Restlessness Là Gì

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StatPearls . Treasure Isl& (FL): StatPearls Publishing; 2021 Jan-.


Continuing Education Activity

Uremia is a clinical condition associated with worsening renal function. It is characterized by fluid, electrolyte, hormonal, và metabolic abnormalities. Uremia most commonly occurs in the setting of chronic and end-stage renal disease, but may also occur as a result of adễ thương kidney injury. This activity nhận xét the evaluation & management of uremia & highlights the role of interprofessional team members in collaborating to lớn provide well-coordinated care & enhance outcomes for affected patients.

Identify the leading causes of uremia.
Ređiện thoại tư vấn the pathophysiology of uremia.
Summarize the evaluation of a patient with suspected uremia.
Employ interprofessional team strategies for improving care coordination và communication to advance the treatment of uremic patients.
Access không tính tiền multiple choice questions on this topic.


Uremia, a clinical condition associated with worsening renal function, is characterized by fluid, electrolyte, and hooc môn imbalances in addition to metabolic abnormalities. The literal meaning of uremia is “urine in the blood,” & the condition develops most commonly in the setting of chronic và end-stage renal disease (ESRD), but may also occur as a result of acute kidney injury.

Putative uremic toxins include parathyroid hormone, macroglobulin, advanced glycosylation over products, and beta2 microglobulin, though no specific uremic toxin has been identified as responsible for all clinical manifestations of uremia.<1><2><3>


Kidney disease can result from some conditions ranging from primary renal disorders, for example, IgA nephropathy, focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, polycystic kidney disease) khổng lồ systemic disorders that can lead lớn renal damage. Systematic disorders can include diabetes mellitus, lupus, multiple myeloma, amyloidosis, Goodpasture disease, Thrombotic thrombocytopenic purpura, or hemolytic uremic syndrome.

The leading cause of ESRD in the United States is diabetes. Additional causes, listed in order of decreasing incidence, include hypertension, glomerulonephritis, interstitial disease, cystitis, và neoplasms.

Uremia may also result from axinh đẹp kidney injury if the injury involves a sudden increase in urea or creatinine.<4><5><6>


It is difficult to determine the exact prevalence of uremia in the United States because patients with ESRD typically begin dialysis before the development of uremic symptoms. Uremic symptoms typically arise once creatinine clearance is less than 10mL/min or 15mL/min in the case of diabetic patients.

There are approximately 354 out of a million individuals diagnosed with end-stage renal disease each year. This number continues to rise as the life expectancy of those with ESRD is increasing. Improved survival in patients with diabetes or cardiovascular disease, in addition lớn increased access to renal therapy, has resulted in the highest increase in the incidence of ESRD in patients aged 75 years or above sầu. On the other hvà, the number of individuals under the age of 60 with ESRD is declining, except for African American or Native American patients with diabetic ESRD.

The majority of patients with ESRD are Caucasian (59.8%), the remainder is African American (33.2%), Asian (3.6%) or Native American (1.6%). The incidence of ESRD among mỏi blaông xã individuals, however, is 3.7 times higher than it is among muốn the trắng population. Similarly, the incidence aước ao Native sầu Americans is 1.8 times greater than it is among whites.

Additionally, minority populations tkết thúc to initiate dialysis care at a later point in the course of renal disease, usually once there is already a significant decline in glomerular filtration rate (GFR). It is unknown, however, whether racial or ethnic background has an effect on predisposition khổng lồ the development of uremic symptoms.

Men are 1.2 times more likely than women lớn develop ESRD, though women are 1.7 times more likely to delay initiation of dialysis. Women are also more prone to lớn the development of uremic symptoms at lower creatinine levels, due khổng lồ the decreased amount of muscle mass & baseline serum creatinine levels that they have.<7><8><9>


When the kidneys are not functioning properly, dysfunction can occur in acid-base homeostasis, fluid & electrolyte regulation, hormone production và secretion, & waste elimination. Altogether, these abnormalities can result in metabolic disturbances and ultimately conditions such as anemia, hypothyroidism, hypertension, acidemia, hyperkalemia, và malnutrition.

Anemia associated with kidney disease is typically normocytic, normochromic, and hyperproliferative. It occurs as a result of decreased erythropoietin production by the failing kidneys. This is associated with a glomerular filtration rate (GFR) of less than 50 mL/min (unless the patient has diabetes, then they may have anemia at GFR less than 60mL/min) or when serum creatinine is greater than 2 mg/mL.

Additional factors associated with chronic kidney disease alone may additionally contribute khổng lồ the development of anemia. These include iron or vitamin deficiencies, hyperparathyroidism, hypothyroidism, or a decreased lifespan of red blood cells.

The buildup of uremic toxins in the blood may additionally contribute to the development of coagulopathy as a result of reduced platelet adhesion khổng lồ the vascular endothelial wall, increased platelet turnover, and a slightly reduced absolute number of platelets. A common finding in patients with ESRD is bleeding diathesis which is the increased susceptibility khổng lồ bleeding and hemorrhage.

Another major metabolic complication associated with uremia & ESRD is acidosis because renal tubular cells are the primary regulators of acid-base homeostasis in the toàn thân. As kidney failure progresses, there is decreased secretion of hydroren ions and impaired excretion of ammonium, & eventually buildup of phosphate and additional organic acids (e.g., lactic acid, sulfuric acid, hippuric acid). In turn, the resulting increased anion-gap metabolic acidosis may lead lớn hyperventilation, lethargy, anorexia, muscle weakness, and congestive heart failure (due to lớn a decreased cardiac response).

Hyperkalemia may also occur in the setting of both adễ thương or chronic renal failure. This condition becomes a medical emergency when serum potassium reaches a cấp độ greater than 6.5 mEq/L. This level may be exacerbated with excessive sầu potassium intake or use of certain medications (e.g., potassium-sparing diuretics, angiotensin-converting enzymes (ACE) inhibitors, angiotensin-receptor blockers, beta blockers, NSAIDs). Acidosis resulting from renal failure may additionally contribute to the development of hyperkalemia.  

Hypocalcemia, hyperphosphatemia, and elevated parathyroid hormone levels may additionally occur as a result of renal failure. Hypocalcemia occurs due to lớn decreased production of active sầu Vi-Ta-Min D (1,25 dihydroxyVi-Ta-Min D) which is responsible for gastrointestinal (GI) absorption of calcium and phosphorus và suppression of parathyroid hormone excretion. Hyperphosphatemia occurs because of impaired phosphate excretion in the setting of renal failure. Both hypocalcemia & hyperphosphatemia stimulate hypertrophy of the parathyroid gland & resultant increased production and secretion of parathyroid hormone. Altogether, these changes in calcium metabolism can result in osteodystrophy (renal bone disease) & may lead to lớn calcium deposition throughout the body (i.e., metastatic calcification).

Declining renal function can result in decreased insulin clearance, necessitating a decrease in dosage of antihyperglycemic medications lớn avoid hypoglycemia. Uremia may also lead lớn impotence in men or infertility (e.g., anovulation, amenorrhea) in women as a result of dysfunctional reproductive hooc môn regulation.

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The buildup of uremic toxins may also contribute to uremic pericarditis, và pericardial effusions leading to abnormalities in cardiac function. Together with metastatic calcification as a result of declining renal function, these may contribute lớn worsening of underlying valvular dysfunction or suppression of myocardial contractility.<10><11>

History và Physical

Symptomatic uremia tends khổng lồ occur once creatinine clearance decreases below 10 mL/min unless kidney failure develops acutely, in which case, some patients may become symptomatic at higher clearance rates.

Patients presenting with uremia typically complain of nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, or changes in mental status. The clinical presentation of uremia can be explained by the metabolic disturbances associated with the condition.

Fatigue as a result of anemia is considered one of the major components of the uremic syndrome. 

Patients with a history of diabetes may report improved glycemic control but are at a greater risk of developing hypoglycemic episodes as kidney function worsens.

Hypertension, atherosclerosis, valvular stenosis và insufficiency, chronic heart failure, and angina may all develop as a result of a buildup of uremic toxins & metastatic calcification associated with uremia and ESRD.

Occult GI bleeding as a result of platelet abnormalities may present with nausea or vomiting. Uremic fetor, ammonia or urine-lượt thích odor of the breath, may also occur in uremic patients.


A diagnosis of renal failure is based on abnormalities in GFR or creatinine clearance.<12>

It is important lớn determine whether a patient presenting with uremic symptoms is experiencing acute or chronic renal failure, as axinh đẹp kidney injury is reversible. Laboratory studies to evaluate for abnormalities in hemoglobin, calcium, phosphate, parathyroid hormone, albumin, potassium, and bicarbonate in addition khổng lồ urinalysis (with microscopic examination) will help point towards any potential abnormalities.

A 24-hour urine collection may provide insight to lớn both GFR & creatinine clearance, though this method is both burdensome & often inaccurate. Alternatively, a nuclear medicine radioisotope (iothalamate) clearance assay may be used to measure GFR. However, this thử nghiệm is also time-consuming và expensive relative sầu lớn the Cockcroft-Gault formula or the Modification of Diet in Renal Disease formula <(GFR (mL/min/1.73 m) = 175 x (S) times (Age) times (0.742 if female) or times (1.212 if African American)> that are often used instead.

As per the National Kidney Foundation, patients presenting with chronic kidney disease are staged based on the estimated GFR (creatinine clearance) as calculated by the Modification of Diet in Renal Disease formula.

A renal ultrasound may be useful khổng lồ determine the kích cỡ và shape of the kidneys, & to lớn evaluate for hydronephrosis or ureteral and/or bladder obstruction. This may occur as a result of kidney stones, neurosúc tích abnormalities, trauma, pregnancy, prostate enlargement, retroperitoneal fibrosis, abdominal tumors (secondary khổng lồ cervical or prostate cancers) or additional structural abnormalities. Early diabetic nephropathy, multiple myeloma, polycystic kidney diseases, and glomerulonephritis associated with làm giảm hệ miễn dịch cấp tiến (HIV) are all associated with enlarged kidneys on ultrasound.  Smaller kidneys are indicative of more chronic, irreversible changes as a result of long-standing kidney disease, ischemic nephropathy, or hypertensive sầu nephrosclerosis.

If a patient presents with significant alterations in mental status, a brain computed tomography (CT) scan may be warranted. Uremic patients with a blood urea nitrogen (BUN) màn chơi greater than 150 mg/dL to 200 mg/dL are also at an increased risk of developing spontaneous subdural hematomas. Given the increased risk of bleeding và hemorrhage in uremia (especially in the setting of a fall or trauma), a CT scan of both the brain & abdomen may additionally be considered. An abdominal CT scan might help further elucidate the underlying cause of hydronephrosis if it was found on ultrasound without any obvious etiology.

Finally, magnetic resonance imaging (MRI) may be considered lớn assess for renal artery stenosis or thrombosis, or aortic & renal artery dissection- all potentially reversible causes of renal failure.

A renal biopsy may be helpful in determining reversibility or treatability of the renal injury, and may ultimately be required lớn make an accurate diagnosis of adễ thương kidney injury or chronic kidney disease. However, a biopsy should not be performed in the case of small kidneys because of the associated comorbidities và increased risk of bleeding. 

Treatment / Management

Dialysis is indicated in a patient with symptomatic uremia (e.g., nausea, vomiting, hyperkalemia, metabolic acidosis) that is not treatable my medical means, and should be initiated as soon as possible, regardless of the patient’s GFR.<13><14><15>

Patients presenting with a uremic emergency (e.g., hyperkalemia, acidosis, symptomatic pericardial effusion, or uremic encephalopathy) require emergent dialysis which should be initiated gently to lớn avoid dialysis disequilibrium syndrome (neuroxúc tích symptoms secondary khổng lồ cerebral edema occurring during or shortly after the initiation of dialysis).

Ultimately, the best renal replacement therapy is renal transplantation, although practitioners may also consider long-term hemodialysis & peritoneal dialysis. Renal transplantation is associated with improvements in both survival and quality of life, và should be considered early (before the need for dialysis) as the waiting list for transplantation is often longer than two to three years.

Iron replacement should be initiated in patients with anemia of chronic kidney disease và underlying iron deficiency (as long as serum ferritin is greater than 100 mcg/mL). This can be done with dialysis treatments, or as oral therapy, if dialysis has not yet been initiated. Erythropoietic stimulating agents, such as erythropoietin or darbepoetin, may additionally be used in low doses (due to lớn the increased risk of cardiovascular mortality) once hemoglobin levels reach below 10 g/dL.

Hyperparathyroidism & associated or isolated hypocalcemia & hyperphosphatemia can be treated with oral calcium carbonate or calcium acetate, oral Vi-Ta-Min D therapy, và oral phosphate binders (e.g., calcium carbonate, calcium acetate, sevelamer or lanthanum carbonate).

A dietitian should be consulted if dietary alterations are being considered.  Patients with chronic kidney disease should reduce potassium, phosphate and sodium intake lớn 2 g to 3 g, 2 g, and 2 g per day of each, respectively. Though there is some conflicting evidence regarding protein intake in patients with kidney failure, the current low-protein diet recommendations before initiation of dialysis are 0.8 g to lớn 1 g of protein/kg of weight per day with an added gram of protein for each gram of protein lost in the urine in patients with nephrotic syndrome.

A low-protein diet is not recommended in patients with advanced uremia or malnutrition, as this type of diet can result in worsening of malnutrition & has been associated with increased risk of mortality with the initiation of dialysis.

Patients with a creatinine clearance of less than đôi mươi mL/min should avoid excessive potassium intake và use certain medications with caution (e.g., potassium-sparing diuretics, angiotensin-converting enzymes (ACE) inhibitors, angiotensin-receptor blockers, beta blockers, NSAIDs).

Due lớn the buildup of uremic toxins và potentially increased risk of bleeding & hemorrhage, extra care needs khổng lồ be taken when prescribing oral anticoagulants or antiplatelet medications to lớn patients who have sầu ESRD.

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Finally, nephrotoxic medications (e.g., NSAIDs, aminoglycoside antibiotics) should be avoided in all patients with renal disease.  To avoid nephrotoxiđô thị, N-acetylcysteine may be administered before administration of intravenous contrast for radiologic imaging, although alternative sầu modes of imaging like MRI should be considered in these patients, to avoid the risk of adễ thương kidney injury altogether.<16>