天 津 医 科 大 学 授 课 教 案
（共
课程名称：
内科学
页）
课程内容：急慢性肾小球肾炎
教师姓名： 韩鸿玲
职称：主任医师
授课对象： 医疗系
年级 留学生 本 科
授课方式：
页、第
授课日期： 2013 年 2 月 28 日 10 时— 12 时
教材版本：留学生教材
大课
学时数：
2
听课人数：80
本单元或章节的教学目的与要求：
1.掌握肾小球疾病的分类
2.掌握急性肾炎、慢性肾炎、急进肾炎的概念
3。掌握急慢性肾炎的临床表现和诊断方法治疗原则
4.了解急慢性肾炎的病理改变和发病机理
授课主要内容及学时分配：
肾小球疾病的分类和急性肾小球肾炎 1 学时
急进性肾炎 慢性肾炎 1 学时
重点、难点及对学生要求（包括掌握、熟悉、了解、自学）
重点：1.肾小球疾病的分类依据和临床的应用 2.各种肾炎的临床特点，
难点：理解各种肾炎的发病机制不同，尽管临床表现类似，在临床中只能称为综合征
掌握：各种肾小球综合征的临床表现特点和诊断依据及治疗原则
了解：各种肾小球炎症的病理改变，但要相对重点了解 RPGN 的病理改变
外语词汇：
辅助教学情况：
幻灯片 加上生动的实际病例
复习思考题：
 Clinical features of PSGN
 What is RPGN？
 Clinical features of IgA nephropathy
参考资料：
留学生教材 肾脏病学
主任签字：
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天 津 医 科 大 学 授 课 教 案
（共 5 页、第 1 页）
AGN
Gross or microscopic hematuria is most common, and is often described by
the patients as smoky- coffee- or cola-colored urine. The erythrocytes in the
urinary sediment are small, distored, fragmented and hypochromic which is
called dysmorphic hematuria. In general, gross hematuria may last a few days
to 1 or 2 weeks and then disappear.
B. Proteinuria
The degree of proteinuria varies according to the nature and severity of the
underlying glomerular lesion. Rarely, protein excretion rates are within the
normal range, but generally they are between 0.2 and 3g/d and nonselective. If
proteinuria is marked and sustained, the NS may appear.
C. Edema
The edema appears in areas of low tissue pressure, such as periorbital areas,
especially in the morning. This is called nephritic faces. Severe edema may
progress to dependent portion of the body and lead to ascites and/or pleural
effusions.
D．Hypertension
Almost 80% of cases have a mild to moderate degree of hypertension,
especially in old patients.
E. Oliguria
Oliguria may be present when nephritis occurs. Usually less than 500ml/d,
which leads to azotemia. Two weeks later the amount of urine may gradually
increase.
F. Renal function lesion
Glomerular inflammation can lead to reduced glomerular filtration that could
lead to azotemia. Usually after a diuretic, azotemia may gradually disappear, if
not, acute renal failure occurs.
G. Others
Other symptoms of PSGN may be vomiting, nausea, sleeping, loin pain etc.
Complications
The complications of PSGN are heart failure, encephalopathy and uremia.
Laboratory findings
RBCs and RBC casts, leukocyte casts, WBCs, FDP, Cз, non-selective proteinuria
(non-nephrotic range) can be detected in urine. In most children and adults,
proteinuria will become negative after 4 to 6 months of onset of nephritis.
Other laboratory features include positive tests for circulating immune complexes,
an elevated antistreptolysis O titer, a low serum complement (usually returning to
normal at 6 to 12 weeks), azotemia, elevated erythrocyte sedimentation rate (ESR)
and mild anemia.
Diagnosis and differential diagnosis
The diagnosis of PSGN can be based on the typical renal presentation following
streptococcal infection, hypocomplementemia, and serologic evidence.
The differential diagnosis is that of AGN with hypocomplementemia and includes
other forms of postinfectious GN, e. g. bacterial endocarditis, shunt nephritis,
systemic lupus erythematosus (SLE), and membranoproliferative GN.
Because the diagnosis is most often straightforward, a renal biopsy is indicated
only of the disease follows an atypical course in children. Most adults with acute
nephritic syndrome require a kidney biopsy to establish the diagnosis.
Course and treatment
Complete recovery occurs in at least 85 to 90% of all patients. However, minor
urinary sediment abnormalities may continue for several years in some patients
(<2%), but progression to chronic renal failure is rare, typically occurring only in
older adults. Fewer than 5% of patients have oliguria for more than 7 to 9 days, and
the prognosis in these patients is less favorable.
There is no specific therapy for PSGN. The treatment is supportive and
symptomatic until all acute signs have abated. It’s reasonable to recommended bed
rest until the signs of glomerular inflammation subside. Mild protein restriction is
desirable for azotemic patients. Seven to 10 days of penicillin or other suitable
antimicrobials should be given with evidence of streptococcal infection. Salt
restriction and, in some cases, diuretics and antihypertensive agents may be required
to manage sodium retention (manifested by hypertension, edema, congestive heart
failure, and other signs). Steroids and cytotoxic drugs are not of value.
Rapidly progressive glomerulonephritis (RPGN)
RPGN is characterized clinically by the rapid deterioration of renal function that
reaches end stage within a period of days or weeks, and histologically by extensive
crescents. It can be an idiopathic primary glomerular disease or can be superimposed
on other glomerular diseases, either primary or secondary.
Classification and pathology
The classification of RPGN is based on immunofluorescence microscopic
findings. The categories are as follows (shown in table -2):
Table -2 Types of RPGN
Types
Light microscopy
Immunofluorenscence
Microscopy
Possible Pathogenesis
Association
Anti-GBM
antibody
Crescents
Necrosis
Linear-IgG
Fibrinogen
Anti-GBM
Pulmonary
hemorrhage
Immune-complex
es
Crescents
Proliferation
Non-immu
ne-complex
es
Crescent
s
Necrosis
Granular IgG
complement
fibrinogen
Immunecomplexes
Negative
ANC
A
Bacterial
infections
Systemic
symptom
s
rash,feve
r
·Glom
erulon
ephriti
s due
to
antibo
dies
directe
d
toward
glomer
ular
basem
ent
membr
ane
antige
ns
(anti-GBM). It accounts for 20% of all cases of RPGN.
·Glomerulonephritis due to the deposition or formation of immune complexes in the
glomeruli. It accounts for 40% of all cases of RPGN.
·Glomerulonephritis in which no immunoglobulins are found in the glomeruli
(so-called nonimmune). It accounts for 40% of cases of RPGN.
By light microscopy, extracapillary proliferation (i.e. crescents) can be detected
which is a feature of RPGN. Usually more than 70% of glomeruli are involved with
crescents (so called crescentic glomerulonephritis Figure-4). Endocapillary
proliferation, if prominent, suggests the presence of infection. Segmental or diffuse
endocapillary necrosis suggests underlying systemic necrotizing vasculitis.
Nonstreptococcal acute postinfectious glomerulonephritis
Nonstreptococcal acute postinfectious glomerulonephritis includes a wide variety
bacterial states and various viral and parasitic diseases e.g. infective endocarditis,
sepsis of other types, visceral abscess, typhoid fever, infectious mononucleosis,
acute viral hepatitis B, falciparum malaria, and toxoplasmosis etc. Circulating
immune complexes play an important role in the pathogenesis of AGN in these
diseases. The clinical and histologic manifestation may vary somewhat, still, most
have features similar to the PSGN. If the underlying infection is eradicated, the
prognosis is good.
Systemic lupus erythematous, Henoch-Schönlein purpura, and mixed essential
cryoglobulinemia may present as an acute GN, but they are usually associated with
other glomerular syndromes.
Asymptomatic urinary abnormalities
This group of patients has proteinuria in the nonnephrotic range and /or hematuria,
unaccompanied by edema, reduced GFR, and hypertension. Abnormalities are often
discovered incidentally and may be persistent or recurrent. In some, this syndrome is
a phase in the natural history of other glomerulopathic syndromes, especially NS or
chronic glomerulonephritis.
Asymptomatic hematuria
A variety of renal lesion may present as asymptomatic hematuria.
IgA nephropathy
IgA nephropathy or Berger’s disease is the most common cause of recurrent
hematuria of glomerular origin. It accounts for 50% of cases with asymptomatic
hematuria and 26 to 34% in primary glomerulopathy.
Light microscopic changes are variable, but diffuse mesangial proliferative
glomerulonephritis or focal and segmental proliferative glomerulonephritis is found
most often. In some cases, glomerular morphology may be normal; uncommonly,
crescents may be found. The diagnosis depends on the finding of prominent IgA
deposits in the mesangium by immunofluorescence microscopy.
The typical presentation is gross hematuria following a viral illness or vigorous
exercise, with men affected two to three times more frequently than women. Most
other patients present with asymptomatic hematuria discovered on an incidental
examination, accompanied by mild to moderate proteinuria. Most patients are
between the ages of 15 and 35. Microscopic hematuria usually remains after gross
hematuria resolves. Mild proteinuria of less than 1g/d is common, but the NS
develops occasionally. Serum complement is normal. Serum IgA levels are increased
in about 50% of cases.
At present, there is no evidence that therapy will influence the natural history,
although intermittent steroid therapy may reduce the frequency of episodes of gross
of hematuria. Steroids may also result in remissions of proteinuria in those patients
with NS.
The prognosis is variable, but the disease tends to progress slowly. Approximately
50% of patients develop end stage renal failure within 25 years of the time if
diagnosis. Poor prognostic indicators include nephrotic range proteinuria,
hypertension, and azotemia. IgA nephropathy recurs in the transplanted kidney in
approximately 30 to 40% of cases, but with minimal long-term effects on renal
function.
Chronic glomerulonephritis(CGN)
The syndrome of chronic glomerulonephritis is characterized by persistent urinary
abnormalities (proteinuria and/or hematuria), by hypertension and the progressive
loss of functioning nephrons. Except for the minimal change, all the disorders
described in this chapter can lead to chronic glomerulonephritis.
At the earliest time points, only mild proteinuria with a slight decrease in GFR
and minimal hypertension may be seen. Inevitably, these patients generally progress
to ESRD.
Treatment is supportive and symptomatic. Hypertension and infections should be
treated vigorously. Nephrotoxic agents should be avoided. Anticoagulants and ACEI
may be beneficial.
The prognosis of CGN depends upon the nature of the underlying disease and
presence or absence of complications, especially hypertension. Ten, twenty, or more
years may elapse from the first discovery of CGN until the development of ESRD.
Renal biopsy is necessary to define the precise nature of the glomerular lesion.
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