The kidney maintains a vast array of integral functions within the human body. Therefore the treatment for chronic kidney disease (CKD) is multifactorial. Some of the most common and necessary treatments for renal disease include regulation of bone and electrolyte abnormalities, hypertension and anemia. CKD is divided into five stages, with higher numeric values reflecting more advanced disease progression.
Preventing Progression of Proteinuria:
Treating CKD patients with renin-angiotensin aldosterone system (RAAS) inhibitors is a current strategy to slow the progression of CKD. Reno-protective benefits happen through vasodilation of the efferent arteriole, which in turn lowers glomerular pressure. Two drug classes used to inhibit the RAAS system are angiotensin conversion enzyme inhibitors (ACEIs) such as lisinopril or benazepril and angiotensin receptor blockers (ARBs) such as losartan or valsartan. These agents usually require checking of potassium and serum creatinine one week after initiation as they can actually worsen kidney injury when hypoperfusion such as renal artery stenosis is the etiology of CKD. Non-dihydropyridine calcium channel blockers also have antiproteinuric effects. The two agents within this drug class are diltiazem and verapamil.
Hypertension (HTN)
CKD patients being treated for HTN usually have a goal blood pressure (BP) between < 120-130 /< 80-90mmHg. Diuretics such as furosemide are helpful BP reducing agents. However, the severity of BP dysregulation from renal dysfunction usually requires multiple medications to attain BP goals. Once again, ACEIs or ARBs are helpful. Other common drug classes for add-on therapy include beta blockers, alpha blockers, vasodilators and calcium channel blockers depending on the patient’s comorbidities and medication tolerability.
Anemia
Healthy renal function is required for generation of red blood cells through erythropoietin synthesis. Therefore, iron and erythropoietin stimulating agent (ESA) therapy are needed as CKD progresses and patients are subjected to inevitable anemia. Oral iron is poorly absorbed, so it is common to administer intravenous iron to patients, with caution, to prevent transfusion reactions and cumulative iron overload. ESA therapy agents such as darbepoetin alfa and epoetin alfa have a goal of keeping a dialysis patient’s hemoglobin > 10mg/dL but less than 13mg/dL. Blood transfusions remain last line therapy for anemia in CKD patients.
Electrolyte Disturbances: Acidosis and Hyperkalemia
Acidosis in advanced CKD is common and will negatively affect bone density and muscle strength. Oral sodium bicarbonate replacement is often necessary. Acidosis also contributes to hyperkalemia which is unfortunately common with CKD due to the reduced glomerular filtration rate (GFR) and common medications such as RAAS inhibitors. Hyperkalemia is considered a medical emergency when levels are > 6mmol/L due to the risk of fatal cardiac arrhythmias. Intravenous calcium, glucose, dextrose, beta agonists and even dialysis are common therapies for hyperkalemia in acute situations. Avoidance of potassium-sparing medications and adherence to a low potassium diet longitudinally are both important tools for patients to prevent severe hyperkalemia.
Bone Disease /Mineral Disorders:
Hyperparathyroidism and Hypercalcemia
Renal dysfunction causes excess parathyroid hormone (PTH) release in the systemic circulation and unfortunately moves calcium from the bones into the bloodstream. Calcitriol, calcimimetics and vitamin D analogues are initiated when hyperparathyroidism is severe with a goal of keeping iPTH levels 2 to 9 times the upper limit of an assay’s normal range. Despite these efforts, a surgical parathyroidectomy is sometimes required. Left untreated, high calcium can deposit into the blood vessels and/or organs which is a significant mortality risk for CKD patients.
Hyperphosphatemia and vitamin D
An additive insult to the bones lies in the fact that Vitamin D can not be activated as the kidney’s progressively fail and phosphorus is no longer normally excreted. Oral phosphorus binders are dosed with snacks and meals with a goal of lowering phosphorus to normal levels. Adhering to a low phosphorus diet remains of utmost importance even with phosphate binder therapy.
Lifestyle (Nutrition/Exercise/Substance abuse):
Sodium intake < 2g/day aids anti-hypertensive efforts in the CKD patient. Low phosphorus containing diets include avoiding canned and preserved foods, dairy products and limiting protein portion sizes. Smoking cessation should be completed and is often required for transplantation as well as moderate consumption of alcohol and abstinence from illicit substances. Moderate-intensity exercise for at least 150 minutes per week is preferred.
In summary, chronic kidney disease will affect many organ systems within the body. Understandably, nephrologists routinely work with other specialists and the patient’s primary care team for best patient care management. Progression leads to end stage renal disease (ESRD) which is treated with either dialysis and/or renal transplant. The journey from CKD to ESRD has differing lengths, even when patients share the same diagnosis. Investigations further examining the role of genetics and environmental factors within chronic kidney disease are ongoing.
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