医学肾脏及泌尿系疾病经常会引起一些临床症状课件

Nephrotic syndrome Figure 1. Nephrotic edema. Figure 2. Nephrotic edema. Clinical Syndrome n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 nNephrotic syndrome nNephritic syndrome nAsymptomatic urinary abnormalities nAcute renal failure or Rapidly progressive renal failure nChronic 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* STAGEDESCRIPTIONGFR (mL/min/1.73m2) 1Kidney damage with normal or GFR90 2Kidney damage with mild or GFR60-89 3Moderate GFR30-59 4Severe GFR15-29 5Kidney failure 3.5g/24h), hypoalbuminemia ( less than 30g/dL ) and edema. Hyperlipidaemia is also present. Primary and secondary causes are summarized in Table 2, 3 In 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 SYNDROMENEPHROTIC SYNDROME n Pathophysiology -Proteinuria -Hypoalbuminemia -Edema -Hyperlipidemia n Cause (diagnosis and differential diagnosis) -Systemic renal disease hepatitis B associated glomerulonephritis, Henoch-Schonlein purpura, systemic lupus erythematosus, diatetes mellitus, amyloidosis -Idiopathic nephrotic syndrome n Complications -Infection -Coagulation disorders -Protein malnutrition and dyslipidemia -Acute renal failure Pathophysiology Proteinuria nProteinuria can be caused by systemic overproduction, tubular dysfunction, or glomerular dysfunction. It is important to identify patients in whom the proteinuria is a manifestation of substantial glomerular disease as opposed to those patients who have benign transient or postural (orthostatic) proteinuria. Heavy proteinuria (albuminuria) Figure 3. Hypoalbuminemia nHypoalbuminemia is in part a consequences of urinary protein loss. It is also due to the catabolism of filtered 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 NS may occur through at least two different major mechanisms. nIn 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 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 nIn some patients, however, the intravascular volume has been measured 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 kidney 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 nMost nephrotic patients have elevated levels of total and low-density lipoprotein (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 thrombophlebitis, 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 patterns and clinical presentations of idiopathic nephrotic syndome nIn 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 change in specific diagnosis, prognosis, and therapy. nSelected 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 SYNDROMEPRIMARY NEPHROTIC SYNDROME n Minimal Change Disease n Focal Segmental Glomerulosclerosis n Membranous Nephropathy n Membranoproliferative Glomerulonephritis (MPGN) Figure 5a. Pathology of glomerular disease. Light microscopy. (a) Normal glomerulus; minimal change disease. Table 4 PRIMARY NEPHROTIC SYNDROMEPRIMARY NEPHROTIC SYNDROME n Minimal Change Disease n Focal Segmental Glomerulosclerosis n Membranous Nephropathy n Membranoproliferative 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 5 PRIMARY NEPHROTIC SYNDROMEPRIMARY NEPHROTIC SYNDROME n Minimal Change Disease n Focal Segmental Glomerulosclerosis n Membranous Nephropathy n Membranoproliferative Glomerulonephritis(MPGN) Figure 7a. Early MN: a glomerulus from a patient with severe nephrotic syndrome and early MN, exhibiting normal architecture and peripheral capillary 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 SYNDROMEPRIMARY NEPHROTIC SYNDROME n Minimal Change Disease n Focal Segmental Glomerulosclerosis n Membranous Nephropathy n Membranoproliferative 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 n Initial 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. nCommon screening tests include the fasting blood sugar and glycosylated hemoglobin tests for diabetes, and antinuclear 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 useful. Once secondary causes have been excluded, treating the adult nephrotic patient often requires a renal biopsy to define the pattern of glomerular involvement. nIt leads to a multitude of other consequences , such as predisposition to infection and hypercoagulability. In general, the diseases associated 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. 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 1、病毒性肝炎：由病毒造成的肝炎按照其病毒系列不同分为甲、乙、丙、丁、戊和庚共六种类型病毒性肝炎。能引起肝脏细胞肿胀，是世界上流传广泛，危害很大的传染病之一。 1908 年，才发现病毒也是肝炎的致病因素之一。1947 年，将原来的传染性肝炎（infectious hepatitis ）称为甲型肝炎（Hepatitis A, HA ）；血清性肝炎（serum hepatitis ）称为乙型肝炎（Hepatitis B, HB ）。1965 年人类首次检测到乙型肝炎的表面抗原。 我国经济和科学技术日益发展，学术文化领域百家争鸣，（df高血压958心脏病983u6 糖尿病87fr）特别是思想家的革新精神，为中医学理论的创新和突破性进展，提供了有利的文化背景。宋代陈无择著三因极一病证方论一书，（45传染病q566 丙肝964jo乙肝28jgsx甲肝gh）提出三因学说；并产生了最具盛名四大学派，刘完素倡导火热论；张从正力倡“攻邪论”；李杲提出“内伤脾胃，百病由生”的理论；朱震亨创造性地阐明了相火的演变规律。 编辑本段明清时期（df肺25s血液f369血小板t5172 红血球gdf55m 白血球fd2） 是中医学理论综合汇编、深化发展，临床各科辨证体系丰富、提高阶段。如明代楼英的医学纲目和王肯堂的证治准绳，清代吴谦等编著的医宗金鉴和陈梦雷主编的古今图书集成医部全录等。王清任著医林改错，注重实证研究，（df高血压958心脏病983u6 糖尿病87fr）纠正了古医籍中关于解剖知识的某些错误，肯定了“脑主思维”，发展了瘀血理论。温病学说的形成和发展，标志着中医理论的创新与突破，吴有性著温疫论，叶天士著温热病篇，吴鞠通著温病条辨等，在药物学研究方面，（45传染病q566 丙肝964jo乙肝28jgsx甲肝gh）李时珍著的本草纲目，总结了16世纪以前我国药物学研究的成就。医的诊察疾病能参考现代医学的微观分析，将辨证与辨病相结合，实现宏观与微观的统一，使中医诊断客观化，即把分析与综合相结合的方法引入中医理、法、方、药的研究，使二者有 机结合，互相借鉴、补充，避免各自的片面性、局限性，这将有利于中西医学的优势互补，“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