Hypertension High blood pressure affects over 80% of chronic kidney disease patients and can be both a cause and consequence of CKD. Hy- pertension is often a result of volume overload and salt retention, due to the reduced ability of the kidneys to remove excess fluid and salts. In addition, the renin– angiotensin–aldosterone system, which plays a significant role in regulating blood pressure, is lo - cated in the kidneys and can be overactivated in chronic kidney Hyperkalemia Hyperkalemia can develop in patients with chronic kidney disease due to a reduced ability to excrete potassium through the kidneys, particularly in patients with GFR less than 20–25 mL/min/1.73m 2 . High potassium levels can also be seen in earlier stages of chronic kidney disease, particularly in patients who eat a potassium-rich diet or those with low aldosterone levels. When kidney function declines, the hormone aldosterone increases excretion of potassi- um in the gastrointestinal tract, but this mechanism is often insuf- ficient to maintain normal potassium levels in patients with severe or end-stage kidney disease (Rosenberg, 2021). Dyslipidemia Abnormal lipid levels are common in chronic kidney disease pa- tients, particularly hypertriglyceridemia. All patients with CKD should be evaluated for dyslipidemia. Since high lipid levels can Metabolic acidosis Acid–based balance is maintained by the renal excretion of acids produced daily in the body. Chronic kidney disease can cause a decreased production of ammonia in the proximal tubules, which aids in the excretion of acids produced by the body by forming ammonium. Lower levels of ammonia production led to increased acid levels. Additionally, accumulation of phosphates, sulfates, and organic anions can also contribute to increased acid levels (Kovesdy, 2021; Rosenberg, 2021). Anemia Anemia often begins early on in chronic kidney disease and pro- gresses in occurrence and severity as renal impairment progress- es, affecting about 8% of CKD stage 1 patients and nearly 53% of CKD stage 5 patients. Decreased renal production of erythro- poietin in CKD patients reduces stimulation of the bone marrow to produce red blood cells, leading to reduced oxygen-carrying capacity of the blood and reduced red blood cell survival. Uremia, or buildup of waste products in the blood, can also cause platelet dysfunction which increases the risk of bleeding (Arora, 2021). Anemia is evaluated in CKD patients when the hemoglobin level is less than 12 g/dL in females and 13 g/dL in males, and other causes of anemia are excluded, such as iron, folate, or vitamin B12 deficiency. Anemia is often associated with the following clinical observations (Arora, 2021; Rosenberg, 2021): ● Decreased exercise capacity. Bone and mineral disease Bone and mineral disorders are a frequent complication of chronic kidney disease, due to the altered balance of mineral levels in the body, and can be collectively referred to as chronic kidney dis- ease bone and mineral disease (CKD-BMD). In healthy individuals, phosphate and calcium levels are carefully balanced in the body and have opposing effects on each other—increases in calcium levels cause decreases in phosphate levels, and vice versa. Dietary calcium and phosphate are absorbed through the small intestine and are filtered and reabsorbed through the kidneys. Phosphate binds with calcium for storage in the bone, which serves as a res- ervoir to provide additional phosphate and calcium when levels are low. To maintain calcium and phosphate in balance, parathy- roid hormone (PTH) aids in lowering blood phosphate levels and increasing blood calcium levels. Activated vitamin D, known as calcitriol , helps to raise blood phosphate and calcium levels (DiP- iro et al., 2019; Rosenberg, 2021).
disease. Since hypertension can cause chronic kidney disease, adequate control of blood pressure and suppression of the renin– angiotensin–aldosterone system are critical to preventing disease progression and reducing cardiovascular complications. The use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are often recommended for this purpose (Rosenberg, 2021). Preventative measures can be applied to patients with CKD to avoid hyperkalemia. Initiation of a low-potassium diet, with restric- tion between 1,500 and 2,700 mg/day, can reduce the amount of potassium available for absorption. Avoiding medications that increase potassium levels such as nonsteroidal anti-inflammatory agents can also be beneficial. Potassium levels should be closely monitored in CKD patients at risk of hyperkalemia (Rosenberg, 2021).
increase cardiovascular risk and cause atherosclerosis, treatment may be required, depending on the level of severity and the pa- tient’s underlying cardiovascular risk (Rosenberg, 2021).
Metabolic acidosis, or high blood acid levels, can occur in late- stage chronic kidney disease. Metabolic acidosis can negative- ly impact protein balance, leading to reduced protein creation and processing and causing protein–energy malnutrition, muscle weakness, and a loss of lean body mass. Since bone can act as a buffer when blood acid levels are high, metabolic acidosis can also lead to bone mineral loss. Metabolic acidosis is associated with higher mortality and more rapid disease progression among CKD and ESRD patients (Kovesdy, 2021; Rosenberg, 2021). ● Fatigue. ● Reduced immune and cognitive function. ● Cardiovascular disease development, leading to increased cardiovascular mortality. ● Development or worsening of heart failure. ● Decreased quality of life. The KDIGO Work Group suggests checking hemoglobin levels when clinically indicated, and at least annually in CKD stage 3 patients, at least biannually in CKD stages 4 and 5 patients, and at least quarterly in patients on dialysis in patients not already di- agnosed with anemia. For those patients diagnosed with anemia, hemoglobin levels should be checked when clinically indicated, at least quarterly in CKD stages 3 to 5 patients, and monthly in patients on hemodialysis (KDIGO Work Group, 2013; Rosenberg, 2021). Patients with chronic kidney disease experience increased secre- tion of parathyroid hormone early in the course of chronic kidney disease, around the time the GFR drops below 60 mL/min/1.73m 2 . This increase in PTH helps to maintain normal blood calcium and phosphate levels. However, when the GFR falls to below 30 mL/ min/1.73m 2 , the kidneys can no longer keep up with excretion of excess phosphate, which results in hyperphosphatemia. High phosphate levels then trigger more release of parathyroid hor- mone, contributing to high parathyroid levels, or hyperparathy- roidism (DiPiro et al., 2019; Rosenberg, 2021). Vitamin D levels are reduced in CKD patients due to reduced ac- tivation of vitamin D in the kidneys. This results in a reduction in calcium absorption from the small intestine, contributing to lower blood calcium levels, as well as a decrease in bone uptake of cal- cium. When phosphate levels are high, calcium can precipitate
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