Renal blood flow
Loss of renal function is commonly
slow and progressive with a profall in glomerular filtration rate (GFR) caused by
increasing loss of functional nephrons. One mechanism by which this progress is believed
to occur is the 'hyperfiltration theory' (Brenner et al. 1982). This theory is based
upon the increased workload on functioning nephrons, in kidneys in which renal reserve
has been lost due to injury. Under such circumstances surviving nephrons are subjected
to intraglomerular hypertension and hyperperfusion which can result in glomerular
injury (sclerosis) and further loss of function.
Ingestion of a meal causes a postprandial increase in renal perfusion and filtration
and by cumulative effect this is thought to be responsible for hyperfiltration and
the<renal hypertrophy seen in animals maintained on high protein diets. In the
dog changing from a carbohydrate to a meat diet increases renal blood flow and filtration
rates by as much as 100% (Shannon et al. 1932; Pitts 1944). This increase in renal
blood flow is thought to be mediated by a hormone (e.g. glucagon) or other factor
(Rocha et al. 1972; Aoki et al. 1976; Johannesen et al. 1977).
In the presence of decreasing renal function, therefore, feeding a low protein diet
is indicated to decrease further glomerular damage caused by the above effects on
It has also been suggested that augmented intrarenal pressures and flows associated
with ad libitum feeding might contribute to age-related glomerular sclerosis (Brenner
et al. 1982), but whether or not diet induced changes can result ultimately in disease,
In experimental models reducing dietary protein intake has been assowith decreased
progression of renal haemodynamics (Hostetter et al. 1981) and improved longevity
(Kleinknecht et al. 1979; Salusky et al. 1981). Other studies have demonstrated accelerated
glomerulosclerosis in uninephrectomised rats fed high protein diets (Blatherwick
& Medlar 1937; Lalich et al. 1975) and retardation of the progression of renal
failure in rats (Farr & Smadel 1939; Neugarten et al. 1982; Friend et al.
1978), and in mice (Farr & Smadel 1939), by feeding a protein restricted diet.
Increasing glomerular pathology as evaluated by light microscopy (including glomerulosclerosis)
has been reported in nephrectomised dogs fed increasing levels of dietary protein
(Bovee et al. 1979; Robertson et al. 1986). Several studies in
dogs with renal failure have shown that dietary protein restriction reduces proteinuria,
an indicator of glomerular injury (Polzin et al. 1983; Polzin et al.
1984; Polzin & Osborne 1988) and recent studies show that glomerular hyperfiltration
may promote the development of glomerular sclerosis in dogs with chronic renal failure
(Polzin et al. 1988).
In humans a prospective, randomised study has recently been reported (Ihle et al.
1989) after which the authors concluded that dietary protein restrictions was effective
in slowing the rate of progression of chronic renal failure.
Protein malnutrition has been shown to be unlikely to occur on a protein intake of
more than 1.9 g protein/kg body weight per day in dogs with chronic renal failure
(Polzin et al. 1991). Protein intake below this amount did not further reduce hyperfiltration
and hence would be of no additional benefit in reducing glomerular injury.
Systemic hypertension has been reported in dogs with acute and subinterstitial nephritis
(Anderson & Fisher 1968) and in 58-93% of dogs with renal failure (Cowgill 1982;
Weiser et al. 1971). The presence of systemic hypertension may result in intraglomerular
hypertension, although it is not necessarily present for the development of the laffer.
Animals with renal insufficiency are unable to regulate sodium excretion properly,
however net loss of sodium (sodium dumping) was not demonin one study in which sodium
intake was decreased abruptly in nephrectomised dogs (Schmidt et al. 1974). Currently
it is recommended that the sodium intake for dogs and cats with renal disease be
limited to 0.1-0.3% in dry mailer, which is considerably less than the levels in
most commercial pet foods (Lewis et al. 1987).
Sodium supplementation is contraindicated, though this was once commonly recommended.
Maintaining blood haemodynamics to avoid hypoperfusion and ischaemia is an important
objective in the management and prevention of acute renal failure, and interestingly
it has recently been suggested that limiting protein intake might reduce the susceptibility
of renal tubular cells to nephrotoxic or ischaemic stress, such as occurs in renal
failure (Andrews & Bates 1986; Polzin & Osborne 1990).
Uraemia is a common occurrence in renal disease, and urea itself may increase renal
blood flow, thus having an effect on renal haemodynamics.