Most physical therapists have treated patients with chronic kidney disease (CKD) at some point, and many have interacted with patients receiving kidney dialysis. Currently, more than 11% of the adult population in the United States — over 19 million people — are now affected by CKD.¹ Unfortunately, kidney problems are rapidly on the rise, with the prevalence of CKD increasing 104% between 1990 and 2001 and with even higher numbers of people developing the disease during the most recent decade.² Because the most common precursors to CKD are diabetes and hypertension, both of which are climbing at alarming rates as a consequence of obesity and the aging population, this may partially explain the sharp upward trend in CKD diagnoses over the past 20 years. As a result, therapists are seeing ever-greater numbers of patients with CKD, a disease associated with poor functional outcomes, high health costs, and a rising mortality rate. Kidney disease is currently the ninth leading cause of death in the U.S., the country with the highest incidence of end-stage renal disease in the world.² Fortunately, although many patients with progressive CKD typically experience fatigue and muscle weakness, these problems are amenable to physical therapy intervention.

Filtration System

Anatomically, the kidneys are fist-sized organs located just distal to the posterior rib cage that function to cleanse the blood of waste products and excess fluids. On a daily basis, a healthy kidney filters approximately 400 pints of blood through its one million nephrons, where it retains normal blood cells and proteins; regulates sodium, potassium, calcium and phosphorus levels; and removes waste materials.³ Each nephron contains tiny capillaries (glomeruli) that are entwined with small tubes (renal tubules) that collect excess fluids. Each glomerulus functions as a tiny filtration system that processes wastes from the circulatory system and allows clean blood to exit the system after trapping the wastes and excess fluids as urine, which is then transported from the kidneys to the bladder via the ureters.

Aside from acting as a sieve to catch and remove waste products from the blood, the kidney also secretes three major hormones: erythropoietin, renin and calcitriol. Erythropoietin functions to stimulate the bone marrow for red blood cell production (erythropoieisis). Renin helps to regulate blood pressure and blood fluid volume, and calcitriol, the active form of vitamin D (1,25 dihydroxy-vitamin D), works to regulate the absorption of calcium and phosphorus to maintain healthy bone. As renal synthesis of these three critical hormones decreases with progressive kidney damage, patients may begin to experience fluid retention, fatigue, changes in urinary habits, loss of appetite, muscle cramps and atrophy, anemia, hypertension and bone disease.³

CKD represents a continuum of damage to the kidneys that is measured in stages, according to the calculated glomerular filtration rate (GFR) and the amount of kidney damage evidenced by abnormalities in blood tests (serum creatinine and blood urea nitrogen [BUN]), urinalysis or abnormal imaging tests.

Because the GFR, or the flow rate of fluid being filtered by the kidneys, naturally varies according to a person’s age, weight and gender, it is calculated by taking the serum creatinine level found on a blood test and entering these factors into an equation. Various GFR calculators are available online, but an estimated GFR (eGFR) can be calculated using the Modification of Diet in Renal Disease formula:⁴

eGFR = 186.3 × (serum creatinine) - 1.154 × (age) - 0.203 × [0.742 if female] × [1.212 if African American]

Although most physicians examine blood levels of the waste products creatinine (a byproduct of muscle metabolism) and BUN (a byproduct of proteins metabolized by the liver), along with certain electrolytes to determine the extent of kidney disease, calculating the GFR is the most accurate measurement of kidney function. But tracking the GFR is not useful in catching CKD in its early stages because creatinine and BUN levels typically do not begin to rise until more than 50% of kidney function is already lost.²

Failure to Filtrate

Kidney damage that occurs quickly in response to certain medications, ingestion of toxins or an accident that causes sudden blood loss is known as acute renal failure. Depending on the amount of damage, acute renal failure may be reversible with rapid treatment. But in most cases, kidney damage occurs slowly and silently — this is called chronic renal failure, also known as CKD. With kidney disease, the nephrons of both kidneys simultaneously and steadily lose their ability to filter blood, allowing waste products such as creatinine and BUN to gradually build up in the bloodstream and important electrolytes to fall out of balance.

The most common cause of CKD is diabetes, which allows unused glucose to spill into the bloodstream in the form of high blood sugar, damaging the nephrons. The second most common cause of CKD is hypertension, which damages the capillary tangle of the glomeruli, rendering the filtration system ineffective.

Other causes of CKD include chronic kidney or urinary tract infections, autoimmune diseases (e.g., systemic lupus erythematosus), hereditary diseases (e.g., polycystic kidney disease), obstruction of urine flow by kidney stones or an enlarged prostate, vascular diseases and nephrotoxic medications like nonsteroidal anti-inflammatory medications and acetaminophen.⁵

Diagnosis: CKD

Because CKD is so pervasive and there is no cure, it is important to identify and begin treatment as early as possible to manage the disease and prevent patients from reaching ESRD, which precipitates dialysis or a kidney transplant. Patients at increased risk for CKD must be regularly screened for kidney damage, which can be accomplished with three basic tests: serum creatinine, urine albumin and blood pressure.⁵ Normal ranges for blood and urine tests can vary according to the individual lab processing the sample, the age of the patient and the patient’s gender — serum creatinine is expected to be lower in females than in males due to their smaller musculature. It is important to obtain and track test results to notice trends in kidney function.

When assessing blood pressure, it is important to know that hypertension is not only one of the leading causes of CKD but is also a complication of the disease — more than 50% of patients with CKD have concurrent hypertension. Uncontrolled hypertension places patients at increased risk that the CKD will worsen toward ESRD and also increases the mortality rate; because of this, most guidelines suggest that seated blood pressure taken in the office or clinic must be controlled to stay below 130/80 mm Hg.² However, recent research now identifies that this goal may not be feasible in older patients and may not save lives nor slow the progression of the disease; a target blood pressure ceiling of 140/90 mm Hg is sufficient, according to recent research.⁸

Other tests used to diagnose CKD include renal ultrasound, which may reveal structural abnormalities, such as the multiple cysts present in polycystic kidney disease; changes in size, with shrinking kidneys apparent in advanced CKD and enlarged kidneys apparent with obstructions; or tumors that present with primary cancers of the kidney. A plain X-ray of the abdominal area can reveal calcific deposits and radio-opaque stones in the kidneys, and a computerized (axial) tomography or magnetic resonance imaging scan can further define renal masses. In such cases, intravenous contrast dye is contraindicated, as processing the dye material places the kidneys at risk for acute renal failure.² If a suspicious mass is found, renal biopsy can be performed percutaneously.

Physical Effects

Although early CKD is virtually undetectable and asymptomatic, once kidney damage is established and waste products in the bloodstream start to accumulate, patients may begin to develop symptoms. As CKD steadily worsens, the kidneys increasingly struggle to maintain fluid and electrolyte balance and begin to lose their ability to concentrate urine, resulting in the increased need to urinate, often first occurring during the night (nocturia).⁴ With time, the kidneys also become less efficient at excreting phosphates, potassium and acids, and as the damage progresses, the GFR declines with a commensurate increase in serum creatinine and BUN.

The accumulation of creatinine and BUN are markers for other systemic changes that cause uremia, the increase of toxins in the blood. With uremia, symptoms of fatigue, malaise, headaches, muscle atrophy, nausea, dry skin, lower extremity edema, muscle cramps and a poor appetite may occur. If hypertension was not a predisposing factor to the CKD, it may develop as kidney function worsens. Most of these symptoms not only impair quality of life and the independent performance of daily functional tasks, but they can impact a patient’s ability to participate in rehabilitative care.

Patients with CKD typically experience significant levels of fatigue on a continuum that roughly parallels the stages of the disease, but fatigue is reportedly worse in older patients, females, patients receiving peritoneal dialysis, and those with lower levels of serum albumin, which occurs when small amounts of albumin leak through the renal glomeruli into the urine (microalbuminuria).⁹ Research shows that dense fatigue (fatigue that is chronic and unrelenting) and reduced muscle strength is also a direct result of renal-associated anemia, muscular atrophy, poor dietary intake and weight loss, and increasing inactivity.¹⁰ Such changes make it difficult for patients with CKD to participate in exercise programs, but exercise can provide an effective means to improving exercise tolerance and physical capacity in both adults and children with CKD at all stages of the disease.^10,11 Although it is generally better tolerated to introduce an exercise program before a patient needs to rely on dialysis, rehabilitation therapy to improve exercise capacity is found to improve quality of life even in patients in ESRD.¹²

It is thought that despite CKD, muscle strength and muscle bulk can be increased with resistance training, which contributes to improved physical functioning and decreased fatigue. Aerobic activities can increase maximal oxygen consumption, reduce hypertension and enhance mental health. But when an exercise program is first introduced to patients with CKD, it is important to begin at a very low level of exercise intensity and progress slowly to reduce the risk of muscle injury and to achieve compliance.¹³ Patients with CKD have a disadvantage in trying to improve their muscle strength because of the recommended low protein diet that is designed to help keep serum BUN levels under control; other disadvantages stem from the tendency of developing metabolic acidosis, which worsens muscle protein loss and slows bone metabolism.¹⁴ One clinical measurement of nutritional status and protein wasting is hand grip strength: In patients with Stage 3 through Stage 5 CKD, poor hand grip strength (approximately less than 20 kg in men and 10 kg in women) is predictive of worse renal outcomes and early mortality.¹⁵ Despite changes in muscle metabolism, patients with pre-dialysis CKD demonstrate the ability to increase their endurance, cardiovascular health and quality of life when exercising consistently for a 12-month period.¹⁶

Patients already receiving dialysis can become a captive audience and may be encouraged to exercise during the treatment, although these patients must be monitored carefully before, during and after physical exercise to ensure that hypotension does not develop: In a recent study, patients who exercised their leg muscles using an elastic resistance band twice a week during dialysis sessions were able to achieve significant improvements in the Timed Up and Go test and Tinetti test, and showed better scores in the six-minute walk test and single leg balance test than non-exercisers.¹⁷ In another study, patients who performed leg ergometry exercise during dialysis for 30 minutes exhibited less fatigue, a higher level of physical fitness and the ability to participate in more activities than controls.¹⁸ The best benefit of exercise may be that it appears to improve kidney function, perhaps by its positive effects on lipid metabolism, in as little as 12 weeks.¹⁹ Exercise therapy appears to improve the metabolic threshold, increase high-density lipoprotein cholesterol levels, and reduce triglyceride levels, all while improving eGFR.¹⁹ Overall, the frequency and/or duration of physical activity should be advanced as tolerated, as exercise may improve quality of life and minimize the catabolic effects of a low-protein diet on the muscles.

Medical Management

Treatment for CKD is typically multifactorial, and it involves controlling underlying disorders (e.g., diabetes and hypertension), diet modification, vitamin supplementation, treatment for anemia when present, dialysis when necessary and renal transplantation if indicated. Patients with diabetes must adhere to strict control of blood sugars, and those with hypertension should receive the appropriate medication to keep blood pressure within the recommended parameters. Patients with diabetes are encouraged to aim for a target A1c reading of 7% or below.²⁰ For those with hypertension, some angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors serve a double benefit in that they not only reduce hypertension but can also reduce the rate of CKD progression in certain patients. Because the failing kidneys are less able to excrete sodium, sodium intake should be limited to less than 2.4 g/day, and must be even more tightly controlled as the patient’s blood pressure and hydration status warrants.²⁰

In terms of nutritional modification, it has long been thought that patients with CKD should adhere to a very low protein diet (between 0.6 g to 0.8 g of dietary protein per kg body weight per day) to slow GFR decline and improve microalbuminuria, but patient compliance with this approach varies. In particular, patients with diabetes often must ingest only a moderately restricted protein diet (0.8 g to 0.9 g of protein per kg body weight per day) or risk protein-energy malnutrition, worse fatigue, loss of lean body mass and unintended weight loss.²⁰

For cardiac health, serum potassium levels must be monitored closely, as they can directly impact cardiac function — potassium that is too low (hypokalemia) or too high (hyperkalemia) can result in cardiac arrhythmias and sudden death. Sodium restriction becomes a more critical necessity if a patient with CKD has developed heart failure. Although the evidence is still being gathered on the direct effect of fish oils and omega-3 fatty acid supplementation on kidney function, there is a beneficial effect on improved lipid profiles in patients with CKD; however, excessive fish oil may impair blood coagulation. Patients with high cholesterol may benefit from statins to improve their cardiovascular risk profiles.

Of great importance is dietary control of phosphorus, as elevated phosphorus levels (hyperphosphatemia) are associated with increased morbidity and mortality. Keeping phosphorus under control also helps prevent bone disease, secondary hyperparathyroidism and soft tissue calcification. Current recommendations are 800 mg to 1,000 mg of phosphorus per day. If the patient is unable to successfully restrict phosphorus intake, phosphorus binders may be added to the diet at mealtimes to prevent excessive phosphorus from being absorbed into the body.²⁰ Calcium intake may also need to be restricted to not more than 2,000 mg/day to prevent leaching of calcium from the bones. Vitamin D must be supplemented as needed to maintain the adequate serum levels (> 30 ng/mL) needed for healthy bones.

To maintain healthy red blood cell production, patients with CKD-related anemia will need supplemental iron when serum ferritin falls below 100 ng/mL and transferrin saturation drops below 20%.²⁰ Vitamin C is recommended to enhance iron absorption, but it should not be over-supplemented secondary to the risk of forming calcium oxalate kidney stones. Vitamin B12 and folic acid supplementation may be necessary if the mean corpuscular volume is found to be > 100 ng/mL.²⁰

As nutritional factors are identified and treated, the underlying CKD anemia may resolve, which helps reduce fatigue and improves the patient’s ability to exercise. But when the decline in kidney function results in significantly impaired secretion of erythropoietin hormone, no amount of nutritional supplementation will solve the problem; patients will need to begin synthetic erythropoietin hormone injections, either epoetin alfa (Procrit) or darbepoetin (Aransep), based on the patient’s blood hemoglobin level. Target hemoglobin levels are 11 g/dL to 12 g/dL, to be attained with extreme caution and by careful calibration of the dose of erythropoietin hormone, as boosting the hemoglobin level higher than the target is directly linked to an increased risk of death by cardiovascular events, such as heart attack, stroke, blood clots and heart failure.

Stage 5 CKD, or ESRD, occurs when the GFR has slowed to < 15 mL/min/1.73 m². It is at this point that patients will need to receive either dialysis or a kidney transplant to survive. However, the mortality rate for patients receiving dialysis is high: Whereas the life expectancy of a healthy 60-year-old person is 20 years, a patient of the same age receiving dialysis can expect to live only four more years.² Regardless of which stage of CKD the patient is experiencing, the leading cause of death in all stages is cardiovascular complications, a fact that makes the ability for the patient to exercise paramount.^21,22 Benefits of exercise can therefore not only be lifesaving, but also contribute to increased physical functioning and the commensurate reduction of one of the most bothersome symptoms reported by patients with CKD — fatigue.

Ambassadors for Exercise

Physical therapists are specialists in helping people with all manner of diseases and conditions improve their neuromuscular capabilities, strength and endurance, and they can help patients with CKD improve their physical functioning just like any other patient group. As therapists work more frequently with this increasingly common patient population to advance strength and endurance and to facilitate functional independence, patients with CKD can only benefit. Although fatigue and weakness from progressive CKD can make patients initially reluctant to engage in physical activity, therapists can become advocates who encourage individualized exercise programs that will in turn reduce fatigue levels and enhance independent functional mobility, restoring quality of life.

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