Effects of dietary protein and phosphorus restriction on the progression of early renal failure

Maschio, Giuseppe; Oldrizzi, Lamberto; Tessitore, Nicola; D’Angelo, Angela; Valvo, E.; Lupo, Antonio; Loschiavo, C.; Fabris, Antonia; Gammaro, Linda; Rugiu, Carlo; Panzetta, Giovanni

doi:10.1038/ki.1982.184

Cited by 226 publications

(69 citation statements)

References 12 publications

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“…In man, a recent study has suggested that moderate protein restriction may also delay the progression of renal functional deterioration in patients with early renal failure (41). While careful hemodynamic measurements were not performed in that study, it is attractive to speculate that the protective effect oflow protein feeding resulted from the prevention of hyperperfusion in surviving nephrons in these patients.…”

Section: Discussionmentioning

confidence: 77%

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Dworkin¹,

Hostetter²,

Rennke³

et al. 1984

J. Clin. Invest.

257

102

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were not different than group 3 but significantly lower than group 4. QA and SNGFR were lower in group 5 (low protein) than in groups 3 and 4. Furthermore, proteinuria and glomerular structural lesions were abolished in group 5. Morphologic studies performed in groups 6 and 7 showed that early DOC-SALT lesions progress to focal glomerular sclerosis. These studies suggest that continued elevations in glomerular capillary flows and pressures predispose to glomerular injury in this model of systemic arterial hypertension.

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Section: Discussionmentioning

confidence: 77%

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Dworkin¹,

Hostetter²,

Rennke³

et al. 1984

J. Clin. Invest.

257

102

View full text Add to dashboard Cite

show abstract

“…Reducing dietary protein content has also been shown to lessen renal damage in nephrotoxic serum nephritis (31,32) and diabetic nephropathy (33) in rats, and in the lupuslike nephropathy of the New Zealand Black/ New Zealand White mouse (34). In humans, studies in both advanced (35) and early renal failure (36) suggest that moderate protein restriction may retard the rate of deterioration of renal function in patients with a variety of renal diseases. Micropuncture studies of glomerular dynamics in rats 1 wk after 90% ablation of renal mass (3) and in rats with DOC-SALT hypertension (2) confirm that, as in the present study, an important effect of protein restriction is to maintain glomerular hemodynamics at near normal levels.…”

Section: Methodsmentioning

confidence: 99%

Glomerular injury in uninephrectomized spontaneously hypertensive rats. A consequence of glomerular capillary hypertension.

Dworkin¹,

Feiner²

1986

J. Clin. Invest.

185

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Micropuncture and/or morphologic studies were performed in intact Wistar-Kyoto rats (WKY) (group 0) intact spontaneously hypertensive rats (SHR) (groups 1 and 5), uninephrectomized (UNX) WKY (groups 2 and 6), and UNX SHR (groups 3 and 4, 7 and 8). UNX was performed when rats were 5 wk of age. Groups 0-4 were observed for 34 wk after which whole kidney clearance and morphologic studies were performed. Groups 5-8 underwent micropuncture study at 10 wk of age. Groups 4 and 8 were fed a diet containing 6% protein. All other rats ingested standard laboratory diet. 5 wk after UNX, normotensive group 6 had higher single nephron glomerular filtration rate (SNGFR) and initial glomerular plasma flow rate (QA) than intact, hypertensive group 5. Glomerular transcapillary hydraulic pressure difference (AP) was similar in these two groups. Hypertensive group 7 exhibited less elevation in SNGFR and QA than group 6, but AP was significantly increased. The presence of glomerular capillary hypertension in UNX SHR at 10 wk was associated with the development of significant proteinuria and an increased incidence of mesangial expansion and glomerular sclerosis at 7 mo (group 3) as compared with groups 0, 1, and 2. Protein restriction prevented the development of increased AP in UNX SHR (group 8) and also conferred long-term protection from increased urinary protein excretion and glomerular injury (group 4). These studies suggest that glomerular capillary hypertension predisposes to glomerular injury in this model of hypertension with reduced renal mass.

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“…Observations in the dog with an advanced degree of renal mass reduction have not demonstrated a tendency for renal failure to progress (Bourgoignie et al 1987), so there may be major differences between species in the behaviour of residual nephrons in renal insufficiency. Studies of dietary protein reduction in patients with chronic renal failure have however yielded similar clinical benefits to those observed in animal studies, though the precise role of protein restriction in progressive chronic renal failure remains controversial (Giordano 1982;Maschio et al 1982; Klahr et al 1983;Mitch 1984). Early studies of angiotensin converting enzyme inhibitor therapy in patients with chronic renal disease have shown marked benefits (Taguma et al 1985), however the demonstration of a specific therapeutic advantage of angiotensin converting enzyme inhibitors over and above conventional forms of systemic blood pressure treatment has yet to be demonstrated.…”

Section: Studies In the Nephrotoxic Serum Nephritic Model Of Renal Famentioning

confidence: 99%

Systemic and Renovascular Hypertension

Jackson

Franze

Whitty

1992

Tohoku J. Exp. Med.

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To ascertain the contribution of systemic hypertension in the progression of renal failure, we have studied the effects of pharmacological treatment of hypertension in rats with the remnant kidney model of renal insufficiency, streptozotocin diabetes, or nephrotoxic serum nephritis.Treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril lowered systemic blood pressure in the remnant kidney and diabetic animals, but did not lower blood pressure in rats with nephrotoxic serum nephritis.Proteinuria was reduced in all three models, and creatinine clearance improved in the remnant kidney and diabetic animals, when compared with untreated controls.In the remnant kidney and diabetic models systemic blood pressure was lowered to a similar degree by treatments with a calcium blocker, with no improvement in either proteinuria, or glomerular filtration rate. Further studies of the long-term effects of enalapril have been undertaken in rats with the two kidney one clip model of hypertension. Rats treated with enalapril had a lower blood pressure and improved survival over one year of treatment, compared with untreated rats. After 1 year of treatment however the clipped kidney was small and fibrotic, and non functional.Following withdrawal of enalapril therapy there was no functional improvement of the clipped kidney.The possibility that ACE inhibitors have a specific intra-renal effect reducing the rate of progression of renal disease now needs confirmation in human studies. In renovascular hypertension however, intra-renal changes induced by ACE inhibitors may cause irreversible renal damage. chronic renal failure ; diabetic nephropathy ; hypertension ; nephrotoxic serum nephritis ; renovascular hypertensionThe contribution of systemic hypertension to the progression of renal failure is controversial.Systemic hypertension is common in chronic renal failure, and may contribute to the progression of glomerular injury (Del Greco et al. 1975). It is well known that malignant hypertension leads to progressive renal failure, where fibrinoid necrosis of the arterioles is associated with progressive loss of renal function, and eventual endstage renal failure. The treatment of severe accelerated hypertension is associated with improvement in renal function, however the effect of antihypertensive therapy on renal functional impairment associated with milder forms of systemic hypertension is still not clear. Studies of blood pressure treatment have yielded conflicting results. In some risk factor surveys, systemic

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Effects of dietary protein and phosphorus restriction on the progression of early renal failure

Cited by 226 publications

References 12 publications

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Glomerular injury in uninephrectomized spontaneously hypertensive rats. A consequence of glomerular capillary hypertension.

Systemic and Renovascular Hypertension

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