Things to note:
- Treat underlying CVD risk factors as appropriate.
- Limit salt intake and stop smoking.
- Avoid nephrotoxic drugs like NSAIDs.
The following interventions may delay progression of renal disease. Proteinuria reduction
Determine the amount of proteinuria with a spot urine specimen.
- If urine dipstick 1plus or greater, request protein creatinine ratio.
- If urine dipstick less than 1plus, request albumin creatinine ratio.
The ideal target is: protein creatinine ratio (PCR) less than 0.03 g/mmol or albumin creatinine ratio (ACR) less than 2.2 mg/mmol. Most benefit is achieved by reducing PCR to less than 0.1 g/mmol or ACR less than 100 mg/mmol. Achievement of these targets must be balanced against side-effects such as hypotension and hypoglycaemia.
- Start treatment with an ACE inhibitor and titrate up to the maximum tolerated dose.
ACE inhibitor, e.g:
- Enalapril, oral, 20 mg 12 hourly.
- Monitor creatinine and potassium after 1-2 weeks if eGFR less than 60 mL/minute and after 4 weeks if eGFR greater than 60 mL/minute.
- If creatinine increases by greater than 20% from the baseline, stop ACE inhibitor and consult a specialist.
- If stable, monitor thereafter at regular clinic visits.
If ACE inhibitor is not tolerated due to intractable cough, consider an angiotensin receptor blocker, e.g:
- Losartan, oral, 100 mg daily.
- Angiotensin receptor blockers are contra-indicated following ACE inhibitor-associated angioedema.
Optimise blood pressure control with additional antihypertensive agents, BP control results in a lowering of proteinuria and slower decline in GFR. Target BP is 130/80 mmHg. Diabetes mellitus
- In diabetics with kidney disease there is an increased risk of hypoglycaemia. Insulin is the preferred medicine to control blood glucose in patients with eGFR <60 mL/minutes.
- Insulin requirements will decrease as renal disease progresses.
- Stop glibenclamide when eGFR less than 60 mL/minute because of an increased risk of hypoglycaemia.
- Stop metformin when eGFR less than 45 mL/minute because of the risk of lactic acidosis.
In patients unable to take insulin, consider:
Fluid overload and oedema
- Gliclazide, oral, 40 mg daily.
- Furosemide, oral, 40 mg 12 hourly.
When fluid overloaded and eGFR less than 60 mL/minute, start:
- Furosemide, oral, 40 mg 12 hourly.
- Titrate to a maximum of 500 mg 12 hourly.
Furosemide is ineffective when patients are on dialysis and anuric. Hypocalcaemia and hyperphosphataemia
- The aim is to lower phosphate levels and maintain normal calcium levels to ensure calcium phosphate product (i.e. Ca x PO4) less than 4.4 mmol/L, to prevent calcium deposition in vessels and tissue which aggravates vascular disease.
Patients with CKD stage 3-5, not on dialysis:
- Calcium carbonate, oral, equivalent to 500 1500 mg daily of elemental calcium.
- Take in divided doses with meals.
- If serum phosphate is low, then take between meals.
In symptomatic patients with CKD stage 5 who are not candidates for renal replacement therapy, the benefits of phosphate binding are unclear. Patients considered suitable candidates for renal replacement therapy
Monitor Ca++ and PO4 and PTH levels regularly.
For hyperphosphataemia uncontrolled on calcium carbonate:
- Aluminium hydroxide BP, oral, 10 mL 8 hourly. Specialist initiated.
- To prevent dementia-associated aluminium toxicity, do not use for longer than 3 months.
For hyperparathyroidism, initiate when PTH levels > 2-3 times normal:
Anaemia associated with CKD in patients on dialysis programmes
- Calcitriol, oral, 0.25-4 mcg daily. Specialist initiated.
Patients on chronic haemodialysis or peritoneal dialysis are often anaemic due to iron deficiency and deficiency of erythropoietin.
In CKD, especially CKD stage 4-5:
- Iron, elemental, oral. Specialist initiated.
- If no response consider parenteral iron.
- Erythropoietin, SC/IV. Specialist initiated.
Definitive treatment, e.g. transplantation, usually improves anaemia. It is important to identify factors likely to aggravate anaemia, e.g. iron deficiency and infection. Acidosis and hyperkalaemia Short furosemide test only after adequate fluid replacement if the status of volume and BP is satisfactory:
- Furosemide, IV, 250 mg in 50 mL dextrose 5% infused over 30 minutes.
- Discuss all cases with the referral center.
INITIATION OF TREATMENT
- Pulmonary oedema and anuria.
- Intractable metabolic acidosis and severe hyperkalaemia (greater than 7 mmol/L).
- Uraemic complications, e.g. pericarditis, encephalopathy and bleeding.
- Drug overdose only if due to dialysable toxin.
Activated charcoal may reduce systemic absorption of a variety of poisonous substances. The greatest benefit is achieved if activated charcoal is given within one hour after ingestion of poisonous substances.
Activated charcoal is of no value after ingestion of the following:
- strong acids or bases,
- other corrosives substances e.g. household detergents,
- iron, lead, mercury, arsenic,
- petroleum products (e.g. paraffin or petrol), and
- ethylene glycol, methanol, ethanol.
* Charcoal, activated, oral, 50 g diluted in 400-800 mL water.
Alkalinisation of urine
- When mixing, add a small amount of water to charcoal in a container.
- Cap and shake container to make a slurry and then dilute further.
This is a high - risk procedure and should be done only in consultation with a specialist.
Urinary alkalinisation may be of benefit in salicylate, lithium and, less clearly, tricyclic antidepressant poisoning. Note:
Salicylate poisoning may cause a respiratory alkalosis, which may aggravate the metabolic acidotic state. The infusion of large volumes of sodium and water may precipitate hypernatraemia and fluid overload. The increase in pH may also be associated with hypokalaemia, which may cause dysrhythmias in a patient with a tricyclic antidepressant overdose. In this setting consider only in the presence of cardiac involvement, i.e. prolonged QRS duration or QRS axis abnormality on ECG.
* Sodium bicarbonate, IV, 50-100 mEq in 1 L sodium chloride 0.45%.
- Administer 250-500 mL over 1-2 hours.
- Attempt to achieve urine pH of equal to or greater than 17.5
Patients with symptomatically severe poisoning due to salicylates, lithium, ethylene glycol, methanol, ethanol and theophylline may benefit from dialysis.
Refer patient to a hospital with dialysis facilities. Note:
HIV infection is not a contra-indication for dialysis. Peritoneal dialysis fluid should be considered potentially infectious for HIV and viral hepatitis.
Both haemodialysis and peritoneal dialysis are acceptable modalities of therapy in the acute setting. Acidosis
If pH less than 7.25 and HCO3 less than 15 mmol/L and the patient is stable and not dehydrated, refer for dialysis. If dehydrated, administer fluid. CAUTION
Avoid fluid overload.
If associated acidosis, see fluid preference below. Hyperkalaemia
- Serum K+ greater than 6.5 mmol/L.
- Beware of spurious hyperkalaemia due to haemolysis during venipuncture.
* Calcium gluconate 10%, slow IV bolus, 10 mL.
* Dextrose 50%, continuous IV infusion, 100 mL with soluble insulin, 10 units administered over 15-30 minutes.
- Monitor blood glucose levels hourly.
* Salbutamol 0.5%, solution, nebulised over 3 minutes preferably driven by oxygen.
- Dilute 1 mL in 3 mL of sodium chloride 0.9%.
If there is no response, patients will require dialysis.
For long-term or chronic, non-urgent need for potassium removal:
* Sodium polystyrene sulfonate, oral, 15 g with 15 mL lactulose, 6 hourly. OR
* Sodium polystyrene sulfonate, rectal, 30-60 g as an enema.
- After 8 hours, wash out with phosphate enema.
Rectal administration is less effective.
- Treat acidosis to prevent cardiac instability.
- Furosemide may also be of benefit.
- Monitor ECG and measure serum K+ frequently.
If the above treatment fails, urgent dialysis is required. Hyperphosphataemia
To decrease absorption of phosphate in acute renal failure:
* Aluminium hydroxide 300 mg/5 mL, oral, 10 mL 8 hourly.
Do not administer aluminium hydroxide and sodium polystyrene sulfonate simultaneously as this may potentiate aluminium toxicity.
When to refer
- Acute renal failure may complicate chronic renal failure.
- A small percentage of patients do not recover kidney function and should be treated as CKD.
- CKD stage 3 and above.
- Unknown cause of kidney failure.
- Rapid deterioration in renal function.
- Resistant hypertension despite appropriate medication and adherence.