1、Nephrotic syndrome,Figure 1. Nephrotic edema.,Figure 2. Nephrotic edema.,Clinical Syndrome,肾脏及泌尿系疾病经常会引起一些临床症状、 体征和实验室表现相似的综合征。识别患者属于哪一种综合征对诊断很有帮助，因为导致每个综合征的病因较之其包含的个别临床症状和体征的致病原因要少，故识别患者属于哪一种综合征对诊断有帮助。,The most common syndrome of kidney disease,Nephrotic syndrome Nephritic syndrome Asymptomatic uri
2、nary abnormalities Acute renal failure or Rapidly progressive renal failure Chronic kidney disease(Table 1),(一)肾病综合征 (二)肾炎综合征 (三)无症状性尿检异常 (四)急性及急进性肾衰竭综合征 (五)慢性肾脏病(表1),肾脏疾病常见综合征,Table 1. STAGES OF CHRONIC KIDNEY DISEASE*,* Chronic kidney disease is defined as either kidney damage or GFR 60mL/min/1.73
3、m2 for 3months. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or image studies.,Nephrotic syndrome,This is characterized by proteinuria (Typically 3.5g/24h),hypoalbuminemia ( less than 30g/dL ) and edema. Hyperlipidaemia is
4、 also present.Primary and secondary causes are summarized in Table 2, 3In practice, many clinicians refer to “nephrotic range” proteinuria regardless of whether their patients have the other manifestations of the full syndrome because the latter are consequences of the proteinuria.,NEPHROTIC SYNDROM
5、E,Pathophysiology Proteinuria Hypoalbuminemia Edema HyperlipidemiaCause (diagnosis and differential diagnosis) Systemic renal disease hepatitis B associated glomerulonephritis, Henoch-Schonlein purpura, systemic lupus erythematosus, diatetes mellitus, amyloidosis Idiopathic nephrotic syndromeComplic
6、ations Infection Coagulation disorders Protein malnutrition and dyslipidemia Acute renal failure,Pathophysiology,Proteinuria,Proteinuria can be caused by systemic overproduction, tubular dysfunction, or glomerular dysfunction. It is important to identify patients in whom the proteinuria is a manifes
7、tation of substantial glomerular disease as opposed to those patients who have benign transient or postural (orthostatic) proteinuria.,Heavy proteinuria (albuminuria),Figure 3.,Hypoalbuminemia,Hypoalbuminemia is in part a consequences of urinary protein loss. It is also due to the catabolism of filt
8、ered albumin by the proximal tubule as well as to redistribution of albumin within the body. This in part accounts for the inexact relationship between urinary protein loss, the level of the serum albumin, and other secondary consequences of heavy albuminuria .,The salt and volume retention in the N
9、S may occur through at least two different major mechanisms. In the classic theory, proteinuria leads to hypoalbuminemia, a low plasma oncotic pressure, and intravascular volume depletion. Subequent underperfusion of the kidney stimulates the priming of sodium-retentive hormonal systems such as the
10、RAS axis, causing increased renal sodium and volume retention, In the peripheral capillaries with normal hydrostatic pressures and decreased oncotic pressure, the Starling forces lead to transcapillary fluid leakage and edema .,Edema,In some patients, however, the intravascular volume has been measu
11、red and found to be increased along with suppression of the RAS axis. An animal model of unilateral proteinuria shows evidence of primary renal sodium retention at a distal nephron site, perhaps due to altered responsiveness to hormones such as atrial natriuretic factor. Here only the proteinuric ki
12、dney retains sodium and volume and at a time when the animal is not yet hypoalbuminemic. Thus, local factors within the kidney may account for the volume retention of the nephrotic patient as well.,Edema,Figure 4.,Hyperlipidemia,Most nephrotic patients have elevated levels of total and low-density l
13、ipoprotein (LDL) cholesterol with low or normal high-density lipoprotein (HDL) cholesterol . Lipoprotein (a) Lp(a) levels are elevated as well and return to normal with remission of the nephrotic syndrome. Nephrotic patients often have a hypercoagulable state and are predisposed to deep vein thrombo
14、phlebitis, pulmonary emboli, and renal vein thrombosis.,Cause,Table 2 CAUSES OF THE NEPHROTIC SYNDROME,Table 3a NEPHROTIC SYNDROME ASSOCIATED WITH SPECIFIC CAUSES (“SECONDARY” NEPHROTIC SYNDROME),Table 3b NEPHROTIC SYNDROME ASSOCIATED WITH SPECIFIC CAUSES (“SECONDARY” NEPHROTIC SYNDROME),Pathology p
15、atterns and clinical presentations of idiopathic nephrotic syndome,In adults, the nephrotic syndrome is a common condition leading to renal biopsy. In many studies, patients with heavy proteinuria and the nephrotic syndromes have been a group highly likely to benefit from renal biopsy in terms of a
16、change in specific diagnosis, prognosis, and therapy. Selected adult nephrotic patients such as the elderly have a slightly different spectrum of disease, but again the renal biopsy is the best guide to treatment and prognosis (Table 2, 3).,Renal biopsy,PRIMARY NEPHROTIC SYNDROME,Minimal Change Dise
17、aseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis (MPGN),Figure 5a. Pathology of glomerular disease. Light microscopy. (a) Normal glomerulus; minimal change disease.,Table 4,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental Glomerulosc
18、lerosisMembranous NephropathyMembranoproliferative Glomerulonephritis(MPGN),Figure 5b. Segmental sclerosis; focal segmental glomerulosclerosis.,Figure 6. Light microscopic appearances in focal segmental glomerulosclerosis. Segmental scars with capsular adhesions in otherwise normal glomeruli.,Table
19、5,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis(MPGN),Figure 7a. Early MN: a glomerulus from a patient with severe nephrotic syndrome and early MN, exhibiting normal architecture and peripheral capill
20、ary basement membranes of normal thickness (Silvermethenamine 400).,Figure 7b morphologically advanced MN,Figure 7c. Morphologically more advanced MN (same patient as in (b),Table 6,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproli
21、ferative Glomerulonephritis(MPGN),Figure 8. Pathology of membranoproliferative glomerulonephritis type I. (a) Light microscopy shows a hypercellular glomerulus with accentuated lobular architecture and a small cellular crescent (methenamine silver).,Table 7,Diagnosis and Differential diagnosis,Initi
22、al evaluation of the nephrotic patient includes laboratory tests to define whether the patient has primary, idiopathic nephrotic syndrome or a secondary cause related to a systemic disease.,Common screening tests include the fasting blood sugar and glycosylated hemoglobin tests for diabetes, and ant
23、inuclear antibody test for rheumatoid disease, and the serum complement, which screen for many immune complex-mediated disease (Table 3), In selected patients, cryoglobulins, hepatitis B and C serology, anti-neutrophil cytoplasmic antibodies (ANCAS), anti GBM antibodies, and other tests may be usefu
24、l. Once secondary causes have been excluded, treating the adult nephrotic patient often requires a renal biopsy to define the pattern of glomerular involvement.,It leads to a multitude of other consequences , such as predisposition to infection and hypercoagulability. In general, the diseases associ
25、ated with NS cause chronic kidney dysfunction, but rarely they can cause ARF. ARE may be seen with minimal change disease, and bilateral renal vein thrombosis.,Complications,Infection Coagulation disorders Protein malnutrition and dyslipidemia Acute renal failure,Treatment 治疗,1. General treatment 2.
26、 Symptomatic treatment (e.g.diuresis to relieve edema, treating dyslipidemias, anticoagulate treatment, etc.) 3. Immunosupressive treatment,一、一般治疗 二、利尿消肿 三、免疫抑制治疗 四、调脂药物 五、抗凝治疗,Thank you,） “和而不同”，多元发展。近年来，中医药在防治非典、禽流感和艾滋病方面发挥的独特作用也证实了二者的有机结合，具有肯定的临床疗效。 编辑本段东西方医学交融（df高血压958心脏病983u6糖尿病87fr）不管是中医学还是西医学
27、，从二者现有的思维方式的发展趋势来看，均是走向现代系统论思维，中医药学理论与现代科学体系（45传染病q566丙肝964jo乙肝28jgsx甲肝gh）之间具有系统同型性，属于本质相同而描述表达方式不同的两种科学形式。可望在现代系统论思维上实现交融或统一，成为中西医在新的发展水平上实现交融慢性胃炎分类慢性胃炎的命名很不统一。依据不同的诊断方法而有慢性浅表性胃炎、慢性糜烂性胃炎、慢性萎缩性胃炎、慢性胆汁返流性胃炎、慢性疣性胃炎、药物性胃炎、乙醇性胃炎等等。 慢性胃炎大体可分为三种类型：慢性肥厚性胃炎、慢性浅表性胃炎以及慢性萎缩性胃炎。慢性肥厚性胃炎在临床上较为少见，一般也不会发生癌变。慢性浅表性胃炎
28、主要是指胃粘膜的浅表性炎症，这类炎症主要表现为胃粘膜的固有膜宽度增大并伴有水肿，被炎症细胞浸润，但胃腺体多属正常这类胃炎在临床上较多见，一般也不会发生癌变。只要经过恰当治疗之后，炎症可消退，但如治疗不当，往往可发展成萎缩性慢性胃炎慢性萎缩性胃炎是指胃粘膜除有浅表性胃炎病变外，胃腺体明显减少，脉管间隙扩大，胃粘膜层有全层性细胞浸润，常伴有肠上皮化生，即胃型上皮变为肠型上皮这种性质的慢性胃炎与胃癌的关系密切，特别是有肠上皮化生者更是如此或统一的支撑点，希冀籍此能给（df高血压958心脏病983u6糖尿病87fr）中医学以至生命科学带来良好的发展机遇，进而对医学理论带来新的革命。 在胃镜问世以前，胃
29、炎的主要诊断依据是依靠临床症状和上消化道钡餐检查。随着纤维胃镜的临床应用，特别是经胃镜对胃粘膜的活组织检查，对越来越多的胃炎有了较明确的认识。1982年，国内胃炎会议上根据国内外经验，将慢性胃炎分为浅表性和萎缩性两大类。而在浅表性胃炎的命名上，又常常使用病理、部位、形态等含义的词，如“慢性疣状胃炎”、“慢性出血性胃炎”、“慢性糜烂性胃炎”、 “慢性胆汁反流性胃炎”等等。1990年8月，在澳大利亚悉尼召开的第九届世界胃肠病学大会上，又提出了新的胃炎分类法，它由组织学和内镜两部分组成，组织学以病变部位为核心，确定3种基本诊断：急性胃炎；慢性胃炎；特殊类型胃炎。加上前缀病因学诊断和后缀形态学描述，并
30、对炎症、活动度、萎缩、肠化、幽门螺杆菌感染分别给予程度分级。内镜部分以肉眼所见描述为主，分别区分病变程度。 1慢性糜烂性胃炎 内镜下常表现为多发性点状或阿弗他溃疡。慢性非糜烂性胃炎可为特发性，也可由药物(特别是阿司匹林和非甾体类消炎药，参见消化性溃疡的治疗部分)，克罗恩病或病毒感染所引起。幽门螺杆菌可能在此不发挥重要作用。 症状多为非特异性的，可包括恶心，呕吐和上腹部不适。内镜下显示在增厚的皱襞隆起边缘有点状糜烂，中央有白斑或凹陷。组织学变化多样。尚无某种方法具有广泛疗效或可治愈。 治疗多为对症治疗，药物包括制酸剂，H2拮抗剂和质子泵。 2慢性胃炎的癌变 对于胃溃疡发生癌变，人们比较容易理解，但对于有些类型的慢性胃炎也会发生癌变，许多人会感到不可思议然而，慢性萎缩性胃炎发生癌变却是事实 编辑本段现代中医史（df4肺炎88gdg青霉素d25f肝炎df6）轴心时代中、西医学的峰巅之作。雅斯贝而斯曾说：“如果历史有一个轴心，那么我们就必须将这轴心作为一系列对全部人类都有意义的事件，发生于公元前800至200年间的这种精神历程似乎构成了这样一个轴心。,医学健康系列精品课件,本文档下载后可以修改编辑，欢迎下载收藏。,
