: Introductionmentioning

confidence: 99%

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Influence of a High Salt Diet on Glomerular Injury and the Preventive Effects of Amiloride in Adriamycin Nephropathy

Nagashima

Okuda

Tamaki

et al. 1995

Nephron

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The effects of a high salt diet on glomerular hypertrophy and sclerosis were examined in a focal glomerular sclerosis rat model. Sprague-Dawley rats were injected twice with Adriamycin (ADR, 2.5 mg/kg body weight) and then divided into 3 groups: (1) ADR rats fed a 1% sodium chloride (NaCl) diet (control ADR rats); (2) ADR rats fed an 8% NaCl diet (ADR-NaCl group), and (3) ADR rats fed a 10% sodium bicarbonate (NaHCO₃) diet (the ADR-NaHCO₃ group), and were then observed for 8 weeks. There were no differences in the blood pressure levels between the control ADR and ADR-NaCl groups. The urinary protein excretion was significantly less in the ADR-NaCl and ADR-NaHCCO₃ groups than in the control ADR group. However, a progressive increase in the blood urea nitrogen and serum creatinine associated with extensive glomerular sclerosis and hypertrophy was only observed in the ADR-NaCl group. An increase in the glomerular diameter preceded the development of glomerulosclerosis in this group. Furthermore, a daily administration of amiloride, a Na⁺/H⁺ exchanger inhibitor, to the ADR-NaCl rats prevented the development of glomerular hypertrophy and sclerosis. These results therefore suggest that the aggravated effect of a high salt diet on glomerular sclerosis may be related to glomerular hypertrophy which is associated with the stimulation of the Na⁺/H⁺ exchanger.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Influence of a High Salt Diet on Glomerular Injury and the Preventive Effects of Amiloride in Adriamycin Nephropathy

Nagashima

Okuda

Tamaki

et al. 1995

Nephron

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“…Experimental work has hypothesized that dietary salt can directly modulate the renal structure. Salt restriction, in fact, diminishes both normal and compensatory renal growth [7,8,21,22]. Furthermore, in experimental models of renal insufficiency, a lower salt intake reduces the rate of GFR decline, proteinuria and renal damage, with the protective effect being superior to the diuretic treatment [7,9,10].…”

Section: Discussionmentioning

confidence: 99%

Salt Intake and Renal Outcome in Patients with Progressive Renal Disease

Cianciaruso¹,

Bellizzi²,

Minutolo³

et al. 1998

Mineral Electrolyte Metab

133

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Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting >200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was <100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 ± 2 vs. 28 ± 2 ml/min) and higher proteinuria (2.9 ± 0.3 vs. 1.5 ± 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 ± 2 mm Hg in LSD and 107 ± 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 ± 0.07 vs. 0.51 ± 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.

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“…This also results in an increased risk of cardiovascular events, and even the earliest stage CKD was associated with an excess risk of subsequent coronary heart disease (CHD) [36]. The interactive effects of hormones and nutrients greatly affect growth, and maternal dietary excesses and/or deficiencies can result in diverse progeny susceptibilities to systemic/local injuries that manifest in a morbidity status later in life [37]. Recent post-hoc analyses of the Modification of Diet in Renal Disease indicate that lower BP, specifically BP < 120/80 mmHg, may provide long-term kidney protection in patients with nondiabetic kidney disease.…”

Section: Discussionmentioning

confidence: 99%

Effects of Perinatal Protein-Nacl Diets on Offspring's Blood Pressure and Renal Function in Lewis Rats

Lee¹,

Azar²

2013

TOHYPERJ

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Perinatal diets may affect the cardiovascular-renal functions of offspring. To understand effects of maternal diet on the renal function and blood pressure (BP) of offspring, protein (10% low, LP; 23% normal, NP) and/or NaCl (4% high salt, HS; 0.6% normal, NS) diets were started at pre-pregnancy through pups' weaning to either a 4% high NaCl (hs) or 0.6% NaCl (ns) diet. Telemetered BP data was analyzed by methods of linear least square rhythmometry. Systolic BPs (circadian mean ±SE mm Hg) were: NPNSns, 131±2; NPNShs, 137±2; NPHSns, 137±0.2; NPHShs, 134±3; LPNSns, 138±1; LPNShs, 138±0.6; LPHSns, 135±2; LPHShs, 142±2. Offspring in NPNShs and NPHSns had significantly increased SBPs versus NPNSns (both P<0.05). Most LP-offspring had increased SBP (P<0.01 to <0.05) and lower body weight (BW) with smaller glomerular filtration rate changes (renal reserve, RR-GFR) following overnight acute highprotein loads: RR-GFRs (inulin, ml/min/g kidney) for groups stated above were, respectively: 0.935; 0.927; 0.537; -0.064; -0.229; 0.057; -0.515; -0.404. The kidney weight/BW ratio of offspring was higher on hs-than on ns-diets (all P<0.001). Rats on a low caloric diet had reduced sclerotic glomerular numbers compared to those on normal diets (11.2±1 vs. 15.7±2, P<0.001), though glomerular numbers were similar in both groups.In summary, perinatal LP-HS diets significantly affected the BW, BP, renal injuries and kidney function of offspring. RR was seriously reduced, especially among offspring in hs-and perinatal LP groups. The most interesting result was the glomerular maturation staging in the pups, which suggests delayed nephrogenesis by a maternal LP diet.

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Enhancement of Renal Compensatory Hypertrophy by Hyperadrenocorticism and its Modulation by Nutritional Factors

Cited by 10 publications

References 14 publications

Influence of a High Salt Diet on Glomerular Injury and the Preventive Effects of Amiloride in Adriamycin Nephropathy

Influence of a High Salt Diet on Glomerular Injury and the Preventive Effects of Amiloride in Adriamycin Nephropathy

Salt Intake and Renal Outcome in Patients with Progressive Renal Disease

Effects of Perinatal Protein-Nacl Diets on Offspring's Blood Pressure and Renal Function in Lewis Rats

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