Managing kidney disease.
The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF KDOQI) and the Kidney Disease: Improving Global Outcomes (KDIGO) foundations have developed clinical practice guidelines, which vary slightly. The KDIGO guidelines are the most up-to-date but refer to sections of the NKF KDOQI that are still relevant. Recent updates to the KDIGO guidelines were undertaken to help with staging the disease process and determining how aggressively to treat the disease.
The glomerular filtration rate (GFR) is the standard used to estimate the degree of renal impairment, follow the course of the disease and assess the patient's response to therapy. The kidneys can respond to damage by increasing the filtration rate in the remaining normal nephrons (adaptive filtration), which will result in near normal serum creatinine and electrolyte levels. Because of adaptive filtration, patients may not experience any signs or symptoms until their renal disease has progressed to the later stages. Therefore, it is important to remember that not all patients will progress at the same rate or have the same signs or symptoms.
The first step is to determine the cause of the renal dysfunction, and then determine if the cause is reversible. CKD treatment involves removal of an offending agent, tight control over contributing disease states and treatment of the complications of renal dysfunction.
Several agents may cause acute kidney damage, such as nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting-enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers (ARBs), radiographic contrast media and some antibiotics. When these medications are initiated, kidney function should be monitored closely. Consideration should be given to discontinuation at the first signs of kidney stress or damage, or the medications should be avoided altogether in patients who already have kidney damage.
Obtaining therapeutic goals in patients with confounding disease states (such as diabetes and hypertension) will help slow the progression to kidney damage. Patients should be informed of the role other diseases have on CKD progression and how good control over other diseases will positively affect their kidney disease. If the cause is not reversible or the damage is permanent, treating the symptoms is prudent.
Treatment of complications of renal dysfunction depends on the complications that the patient is experiencing. Unique complications of renal dysfunction include hyperkalemia, metabolic acidosis, hyperphosphatemia, bone mineral disorders and anemia. High levels of potassium are related to a high potassium diet (including the use of potassium salt substitutes), increased tissue breakdown, hyperaldosteronism (which may be related to ACE-I or ARB use), use of certain diuretics or oliguria. Monitor potassium levels and remove the offending agent, if possible.
Metabolic acidosis occurs when the body is producing too much acid and cannot remove it. Monitor the bicarbonate level and, if needed, initiate sodium bicarbonate. Hyperphosphatemia occurs from a reduction in the filtered phosphate load and results in cardiovascular disease risk. Treatment for hyperphosphatemia includes dietary restriction to food with high biological value protein only (meat and eggs) and the introduction of phosphate binders.
Dietary restriction is absolutely necessary because of the limited binding capacity of the phosphate binders. All binders should be taken with food to bind dietary phosphate. Calcium salts (carbonate and acetate) are the first line agents because of their binding capacity and lower cost. Sevelamer binds phosphate through ion exchange. A newer version of sevelamer--a carbonate versus the original hydrochloride --was created to lessen the gastrointestinal side effects and help better maintain bicarbonate in the normal range. Sevelamer is not absorbed and can be used in addition to or instead of calcium binders.
Lanthanum is another phosphate binder that forms a water-insoluble complex with phosphate. All of the phosphate binders can cause constipation and should be separated from other medications due to possible interactions. Hypocalcemia, hyperphosphatemia, decreased vitamin D levels and hyperparathyroidism can contribute to bone mineral disorders related to CKD.
When calcium levels fall, the parathyroid gland releases parathyroid hormone, and blood calcium levels rise again. If there is not enough calcium available in the blood, the body will steal it from the bones, resulting in a bone mineral disorder. Vitamin D analogs such as calcitriol, paricalcitol and doxercalciferol work to provide the vitamin D needed to absorb calcium and correct hyperparathyroidism. A product with a different mechanism of action, cinacalcet, increases the sensitivity of the calcium-sensing receptor on the thyroid gland, which through a cascade of events prevents bone-related metabolism disorders.
Last but not least, anemia can occur as a result of blood loss, insufficient iron stores or reduced erythropoietin production. Oral or IV iron may be needed to return iron levels to normal, or erythropoietic agents may be initiated to avoid a transfusion.
Prevention is the key to kidney health. Healthy lifestyle choices and regular checkups can prevent or significantly delay kidney disease. If kidney disease has already occurred, maintaining a healthy lifestyle and treating the complications will help slow or prevent the progression to end-stage renal disease.
Tara Muzyk, Pharm.D., is a clinical pharmacy writer based in Lebanon, Pa.