Chronic renal failure (CRF) implies that there is significant irreversible reduction in renal function; here we are using it to mean CKD stages 4-5, but that isn't a generally accepted convention. There is a separate page on less severe CKD (stages 1-3). Common causes of CKD/CRF are:
• Circulatory problems such as renal artery stenosis
• Inflammation within the kidneys - interstitial nephritis or glomerulonephritis
• Diabetes is very important cause - diabetic kidney disease also affects glomeruli
• Urinary tract obstruction - in ureters, bladder, or below - more on obstruction
• Inherited diseases - more info on inherited/congenital diseases
Preventing progression of CKD
It is common for renal impairment to worsen slowly with time, even if the cause of damage is no longer present. There are various theories for this, including hyperfiltration stress on residual nephrons, and direct toxicity from proteinuria to the renal tubules. The following markers identify patients at greater risk of deterioration of renal function:
- Worse renal function - higher serum creatinine (lower eGFR)
- Proteinuria - the higher, the greater the risk of progression
- Hypertension - the higher, the greater the risk
- Renal biopsy shows fibrosis, or continuing inflammation
- Young age - they have longer for trouble to develop
However this process can be slowed in many cases by the following:
- Blood pressure control to stringent targets. More on BP control
- ACE inhibitors if there is proteinuria. More on ACEI
- Prevention of acidosis by treatment with bicarbonate may play a role
- Dietary restriction - the role of protein restriction is controversial. The gains is small if blood pressure control is good and ACE inhibitors are prescribed. Severe protein restriction does not retard progression in patients whose blood pressure is well controlled, but risks malnutrition. High protein intake is almost certainly a bad thing. Many nephrologists follow an intermediate course, recommending moderate protein restriction (0.6-0.8g/kg/day) but ensuring adequate calorie intake. Salt (sodium) restriction (<100mmol/d, maybe should be less) is indicated for most patients, but difficult to achieve with modern Western eating habits. Phosphate and potassium restriction may also be necessary.
Further info for all on diet (edren/info)
Diet in the Edren Handbook
Become increasingly evident as renal function deteriorates.
- Hypertension is often an early feature. More on hypertension in renal disease
- Fluid retention commonly becomes a major problem in late renal failure, requiring large doses of diuretics.
- Anaemia can be treated by recombinant erythropoietin injections after other causes have been excluded and adequate iron stores demonstrated. This often requires intravenous iron therapy. This is not usually a serious problem until GFR falls below 20. More on anaemia.
Bone disease (renal osteodystrophy) is prevented by
- prescription of alfacalcidol or calcitriol, vitamin D metabolites that do not require 1-α hydroxylation, a function normally carried out by the kidney. This controls hypocalcaemia (but may cause hypercalcaemia).
- prevention of high serum phosphate by dietary restriction and use of dietary phosphate binders such as calcium carbonate or acetate preparations, or aluminium hydroxide (risk of aluminium toxicity, now generally reserved for short-term use), or sevelamer (‘Renagel’), or lanthanum carbonate. Phosphate retention is not usually a severe problem until GFR is less than 20-25.
Gastrointestinal symptoms - anorexia, progressing to nausea and ultimately vomiting - are usually late symptoms, GFR usually well below 20, and sometimes not becoming prominent until GFR <10. They may be helped by dietary modification but are often an indication that dialysis is required.
Other complications such as itching, neuropathy, pericarditis are usually late manifestations that are prevented or controlled by dialysis.
- Patient info about CKD 4/5 (EdREN)
- CKD eGuide - guidance on management of mostly stages 1-3 CKD in the community.