In the face of loss of nephron mass, the kidney tries to maintain function by increasing the work of the remaining nephrons. This increase in individual nephron GFR is achieved by increasing the glomerular capillary pressure and this ultimately leads to further nephron loss and a down-hill spiral in renal function. Progression is perpetuated by all factors that contribute to the increase in single nephron GFR and glomerular pressure, particularly by hypertension and high dietary protein load.
Any treatment that reduces blood pressure will help reduce intraglomerular capillary blood pressure, which is the main driving force behind hyperfiltration injury. This therefore includes calcium channel blockers such as nifedipine and beta-blockers such as atenolol. ACE inhibitors such as enalapril will also be of benefit through their antihypertensive action, but have been found to have an additional benefit, independent of improved renal haemodynamics. This benefit is reflected in a reduction in proteinuria.
The benefits of reducing blood pressure are such that targets for blood pressure control are being reduced to well below the defined upper limit of normal i.e. the 95th centile.
Animal experiments have demonstrated that reduced protein intake slows progression of renal failure. Studies in humans have been equivocal. However, in western societies dietary protein intake is approximately 1.4 g/kg/day, against a recommended intake of 0.8 g/kg/day (these values are higher in children). While the benefits of dietary protein restriction are unclear and potentially harmful in growing children, it seems sensible to avoid excessive protein intake and therefore reduce protein intake to the recommended dietary allowance (RDA).
Diuretics may be helpful to stimulate urine output and help manage fluid overload but have no significant effect on rate of decline of renal function.
Patients with CKD continue to need to excrete an osmotic load to balance their dietary intake. In the face of CKD the renal concentrating ability is reduced and therefore the volume of urine which must be passed to excrete this solute load is increased. This must be matched by an increase in fluid intake. An inadequate fluid intake will therefore lead to dehydration, but equally the impaired kidney function means that they are unable to excrete a high water load. Excessive fluid may lead to hyponatraemia. Animal experiments have suggested that water restriction may accelerate progression of CKD by increasing glomerular filtration pressure. The advice is therefore to maintain a good fluid intake, but avoiding fluid overload.