Family Practice Vol. 19, No. 5, 563-565
© Oxford University Press 2002
Selections from the Current Literature |
A simplified approach to the management of early chronic renal failure
Department of Family Medicine, Health Sciences Center L-4, 050, SUNY at Stony Brook, Stony Brook, NY 11794, USA.
Kopes-Kerr CP. A simplified approach to the management of early chronic renal failure. Family Practice 2002; 19: 563–565.
Received 1 March 2002; Accepted 13 May 2002.
After medical school, our comfort with renal pathophysiology tends to diminish rapidly. Most of us get enough hospital-based experience so that we are familiar with the basic parameters of acute renal failure; few of us ever get substantial experience managing chronic renal failure (CRF). CRF is estimated to occur in ~200 persons per 1 000 000 in the USA. The most common causes are diabetes and chronic hypertension. It is estimated that there are 240 000 patients with end-stage renal disease (ESRD) in the USA, and this number is increasing at ~6–7% per year; 71% of these patients go on dialysis and 29% have a functioning kidney transplant. The annual mortality for ESRD is ~22%, and the most common cause of death is cardiovascular..
A common primary care approach, once an elevated creatinine has been obtained and confirmed, is simply to refer to a specialist. Early CRF, however, is primarily a primary care disease. These patients live in the community and frequent our offices. Our patients with heart disease, chronic hypertension, diabetes, generalized vascular or immune disease and various congenital conditions are the ones most likely to develop CRF. Patients will often be in this state for years before the condition is recognized appropriately. If there were nothing to do for this condition other than to wait for the creatinine to become high enough to refer for dialysis, then clinical recognition and primary care would not matter, but, in fact, there is much we can do. Through appropriate, simple, systematic management of CRF in its pre-clinical stage, we can make a huge difference to both the length and quality of life for these patients. Several recent articles enable us to outline a very simple approach for primary care physicians to render the most effective care for this condition available anywhere.
CRF and its secondary effects constitute a very complex process, but it is not necessary to master all the basic science to do a good job for these patients. Several recent articles have outlined a process that is simple, practical and efficient.
Barrett BJ. Managing progressive renal disease before dialysis. Can Fam Physician 1999; 45: 977–984.
McCarthy JT. A practical approach to the management of patients with chronic renal failure. Mayo Clin Proc 1999; 74: 269–272. (Take Care of the ‘BEANS’)
Pennell JP. Optimizing medical management of patients with pre-end-stage renal disease. Am J Med 2001; 111: 559–568.
Setting your priorities
Comprehensive effective management of patients with CRF can be broken down into five primary goals.
1. Control the blood pressure
This is by far the most important clinical intervention. While the management of most mild-to-moderate hypertension does not mandate rigid control, patients with CRF will benefit from tight control of pressure—with a target of ~130/80 mmHg. Among patients with CRF and proteinuria >1 g/day, the Modification of Diet in Renal Disease (MDRD) study showed in this subgroup that lowering the pressure even further can lead to a slower decline in glomerular filtration rate (GFR). The greater the proteinuria, the greater the benefit with lower target blood pressure. Angiotensin-converting enzyme (ACE) inhibitors currently are considered the most effective therapy for hypertension associated with CRF.
2. Maintain the haemoglobin level above 10 g/dl
Renal failure leads to a normochromic and normocytic anaemia due to deficient erythropoietin production. Several randomized trials suggest that partial correction of anaemia to a haemoglobin level of ~10 mg/dl improves both the quality of life and cardiac function in pre-dialysis patients. The most effective treatment is with erythropoietin subcutaneously at a starting dose of 4000 U weekly. The haemoglobin should rise by ~1 g/dl per month. If the level changes by more than this, adjust the dose up or down in 2000 U increments. The drug is available in pre-filled syringes containing 1000, 2000, 3000, 4000 or 10 000 U. Iron intake should be maintained but, because the problem is due to erythropoietin deficiency, iron alone will not be adequate. Patients receiving erythropoietin should also receive 300 mg of ferrous sulfate b.i.d. or t.i.d. Note, if the patient is also taking calcium compounds, which reduce iron absorption, it may be preferable to give iron as a single 600 mg dose at bedtime.
3. Prevent renal bone disease
The first step is to limit phosphate intake. Simple measures include educating patients to avoid foods high in phosphates—particularly cola-based soft drinks, nuts, seeds, peanut butter, dried peas and beans, baked beans, processed bran cereals, sardines and fish pastes, cheese, milk and other dairy products. The next step is to use a calcium-based phosphate binder with meals (e.g. Tums, calcium carbonate, 500–1500 mg with each meal). Adjust the dose to keep the serum phosphate in a range of 3.5–5.0 mg/dl (or <1.5 mmol/l) and serum calcium on the high side of normal (9.6–10.4 mg/dl or 2.4–2.6 mmol/l), if the serum albumin is normal. Plan to check the serum intact parathyroid hormone (PTH) levels periodically to ensure that this does not increase beyond a range of 1–3 times normal. If the PTH level rises to more than three times normal and serum calcium and phosphate levels are not elevated, then add activated vitamin D [calcitriol or alfacalcidol (0.25 µg/day or 0.5 µg three times a week orally)]. Ongoing laboratory monitoring should include calcium, phosphate and PTH levels.
4. Maintain acid–base balance
Renal failure generally does not lead to serious acidosis until the GFR falls to <0.33 ml/s. The more common chronic, low-grade acidosis can have detrimental effects on protein metabolism, bone mineralization and cardiovascular function. Correction of acidosis also reduces hyperkalaemia, which allows ACE inhibitors to be continued for longer, which is highly desirable for CRF. There is also some evidence from trials that correction of acidosis leads to positive nitrogen balance and less severe bone disease. Current recommendations are to start treatment when the pH level falls below 7.2 or the serum bicarbonate falls below 15 mmol/l. Measurement of pH from venous blood is adequate for monitoring acid–base status. Give either sodium citrate, sodium bicarbonate or calcium carbonate orally until the serum bicarbonate level is >20 mmol/l. The choice of agent should be determined by whether one needs to use calcium carbonate as a phosphate binder. Aluminium-containing antacids should be avoided, particularly those with citrate. An oral multivitamin should be recommended, particularly for patients whose bicarbonate is <20 mEq/l.
5. Treat dyslipidaemia
CRF itself tends to increase triglycerides and lipoprotein A, but not cholesterol. While there are no randomized, controlled trials to show that lipid-lowering therapy improves cardiovascular or renal outcomes in this particular subset of patients, these patients are at much higher than normal risk from coronary artery disease; such therapy dramatically benefits other groups of patients with coronary artery disease and is highly likely to be effective in the group of patients with CRF.
For those preferring mnemonics over numerical listing of goals, an alternate approach to chronic renal failure has been suggested in the form of ‘Take care of the BEANs’, where BEANS is a mnemonic for Blood pressure, Erythropoietin, Access, Nutritional care and Specialist referral. I find that a combination of these approaches will reinforce each other nicely while keeping the overall mental task simple. The BEANS mnemonic places the same primary emphasis on blood pressure control and prevention of anaemia but relabels the concerns about calcium and phosphorus metabolism, acid–base balance and lipid control under the single category of nutrition, and adds a clear guideline for the two other important issues for the primary care physician—when to refer and when to begin planning for access for dialysis, if appropriate.
The author of the BEANS mnemonic addresses the subject of dietary protein more directly, specifically urging that we avoid protein malnutrition in our patients. While much older literature emphasized protein restriction in CRF, current recommendations emphasize maintaining a normal serum albumin level. Hypoalbuminaemia at the time of initiation of dialysis is associated with increased mortality. Many patients with CRF have spontaneous protein restriction to ~0.8 mg/kg/day once the GFR declines below 20 ml/min. This anorexia may be exacerbated by encouragement of a strict protein-restricted diet as was common formerly. The author believes that protein restriction to <0.6 g/kg/day (~40 g/day for the average adult) is "expensive, impractical, and unlikely to be rigorously followed". He specifically recommends monitoring urinary creatine, BUN and protein excretion. Urinary protein nitrogen <0.8 g/kg/day suggests possible malnutrition. Protein intake can be liberalized to 1.0–1.2 g/kg/day after the initiation of dialysis.
For specialist referral, the simple recommendation is just to refer the patient to a nephrologist when either the creatinine rises above 3.0 mg/dl or the GFR falls below 30 ml/min. The National Kidney Foundation in the USA recommends that long-term haemodialysis access should be created when the creatinine rises above 4 mg/dl or the GFR falls below 20 ml/min. The author of the BEANS mnemonic suggests that access should be established whenever the need for long-term dialysis is anticipated to occur within 6 months. Best results are generally obtained with a native A–V fistula, but these require 3–6 months for maturation. An A–V synthetic graft can be used 2–4 weeks after insertion, and peritoneal dialysis catheters are usually allowed to heal for 4–6 weeks.
The final recommendation to this simple package of care that I would add is an emphasis on organizing your medical records into a flow-sheet for these patients. Specifically, I would recommend something as that below.
While all of the concepts mentioned above are quite simple, keeping track of the numbers is the difficult part. You want to make it easy for yourself to see trends at a glance. It is rare that any single value is critical. There is no definitive guideline for how frequently any of these need to be tested. A reasonable interval would be every 3–6 months depending on whether a value has been stable over time or appears to be accelerating in its trend. Monthly testing is probably too frequent for most patients not on dialysis, since the early phase of CRF tends to evolve slowly over years; it is likely to evolve even more slowly if these parameters are monitored actively by the family physician.
Conclusion
Early recognition of chronic renal disease lies squarely in the domain of the family physician who is most often the one taking care of otherwise asymptomatic patients with hypertension and diabetes. Our role does not simply end with the incidental discovery of an elevated creatinine on routine monitoring of these conditions. Once identified, we have a very important role for the next many years. Careful attention to medical records and five simple clinical goals will provide optimal care for most patients.
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