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108321106李雯婷Renal Failure, Kidney Disease (AKI (Acute tubular necrosis…
108321106李雯婷Renal Failure, Kidney Disease
AKI
AKIN: Acute Kidney Injury Network腎損傷分成 stage 1-3，在 48小時內，病患 SCr上升 50-100% (1.5-2倍)或 ≥0.3 mg/dL為 stage 1，上升 100-200% (2-3倍)為 stage 2，上升 >200% (>3倍)為 stage 3。排尿情況則是和 RIFLE criteria的三階段相同 (stage 1=risk, stage 2=injury, stage 3=failure)。
Acute tubular necrosis
exposure to nephrotoxic drugs or chemicals, tubular obstruction, and toxins from massive infection
Reversible, depending on whether necrotic cells and intratubular casts are removed and renal cells regenerate
Severe ischemia that causes cortical necrosis, however, leads to irreversible renal failure
occurs:major surgery, severe hypovolemia, overwhelming sepsis, trauma, burns
RIFLE：risk, injury, failure, loss, end-stage, 7天內 SCr上升50-100% (1.5-2倍)為risk，上升100-200% (2-3倍)為 injury，上升 >200% (>3倍)為 failure，需要接受透析>4週為loss，接受透析>3月為end-stage。
KDIGO criteria:
stage 1為：在 48小時內SCr上升 ≥0.3 mg/dL或 7天內 SCr上升50-100% (1.5-2倍)
stage 2為：SCr上升100-200% (2-3倍)
stage 3為：SCr上升 >200% (>3倍)，或SCr≥4 mg/dL或病患接受透析，或在小於 18歲的病患eGFR<35 ml/min per 1.73 m2
歷時數小時或數天的突然腎功能降低，GFR突然下降，由含氮物質產物（Serum creatinine↑; GFR↓）所累積的表現，且有時伴隨寡尿，通常是可逆的。
腎前性：妨礙腎臟的灌流，腎臟血流量減少，減低腎絲球過濾率。如出血、腹瀉、心輸出量減少、血管阻塞。
腎因性：疾病或腎毒性物質引起的腎實質性病變。如急性腎小管壞死、手術、電擊休克、代謝性疾病、血管炎、腫瘤等
腎後性：泌尿道阻塞引起的。如前列腺肥大、結石、腫瘤等
OBSTRUCTION
Uric acid:They can occur in people with gout or those going through chemotherapy.
Calcium(Primery):calcium oxalate (though they can consist of calcium phosphate or maleate).
Complete:hydronephrosis, decreased GFR,ischemic kidney damage ,Prolonged postrenal( acute tubular necrosis )(intrarenal AKI) and CKD
causes: stones, tumors, prostatic hypertrophy, and strictures of the ureters or urethra.
Complications: infection, sepsis, AKI ,CKD
Struvite:mostly in women with UTI
Cystine:stones are rare,genetic disorder cystinuria
Secondary medication induce
Glomerulonephritis
AGN(inflammatory glomerulopathies)
• Infection(Bacteria/Virus/Parasite), Primary disease, Systemic disease, and others.
•Hematuria, proteinuria, oliguria
•Abrupt onset
•Azotemia
•Edema, HTN
•DM、HTN → glomerulopathies(in US)
•Glomerulonephritis → ESRD(second most common cause)
Chronic Glomerulonephritis
• Proteinuria, Hematuria(+/-), Renal function↓
• Advancing renal damage: Proteinuria and HTN
Extension of that seen in AGN
• Proliferative and membranous lesions
• Sclerotic injury → Fibrotic changes
• Tubulointerstitial damage → renal function ↓
• Nephrons atrophy → kidneys become small, scarred, and nonfunctional.
•Glomerular diseases →→→ CKD
• autoimmune, metabolic, malignant, or infectious systemic disorders.SRD(second most common cause)
Nephrotic syndrome
Urinary elimination of protein >3 to 3.5 g/day
Manifestations: hypoalbuminemia, hyperlipidemia, edema, and a propensity for thrombus formation.
The most common primary causes
minimal change disease (lipoid nephrosis)
idiopathic focal segmental glomerulosclerosis
membranous nephropathy.
Several systemic diseases
SLE and Henoch-Schönlein purpura, infections, malignancies, and vasculitis
DM is the most common cause in adults
Nephrotic(NS):Massive proteinuria、Hypoalbuminemia、Edema、Hyperlipidemia
Nephritic(AGN): Hematuria、Oliguria、Azotemia、Hypertension
:red_flag:
RAAS
再經過肺製造的血管收縮素轉換酵素(Angiotensin Converting Enzyme，ACE)作用後，變成血管收縮素II (Angiotensin II)
使血管收縮→血壓上升刺激腎上腺皮質分泌醛固酮(Aldosterone) →造成Na+與水分滯留→血壓上升
接著會產生負回饋，以抑制Renin的釋放，導致Angiotensin II釋出減少，所以血壓不會一直上升
肝臟合成的血管張力素原 (Angiotensinogen) 經由腎素(Renin)蛋白酶催化形成血管張力素 I (angiotensin I)
血液滲透壓過高時，腦下垂體會分泌抗利尿激素ADH使得集尿管對水的通透性增加（減少排尿量），經由增加水分的吸收來降低血液滲透壓
腎臟經過濾及再吸收功能將身體多餘及有害物質由尿液排泄，來調節身體內的電解質和酸鹼值等體液恆定，以及水的含量來維持血液滲透壓及血壓的恒定
CKD
CKD之分期
腎臟結構或功能異常超過三個月， 並對健康造成影響，GFR<60 ml/ min/1.73m2 及ACR≧ 30 mg/g
stage 1：腎臟傷害 + 正常或 GFR > 90 mL/min/1.73m
stage 2：腎臟傷害 +輕度腎功能下降 GFR60 － 89 mL/min/1.73m
stage 3：中度腎功能下降 (GFR 30-60 ml/min/1.73m2 再細分為 G3a (45-59 ml/min/1.73m2)、G3b(30-44 ml/min/1.73m2))
stage 5：末期腎衰竭 GFR < 15 mL/min/1.73m
Complications：Hypertension and Cardiovascular Disease,Uremic Syndrome,Metabolic Acidosis,Electrolyte Imbalances,Mineral and Bone Disorders,Malnutrition,Anemia,Pain,Depression
APN
通常是單側的，右腎（50％）>左腎（25%）,雙側腎（25%)
通常起源於泌尿道網上升感染，但也可能通過血液到達腎臟有關，一旦進入腎臟，細菌就會與上皮細胞受體結合，引發炎症反應
常見原因：妊娠、糖尿病、
泌尿道解剖異常和阻塞
遺傳易感性、由尿路中的生理變化
