Uremia

Japanese: 尿毒症

(7) Uremia
Concept In patients with chronic kidney disease (CKD), the renal function gradually declines and although there were no symptoms in the early stages, when the glomerular filtration rate (GFR) progresses to <30 mL/min and renal failure, chronic symptoms of uremia such as hypertension, hyperkalemia, renal anemia, peripheral neuropathy, renal osteodystrophy, and metabolic acidosis are observed. Furthermore, when the GFR reaches <5 mL/min and the patient reaches end-stage renal failure, acute symptoms appear. Symptoms of uremia include central nervous system symptoms such as anorexia, nausea, vomiting, pericarditis, impaired concentration, convulsions, and coma. There is no direct correlation between the absolute values of blood urea nitrogen (BUN) and creatinine (Cr) and the onset of these symptoms. Symptoms of uremia may appear even when BUN or Cr is low, and conversely, symptoms may not appear even when BUN or Cr is high. In any case, if acute symptoms of uremia appear, dialysis or kidney transplantation is necessary to prolong life. Not all CKD patients develop progressive kidney damage; the cause of kidney failure varies according to the underlying disease, comorbidities, treatment, socioeconomic status, genetics, and ethnicity.
Pathogenesis: Most of the final metabolic products of nitrogen compounds, such as BUN, Cr, and uric acid, are excreted by the kidneys, and a decrease in GFR leads to azotemia. Traditionally, uremia was thought to result from the abnormal accumulation of metabolic products of nitrogen compounds, and these substances were collectively called uremic toxins. Recently, uremic toxins have been classified into small molecular weight substances, medium molecular weight substances, and protein-bound substances, and the normal values of each substance and the values in a uremic state are becoming clear. The pathology of uremia is thought to be caused by all functional disorders controlled by the kidney, and is related to many factors such as water and electrolyte abnormalities, metabolic acidosis, increased production of parathyroid hormone, active vitamin D deficiency, calcium and phosphorus metabolic disorders, and decreased production of erythropoietin.
Clinical symptoms
Symptoms and CountermeasuresClinical symptoms of uremia are broadly divided into chronic and acute symptoms. Chronic symptoms are seen in a state of renal failure with a GFR of 30 mL/min or less. Acute symptoms are seen in end-stage renal failure or acute renal failure when the GFR drops to 5 mL/min or less and rapid and severe azotemia appears. This can be fatal, but can be corrected with dialysis therapy.
1) Chronic uremia symptoms:
Chronic uremia symptoms appear when the GFR falls below 30 mL/min, and include renal anemia due to decreased erythropoietin production, secondary hyperparathyroidism due to impaired vitamin D activation, and hypertension and congestive heart failure due to increased extracellular fluid volume caused by impaired sodium excretion. A typical symptom with an unclear mechanism of onset is peripheral neuropathy.
a) Changes in urine: In chronic renal failure, osmotic diuresis, sodium diuresis, and renal tubular damage cause a decrease in the ability to concentrate and dilute urine, resulting in isotonic urine, but oliguria is rare until the end of the disease. Nocturnal urination begins at this stage. Extreme salt restriction or administration of diuretics during this stage can cause a decrease in extracellular fluid volume and GFR.
b) Cardiovascular symptoms:
i) Hypertension: Hypertension frequently occurs during this stage. The causes of hypertension can be broadly divided into volume-dependent hypertension and hypertension due to activation of the renin-angiotensin system (RAS), but abnormalities in the antihypertensive system, such as nitric oxide, prostaglandins, kallikrein, and kinins, are also involved. Hypertension is not only a factor in the progression and aggravation of renal failure, but also contributes to the progression of arteriosclerosis and is the greatest risk factor for cerebrovascular and cardiovascular complications. RAS inhibitors are useful for treating blood pressure associated with CKD and are the first-choice drug. For volume-dependent hypertension, loop diuretics are added in CKD stages 3 and above. Furthermore, calcium channel blockers are added if cerebrovascular and cardiovascular complications are a concern. When using RAS inhibitors, it is best to start with a small dose to prevent a sudden decline in renal function and hyperkalemia. ii) Heart failure: In conservative renal failure, some cases present with high output failure due to anemia. Clinically, there are many cases where there are no symptoms, but ultrasound examination reveals a reduced ejection fraction. Myocardial ischemia, coronary artery calcification, renal anemia, increased extracellular fluid volume, hypertensive heart disease, and arteriosclerosis contribute to the pathology. On the other hand, cases presenting with severe cardiac enlargement, hypotension, arrhythmia, right heart failure, etc. are called uremic cardiomyopathy.
c) Uremic peripheral neuropathy: Both sensory and motor nerves are affected, symmetrically on both sides, and severely in the lower limbs, beginning in the distal area and progressing upwards. This results in a decrease in vibration sense and deep sensation, weakened or absent tendon reflexes, and slowed peripheral nerve conduction velocity. Subjective symptoms are known as restless legs syndrome, with patients complaining that they "can't find where to put their feet," and symptoms are severe at night and relieved by movement. Other symptoms include numbness, burning foot syndrome, weakness, and muscle spasms. This condition is resistant to treatment, including dialysis, but dopamine agonists have recently been shown to be effective.
d) Gastrointestinal symptoms: Patients with chronic renal failure often complain of nausea, vomiting, and loss of appetite. Stimulation of the vomiting center in the lateral ciliary body of the medulla due to accumulation of uremic substances and gastrointestinal motility disorders due to autonomic nerve disorders have been proposed as possible mechanisms of onset. Hypergastrinemia due to impaired gastrin metabolism, hypoproteinemia, and reduced blood flow to the gastric mucosa due to anemia may contribute to the development of gastric and duodenal erosions and ulcers. e) Skin symptoms: Cutaneous pruritus occurs frequently in patients with chronic renal failure. There are many causes of cutaneous pruritus, and some of these include accumulation of uremic substances, abnormal Ca and P metabolism, reduced sweat gland count and atrophy, peripheral nerve disorders, and histamine release from mast cells. Cutaneous pruritus is resistant to treatment and is often managed by applying antipruritic drugs or taking antihistamines as needed, but many cases do not improve even with dialysis. Selective opioid kappa receptor agonists are effective for refractory dialysis pruritus, but have not been studied in conservative renal failure. f) Renal anemia: Anemia becomes evident when the GFR falls below 30 mL/min, and worsens as renal failure progresses [⇨11-1-2)-(4)]. The main cause is a decrease in erythropoietin production, but shortening of red blood cell life span and suppression of hematopoiesis by uremic substances are also involved. The anemia is basically normocytic normochromic, but it may occasionally be complicated by iron deficiency anemia and present as microcytic hypochromic anemia. Secondary hyperparathyroidism and malnutrition also contribute to anemia. Regarding treatment, the development of recombinant human erythropoietin preparations and long-acting preparations has made management easier, and the risk of developing hepatitis has drastically decreased with the reduced need for blood transfusions. g) Renal osteodystrophy: In patients with chronic renal failure, characteristic bone lesions collectively known as renal osteodystrophy appear, with osteitis fibrosa and osteomalacia being typical pathologies [⇨11-1-2)-(5)]. i) Osteitis fibrosa: This is a bone lesion caused by hyperparathyroidism, primarily bone resorption. Bone X-rays show subperiosteal resorption on the radial side of the phalanges and middle phalanges, loss of the fingertips, spotted shadows (salt and pepper appearance) on the skull, and enlargement of the pubic symphysis. In the vertebrae, bone sclerosis occurs above and below the vertebral body, characteristically giving the Rugger Jersey appearance. The pathology is characterized by hyperphosphatemia and hypocalcemia due to impaired activation of vitamin D and impaired phosphorus excretion, which causes persistent excessive secretion of parathyroid hormone, which promotes bone turnover, resulting in increased bone resorption and fibrosis of the bone trabeculae.
ii) Osteomalacia: This is caused by a deficiency of active vitamin D and impaired mineralization of osteoid tissue due to hypocalcemia. It is accompanied by hyperparathyroidism, and is characterized by subjective bone pain throughout the body, especially in the lower body. Bone X-rays show increased radiolucency and pathological fractures, and if there are any pseudofractures, this is of great diagnostic significance.
h) Other symptoms: Patients with long-term chronic renal failure frequently suffer from conditions resulting from renal failure such as impaired glucose tolerance, lipid metabolism disorders, hypothyroidism, gonadal dysfunction, and infections.
2) Acute uremic symptoms:
a) Gastrointestinal symptoms: In the early stages, loss of appetite occurs, and in the terminal stages, nausea, vomiting, diarrhea, hematemesis, and bloody stool occur.
The gastrointestinal mucosa becomes edematous and numerous erosions are observed. These changes disappear with strict protein restriction and dialysis, so the cause is thought to be uremic substances. If the gastrointestinal symptoms are severe, dialysis therapy is indicated, but in clinical practice, these are clear clinical signs of uremia.
b) Cardiovascular disorders:
i) Pulmonary edema and heart failure: In end-stage renal failure, the extracellular fluid volume increases, resulting in left heart failure accompanied by pulmonary edema.
Symptoms include marked orthopnea, hemoptysis, and frothy sputum, and chest X-rays are characterized by cardiomegaly and an increased hilar shadow (butterfly shadow). The onset of this disease is mainly due to an increase in extracellular fluid volume, with acidosis, activation of the RAS system, and hypertension contributing to its onset. Usually, dialysis can dramatically improve the condition by removing excess extracellular fluid. If dialysis alone does not improve the condition, it is necessary to differentiate organic myocardial damage. ii) Uremic pericarditis: Uremic substances and bleeding tendency are thought to be involved in the onset of this disease, but it can also be triggered by viral infection. If fever, chest pain, hypotension, decreased pulse pressure, pericardial rub, or an enlarged cardiac shadow is present on chest X-ray, this disease should be suspected and confirmed by echocardiography. Pericardial fluid is usually bloody, and if it becomes severe, cardiac tamponade may occur. If this disease occurs in a patient with end-stage renal failure before the start of dialysis, it is considered an indication for the start of dialysis. In many cases, recovery is achieved by increasing the amount of dialysis, i.e., by performing dialysis more frequently. iii) Hyperkalemia: In renal failure, the reduction in nephrons reduces potassium excretion, resulting in hyperkalemia, but severe hyperkalemia is rare if the urine volume is 400 mL/day or more. However, in patients with diabetic nephropathy or tubular/interstitial damage, hypoaldosteronism or reduced tubular reactivity to aldosterone is likely to cause hyperkalemia. In patients with end-stage renal failure, hyperkalemia is likely to occur due to metabolic acidosis and increased catabolism. In emergency cases, hyperkalemia and acidosis can be corrected by dialysis, but treatment is usually with sodium bicarbonate, ion exchange resin, a combination of glucose and insulin, or calcium gluconate.
c) Metabolic acidosis: In end-stage renal failure, phosphate and sulfate accumulate, causing severe metabolic acidosis accompanied by an increase in the anion gap. When the pH drops below 7.20, hyperventilation due to respiratory compensation becomes severe, and deep, regular breathing (Kussmaul respiration) occurs. When the condition becomes severe (pH < 7.10), ventricular arrhythmias and decreased myocardial contractile function occur.
d) Bleeding tendency: End-stage renal failure is associated with a high rate of bleeding tendency, with complications including subcutaneous bleeding, nosebleeds, and gingival bleeding as well as gastrointestinal bleeding, genital bleeding, and pericardial cavity bleeding. Although the clotting time is usually within the normal range, the bleeding time is significantly prolonged and the platelet count is often low.
e) Uremic encephalopathy: When azotemia becomes pronounced with the decline in renal function, symptoms such as fatigue, impaired memory and concentration, irritability, and impaired ability to perform repetitive calculations appear. As renal function declines further, mental symptoms such as avolition, lethargy, insomnia, euphoria, depression, disorientation, hallucinations, and confusion appear as the level of consciousness decreases, and as the condition progresses, it can lead to drowsiness, stupor, and coma. This series of symptoms is collectively referred to as uremic encephalopathy. Muscle irritability can cause asterixis, muscle spasms, and pathological reflexes, and may lead to generalized convulsions and decorticate rigidity or decerebrate rigidity. These symptoms can be improved relatively quickly with dialysis. Uremic substances are thought to be the main cause of this condition, but electrolyte metabolism disorders such as acidosis, hyponatremia, hypernatremia, and hypermagnesemia, as well as mechanisms similar to hypertensive encephalopathy, are also involved. Among the conditions that should be differentiated are metabolic encephalopathies such as hypoglycemia, hypoxic encephalopathy, and hepatic encephalopathy, as well as vascular disorders. [Eiji Kusano]

Source : Internal Medicine, 10th Edition About Internal Medicine, 10th Edition Information

Japanese:

（7）尿毒症（uremia）
概念
　慢性腎臓病（chronic kidney disease：CKD）を有する患者では，徐々に腎機能が低下すると初期には無症状だったものが，糸球体濾過値（GFR）が＜30 mL/分以下の腎不全に進行すると，尿毒症の慢性症候である高血圧，高カリウム血症，腎性貧血，末梢神経障害，腎性骨異栄養症，代謝性アシドーシスなどが観察されるようになる．さらにGFR＜5 mL/分以下の末期腎不全に至ると急性症候が出現する．尿毒症症状としては食欲不振，悪心，嘔吐，心外膜炎，集中力低下，痙攣発作，昏睡などの中枢神経症状がみられる．血中の尿素窒素（BUN）やクレアチニン（Cr）の絶対値とこれらの症候の発現の間には直接的な相関は存在しない．BUNやCrが低い場合にも尿毒症の症候が出現することもあるし，逆にBUNやCrが高い場合でも症候が出ない場合もある．いずれにしても尿毒症の急性症候が出現したら延命のためには透析療法や腎移植などが必要である．すべてのCKD患者が進行性腎障害を呈するわけではなく，腎不全の原因疾患，合併症，治療，社会経済的状況，遺伝，民族性などによって異なる．
病態
　BUN，Crや尿酸など窒素化合物の最終代謝産物のほとんどは腎から排泄され，GFRが低下すると高窒素血症（azotemia）を呈する．従来，尿毒症は窒素化合物の代謝産物が異常に蓄積した結果と考えられ，これらの物質を総称して尿毒症物質（uremic toxins）とよぶ．最近では尿毒症物質は，小分子量物質，中分子量物質，蛋白結合物質に分類され，各物質の正常値，尿毒症状態での値なども判明しつつある．尿毒症の病態は，腎が司るすべての機能障害によって生じると考えられ，水･電解質異常，代謝性アシドーシス，副甲状腺ホルモンの産生亢進，活性型ビタミンDの欠乏，Ca，P代謝異常，エリスロポエチンの産生低下など多くの要因が関連する．
臨床症
状・対策
　尿毒症の臨床症候は大きく慢性症候と急性症候に分けられる．慢性症候は，GFR 30 mL/分以下程度の腎不全状態でみられる症候である．急性症候は腎不全末期や急性腎不全でGFRが5 mL/分以下に低下し，急激で高度のazotemiaが出現した場合にみられ，ときに致命的であるが透析療法によって是正可能である．
1）慢性尿毒症症候：
慢性尿毒症症候はGFRが30 mL/分以下に低下した頃より出現する症候で，エリスロポエチン産生低下による腎性貧血，ビタミンD活性化障害による二次性副甲状腺機能亢進症，Na排泄障害による細胞外液量増加による高血圧やうっ血性心不全などがあり，発症機序が明らかでない症候としては末梢神経障害などが代表的である．
a）尿の変化：慢性腎不全では浸透圧利尿，Na利尿，尿細管障害により尿濃縮能と希釈能が低下し等張尿となるが，末期に至るまで乏尿をきたすことはまれである．この頃から夜間尿がみられる．この時期の極端な塩分制限や利尿薬投与は，細胞外液量やGFRの低下をきたす．
　b）心血管系症候：
　ⅰ）高血圧：この時期には高血圧を高頻度に合併する．高血圧の成因は大きく，容量依存性高血圧（volume-dependent hypertension）と，レニン-アンジオテンシン系（RAS）の活性化による高血圧（renin-dependent hypertension）に分けることができるが，一酸化窒素やプロスタグランジン，カリクレイン，キニンなどの降圧系の異常も関与している．高血圧は腎不全の進展，増悪因子であるのみならず，動脈硬化症の進展に寄与し，脳･心血管系合併症の最大の危険因子である．CKDに合併する血圧の治療はRAS系阻害薬が有用で，第一選択薬である．容量依存性高血圧にはCKD 3期以上ではループ利尿薬を追加する．また，脳･心血管系合併症が懸念される場合にはカルシウム拮抗薬を追加する．RAS系阻害薬の使用に際しては腎機能の急激な低下や高カリウム血症を予防するために少量から始めるのがよい．　ⅱ）心不全：保存期腎不全では貧血により高拍出性心不全（high output failure）を呈する症例がある．臨床的には無症状であることが多く，超音波検査により駆出率の低下を認める．心筋虚血，冠動脈石灰化，腎性貧血，細胞外液量増加，高血圧性心疾患，動脈硬化症などが病態に寄与している．一方，高度の心拡大，低血圧，不整脈，右心不全などを呈する場合には尿毒症性心筋症（uremic cardiomyopathy）と呼称される．
c）尿毒症性末梢神経障害（uremic neuropathy）：知覚神経と運動神経ともに障害され，両側対称性で下肢に高度で，遠位部にはじまり上行する．振動覚や深部知覚の低下，腱反射の減弱･消失，末梢神経伝導速度の遅延をきたす．自覚的には，下肢静止不能症候群（restless legs syndrome）と呼称され，「足のおきどころがない」と訴え，夜間に高度で，体動時に楽になる．その他，しびれ感，灼熱感（burnig foot syndrome），脱力，筋痙攣などがある．透析療法を含め，治療には抵抗性であるが，最近ドパミンアゴニストが有効とされている．
d）消化器症状：慢性腎不全では，しばしば悪心，嘔吐，食欲不振を訴えるようになる．尿毒症物質の蓄積による延髄外側毛様体の嘔吐中枢の刺激や自律神経障害による消化管運動障害が発症機序として提示されている．ガストリン代謝障害による高ガストリン血症，低蛋白血症，貧血による胃粘膜の血流低下などは，胃･十二指腸のびらんや潰瘍の発症に寄与している可能性がある．　e）皮膚症状：慢性腎不全では皮膚瘙痒症が高頻度に発現する．皮膚瘙痒症の原因は多彩で，尿毒症物質の蓄積，Ca･P代謝異常，汗腺の減少や萎縮，末梢神経障害，マスト細胞からのヒスタミン放出の関与などが指摘されている．皮膚瘙痒症は治療抵抗性で，止痒薬の塗布や抗ヒスタミン薬の頓用で対応することが多いが，透析療法によっても改善しない例が多い．選択的オピオイドカッパ受容体作動薬が治療抵抗性の透析瘙痒症に有効とされているが，保存期腎不全では検討されていない．　f）腎性貧血（renal anemia）：GFRが30 mL/分以下に低下すると貧血が明らかになり，腎不全の進行とともに増悪する【⇨11-1-2）-（4）】．主因はエリスロポエチン産生低下であるが，赤血球寿命の短縮や尿毒症物質による造血抑制も関与している．基本的に正球性正色素性貧血であるが，時折鉄欠乏性貧血を合併し小球性低色素性貧血を呈することもある．また，二次性副甲状腺機能亢進症，低栄養なども貧血に寄与する．治療に関しては，遺伝子組換えヒトエリスロポエチン製剤に始まり，長時間作用型の製剤の開発で管理が容易となり，輸血の必要性の減少に伴い肝炎発症の危険性が激減した．　g）腎性骨異栄養症（renal osteodystrophy）：慢性腎不全患者では腎性骨異栄養症と総称される特徴的な骨病変が出現し，線維性骨炎と骨軟化症が代表的病態である【⇨11-1-2）-（5）】．　ⅰ）線維性骨炎（osteitis fibrosa）：副甲状腺機能亢進症に基づく，骨吸収を主体とする骨病変である．骨X線上，手指骨，中指骨の橈骨側の骨膜下吸収像，指尖骨の消失，頭蓋骨の斑点状陰影（salt and pepper像），恥骨結合の開大などがみられる．脊椎骨では椎体の上下部に骨硬化像が生じてrugger jersey像が特徴的である．病態はビタミンDの活性化障害とリン排泄障害による高リン血症，低カルシウム血症により副甲状腺ホルモンの過剰分泌が持続し，骨代謝回転が促進する結果，骨吸収が亢進し，骨梁が線維化することである．
　ⅱ）骨軟化症：活性型ビタミンDの欠乏，低カルシウム血症による類骨組織の石灰化障害による．副甲状腺機能亢進症を伴い，自覚的には，全身，特に下半身の骨痛が特徴的で，骨X線上，X線透過性の亢進，病的骨折がみられ偽骨折像があれば診断的意義が大きい．
　h）その他の症候：長期に経過した慢性腎不全患者では，腎不全に起因する病態として，耐糖能障害，脂質代謝異常，甲状腺機能低下症，性腺機能障害，感染症などを高頻度に合併する．
2）急性尿毒症症候：
a）消化器症状：初期には食欲不振，末期に至れば悪心・嘔吐，下痢，吐血，下血をきたす．
　消化管粘膜は浮腫状となり多数のびらんを認める．これらの変化は厳重な蛋白制限や透析療法によって消失することから，成因は尿毒症物質が考えられている．消化器症状が高度であれば透析療法の適応となるが，臨床現場では尿毒症の明確な臨床症候である．
b）心血管系障害：
　ⅰ）肺水腫・心不全：末期腎不全では細胞外液量が増加し，肺水腫を伴う左心不全を呈する．
　著明な起坐呼吸，血痰，泡沫状の痰などの症状を呈し，胸部X線写真で心拡大と肺門部陰影の増強（butterfly shadow）が特徴的である．発症には細胞外液量の増大，アシドーシス，RAS系の亢進，高血圧などが寄与し主因は細胞外液量の増大である．通常は透析療法により過剰な細胞外液量を除去することで劇的に改善する．透析療法のみで改善しない場合には器質的な心筋障害を鑑別する必要がある．　ⅱ）尿毒症性心外膜炎（uremic pericarditis）：発症には尿毒症物質と出血傾向が関与すると考えられているが，ウイルス感染を契機として発症することもある．発熱，胸痛，低血圧，脈圧減少，心膜摩擦音，胸部X線写真で心陰影の拡大などがあれば本症を疑い心エコー検査で確認する．通常，心膜液は血性で，高度になれば心タンポナーデを呈する．透析導入前の末期腎不全患者に本症が合併すれば，透析導入の適応と考える．多くの症例で透析量増加，つまり頻回に透析を施行することで回復することが多い．　ⅲ）高カリウム血症：腎不全ではネフロンの減少からK排泄能が低下し高カリウム血症を呈するが，尿量が400 mL/日以上あれば重篤な高カリウム血症を生じることは少ない．しかし，糖尿病性腎症や尿細管・間質障害を伴う例では低アルドステロン血症あるいはアルドステロンに対する尿細管の反応性が低下し高カリウム血症をきたしやすい．末期腎不全に至れば，代謝性アシドーシス，異化亢進などから高カリウム血症が出現しやすくなる．緊急例では透析療法により，高カリウム血症やアシドーシスは是正されるが，通常は，炭酸水素ナトリウム，イオン交換樹脂，ブドウ糖とインスリン併用，グルコン酸カルシウムなどで治療する．
c）代謝性アシドーシス：末期腎不全ではリン酸や硫酸などが貯留し，アニオンギャップの開大を伴った高度の代謝性アシドーシスを呈する．pHが7.20以下に低下すると呼吸性代償による過換気が高度となり，深く規則正しい呼吸（Kussmaul呼吸）を呈する．さらに，高度（pH＜7.10）になると心室性不整脈，心筋収縮機能低下をきたす．
d）出血傾向：末期腎不全で出血傾向を高率に認め，皮下出血，鼻出血，歯肉出血から消化管出血，性器出血，心膜腔出血などを併発する．通常，凝固時間は正常域を示すが，出血時間が著明に延長し，血小板数も低値を示すことが多い．
e）尿毒症性中枢神経障害（uremic encephalopathy）：腎機能低下に伴いazotemiaが顕著になると，易疲労感，記銘力，集中力の低下，易刺激性，反復計算力の低下などが発現する．さらに腎機能が低下すると意識レベルの低下として無欲，嗜眠傾向，不眠，多幸症，抑うつ感，見当識障害，幻覚，錯乱などの精神症状が発現し，さらに進行すれば傾眠，昏迷，昏睡に至る．これら一連の症候をuremic encephalopathyと総称する．筋の易刺激性では羽ばたき振戦，筋攣縮，病的反射を認め，全身痙攣から，除皮質硬直や除脳硬直状態を呈することもある．これらの症候は，透析療法により比較的速やかに改善しうる．成因としては，尿毒症物質が主因と考えられているが，アシドーシス，低ナトリウム血症，高ナトリウム血症，高マグネシウム血症などの電解質代謝異常とともに高血圧性脳症様の機序も関与する．鑑別すべき病態としては，低血糖，低酸素脳症，肝性脳症などの代謝性脳症とともに血管障害が重要である．［草野英二］

出典　内科学第10版内科学第10版について　情報

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