1. Renal Insufficiency 薛冰 Department of Pathophysiology,
Shandong University School of Medicine 薛冰

2. INDEX
Acute renal failure(ARF)
Chronic renal failure(CRF)

3. Functions of the Kidney
1.Excretion
Remove waste product from the body；
Regulate electrolyte and acid-base balance.
2. Endocrine
Produce renin、EPO、and prostaglandins
Active VitD3
Inactivate gastrin、PTH.

4. Renal insufficiency Dysfunction of excretion Diseases Symptoms
and endocrine
Diseases
Symptoms
and signs
Edema, hypertension, oliguria, polyuria, proteinuria, anemia, osteodystrophy.

5. Causes 1. Primary renal diseases
Primary glomerular diseases, Primary tubular diseases, Interstitial nephritis, et al.
2. Secondary renal lesion
Circulatory system diseases, immunity diseases, metabolic diseases, hematopathy(血液病）, et al.

6. Part I Acute Renal Failure(ARF)
Definition
Etiology & classification
Pathogenesis
Alteration of Metabolism and Function
Prevention & Treatment

7. I Definition water intoxication, azotemia,
Acute renal failure (ARF) is defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.
water intoxication, azotemia,
hyperkalemia, metabolic acidosis

8. Morbidity and mortality
急性肾衰竭迄今为止仍是威胁人类生命的危重病症，第二次世界大战时其死亡率高达91%，越南战争时期由于透析技术的应用，其死亡率降为68%。近年来单纯急性肾衰竭的死亡率为7%~23%，而复杂性急性肾衰竭的死亡率仍高达50%~80%。急性肾衰竭的死亡率取决于原发病的严重程度，以往的研究表明，急性肾衰竭的病因不同，其死亡率有明显差别，如缺血性原因者死亡率为30%，而中毒性原因者死亡率仅为10% .

9. II Etiology and Classifications
1. causes
Prerenal ~
Intrarenal ~
Postrenal ~
2. urine volume
Oliguric ~
(<400ml/day)
Nonoliguric ~
(>400ml/day)
3. renal lesion
functional~
organic ~
obstructive ~

10. Causes and classification
Pre-renal (~70% of cases)
functional renal failure; prerenal azotemia
Intra-renal (~25% of cases)
parenchymal renal failure
Post-renal (<5% of cases)
postrenal azotemia
adrenal gland
ureter
renal pelvis
urinary bladder

11. Cause and classification
(I) Prerenal failure - Diseases that compromise renal perfusion
Decreased effective arterial blood volume - Hypovolemia (ECF↓ 50% → RBF ↓ 90-95%)
Congestive heart failure (CO ↓ 40 % → RBF ↓ 72 %)
sepsis (vasodilatation)

12. pathogenesis of pre-renal ARF
pre-renal factors
shock caused by haemorrhage 、infection、AHF、
serious anaphylactic reaction and others (hepatorenal syndrome )
ADH effective blood volume Ald
BP decrease
kidney perfusion renal blood vessel contraction
  renal blood flow 
  Glomerular EFP
  GFR
urine
pathogenesis of pre-renal ARF

13. Characteristics of prerenal ARF
(A) Decreased perfusion without cellular injury
(B) Intact renal tubular and glomerular functions
(C)Reversible if underlying cause is corrected in time. ( Hypovolemia, Renal hypoperfusion, Hypotension)
early stage: functional~ late stage: organic ~
(D) Characteristics of urine: oliguria, specific gravity ,
sodium , urinary sediment(-)

14. Cause and classification
(II) Intrarenal failure - Diseases of the renal parenchyma（肾实质）, specifically involving the renal tubules, glomeruli, interstitium
Vascular diseases
Interstitial diseases
Acute glomerulonephritis
Diseases in tubules
Acute tubular necrosis (ATN)

15. ■Long time of renal ischaemia
Diseases in tubules:Acute tubular necrosis (ATN)(80%)
■Long time of renal ischaemia
shock, dehydration, hemorrhage denaturalization
■Renal poisoning:
Extrinsic：chemical agents (carbon tetrachloride四氯化碳)
heavy metals (mercury水银)
X-ray contrast medium
biological toxin ：some mushroom, snake venoms drugs : sulfonamides磺胺药物, kanamycin卡那霉素
Intrinsic:hemoglobin, myoglobin，uric acid

16. Difference between pre-renal and intrarenal ARF
Pre-renal Intra-renal
Urine specific gravity > < 1.015
Urine osmotic pressure (mmol/L) > < 350
Urine sodium(mmol/L) < > 40
Ucr/Scr > 40: < 20:1
Urinary sediment (±) (+)
Urine protein (-) ＋～＋＋＋＋
Mannitol test urine volume urine volume(-)
　尿比重是指在4摄氏度下与同体积的水的重量之比。是尿液中所含溶质浓度的指标。　健康人24小时尿比重在1.015～1.025之间，比重高低与进水量有关，进水多则尿比重低。
A成人一般600MMOL /L到1000MMOL /L,平均800MMOL /L；尿渗透压亦称尿渗量，是反映单位容积尿中溶质分子和离子的颗粒数。尿比重和尿渗量都能反映尿中溶质的含量，但尿比重易受溶质微粒大小和分子质量大小的影响，而尿渗透压仅与溶质分子浓度相关，并不受溶质分子质量的影响。因此，尿中蛋白质及葡萄糖等含量的变化均可影响尿比重的结果，而对尿渗透压的影响较小，故测定尿渗透压变化更能真实地反映肾小管的浓缩和稀释功能。

17. Cause and classification
(III) Postrenal failure - Diseases causing urinary obstruction from the level of the renal tubules to the urethra
Tubular obstruction from crystals
Ureteral（输尿管） obstruction
renal pelvis
ureter
urinary bladder

18. Characters of Post-renal ARF
1) intact renal tubular and glomerular functions
2) reversible if underlying cause is corrected in
time (To rule out the obstruction quickly is very important.)

19. III Pathogenesis of ARF
Most of the manifestations of ARF are caused by the decreased urine volume.
Waste substance↑
The basic pathogenesis of ARF is to explain the reasons of decreased urine volume.

20. Glomerular-tubular balance 1% excrete
efferent
arteriol
GFR and tubular reabsorption are the main factors to determine the urine volume.
Glomerular-tubular balance
1% excrete
Decreased GFR and increased reabsorption in tubule will lead to decreased urine volume.
GFR

21. Pathogenesis of ARF (induced by ATN)
(I) Changes of renal hemodynamics (effects on glomerular function)
(II) Effects of tubular injury
(III) Glomerular Kf↓

22. (I) Changes of renal hemodynamics
1 Decreased renal blood flow

23. Inferior vena cava Adrenal gland Kidney Aorta Ureter Bladder Urethra
Renal blood flow: 20%～30% of cardiac output(1200 ml/min).
Inferior vena cava
Adrenal gland
Kidney
Aorta
Ureter
Bladder
Urethra

24. Net Filtration Pressure
60 out
BHP
10 out
18 in
COP
32 in
NFP CP
Blood hydrostatic pressure(BHP) mmHg out
Colloid osmotic pressure(COP) mmHg in
Capsular pressure(CP) mmHg in
Net filtration pressure(NFP) mmHg out

25. 1)Decreased renal blood presure
(A)Decreased systemic pressure (B)Increased tubular pressure
Systemic BP<80mmHg
Renal artery BP is decreased
Obstruction of urinary tract
Glomerular hydrostatic pressure is decreased
Increased Bowman’s capsule pressure
Glomerular effective filtration pressure is decreased Decreased urine volume
Glomerular hydrostatic pressure
Glomerular colloid osmotic pressure
efferent arteriole
Afferent arteriole
Bowman’s capsule pressure

26. BP < 80mmHg
CO RBF
BP (50-70mmHg) GFR (1/2 – 2/3)
BP(40mmHg) GFR = 0

27. 2) Renal vasoconstriction
(A)Increased activity of sympathetic system
Shock and trauma (low CO)
Baroreceptor in aortic arch and carotid sinus
Increased activity in sympathetic system
Contraction of renal artery
Constriction of afferent arteriole
RBF decrease
Decreased urine volume

28. Constriction of afferent artery(AII)
(B)Increased activity of renin-angiotension system
Ischemia and poisoning
Low renal artery
pressure
Injury of proximal tubule and reduced Na+ reabsorption
Increased Na+ in the distal tubule stimulate the Macula densa
Stimulate the release of renin from the
juxtaglomerular apparatus
Constriction of afferent artery(AII)
Decreased GFR

29. (C) unbalance of endothelin and NO
Injury of endothelium of renal vessels by hypoxia, acidosis
Increased synthesis and release of endothelin
decreased synthesis and release of NO
Constriction of afferent arteriole
Decreased effective filtration
pressure and GFR
Decreased urine volume

30. (D) Decreased production of vasodilatory prostaglandins (PGE2)
Kidney is the main organ to produce PGE2.
The role of PGE2 is dilating blood vessels.
The production of PGE2 is reduced before the development of ARI caused by gentamycin(庆大霉素 )poisoning.

31. 3）Renal vessel obstruction A swelling of endothelial cell
ischemia Na+ - K+ - ATPase
Renal toxic substances
cell membrane permeability
calcium pump dysfunction
free radical endothelial cellular injury
B microthrombus formation in renal vessel
Cell edema
Calcium overload

32. (I) Changes of renal hemodynamics
2. Renal blood flow re-distribution
renal cortex ischemia GFR
renal medulla hyperemia Renal tubular injury

33. (II) Renal tubular injury
1 Morphologic changes
①morphologic change

34. Red blood Cell Cast
Muddy Brown Cast
White blood Cell Casts

35. ② character of renaltubule cell damage
A.Necrotic lesion
tubulorrhexis lesion( renal poisoning and renal ischemia persistently )
：involve all renal tubule，especially loop of Henle.
focal necrosis of nephron,
epithelial cell necrosis
basement membrane is destroyed
nephrotoxic lesion (Renal poisoning) :
involve proximal tubule，
all Nephron damage ，
epithelial cells necrosis,
basement membrane is integrity
B.Apoptotic lesion： distal tubule

36. 细胞损伤机制（了解） 缺血、中毒 细胞损伤 (坏死；凋亡) ADP、毒物 OFR生成↑ 清除↓ GSH ↓ ATP ↓
Na+、K+-ATP酶↓ Ca2+-ATP酶↓
线粒体Ca2+↑
细胞内钠水潴留 胞浆内游离钙↑
磷脂酶活性↑
细胞内Ca2+超载
PGs、LTs
细胞水肿
脂质过氧化
细胞损伤 (坏死；凋亡)

37. 2 Effect of tubular injury
1）Tubule obstruction
2)Loss of tubule integrity: initial urine back-leakage

38. 1） Tubule obstruction Long time of renal ischemia Renal poisoning
Injury of proximal tubule cells ( necrosis)
Detach from basement membrane
and slough into the tubule lumen
and become impacted (tube cast)
Tubule obstruction
Increase Bowman’s capsule pressure
Reduced urine volume

39. Urine flow
Denuded
tubular
membrane
Injured
tubular
cells
Obstruction
from debris and
necrotic cells

41. ②Loss of tubule integrity （passive back-leakage）
Severe ischemia and poisoning of tubule
Epithelial cell necrosis and loss of tubule integrity (become leaky)
Back leaking of urine to peritubular interstitial space
high interstitial pressure
Press the tubule
Press blood vessels
↑ intratubular pressure
↓ RBF
Decreased urine volume

43. Glomerular lesion (III) Glomerular Kf↓ filtration surface area
Glomerular permselectivity
GFR 43

44. IV Clinical Course and manifestation
Two types of ARF:
oliguric (<400ml/d) ARF
nonoliguric (>400ml/d) ARF.

45. Clinical Course and manifestation
（I） oliguric ARF
1 Oliguric phase（days～weeks）
Manifestations:
a) changes of urine
b) azotemia
c) metabolic acidosis
d) hyperkalemia
e) Water intoxication

46. A changes of urine
(a) reduced urine volume:
less than 400 ml /24h (oliguria)
less than 100 ml/24h (anuria)
Mechanism:RBF decrease, renal tubule obstruction and urine back-leakage
(b) urine sediment investigation:
In prerenal ARF: (- or +?)
In ATN: (+)
contain : RBC, WBC, epithelial cells
and casts

47. (c) specific gravity and osmolality:
ATN: Low specific gravity =1.010~ (N: )
Osmolality of urine = or < plasma
Cause:
The ability of concentration and dilution is lost
in ATN.
Pre-renal AFR:

48. (d) urinary Na+ concentration:
In pre-renal ARF with normal reabsorption of tubule, urine [Na+] <20 mmol/L
In ATN, urine [Na+] >40 mmol/L
Actually, during oliguria, the amount of sodium entering Bowman’s capsule is decreased, the [Na+] in urine is elevated because of deficient tubular reabsorption of sodium.

49. Hypervolemic hyponatremia
B Water intoxication (Hypotonic hypervolemia, dilutional hyponatremia )
Causes:
(a) oliguria with more water intake
(b) increased production of metabolic water
(catabolism)
(c) Transfuse fluid↑
Fluid retention
Hypervolemic hyponatremia
Cell edema

50. C Azotemia (NPN>40 mg/dl)
(a) Concept of azotemia:
increased concentration of nonprotein nitrogens (NPN) in the blood. (normal: 20~35 mg/dl)
The nonproteins include urea, uric acid, creatinine etc.
(b) Reasons :
a) oliguria
b) increased catabolism of proteins.

51. 常用指标 血浆尿素氮 (blood urea nitrogen，BUN) 血浆肌酐 (serum creatinine, SCr)
内生肌酐清除率(creatinine clearance rate, CCr )

52. D Hyperkalemia most serious
Urinary excretion of K+
Tissue destruction
Metabolic acidosis
Transfuse non-fresh blood, high K+ diet
Movement of K+ from cells into ECF
Hyperkalemia

53. E Metabolic acidosis progressive, difficult to correct
GFR excretion of acid production
Secretion of H、NH3 , reabsorption of HCO3–
Catabolism ， acid production
Metabolic acidosis
Hyperkalemia

54. 2 Diuresis phase （4W） (A) Causes of diuresis:
Diuresis phase begins if the urine volume is over 400 ml/L, which reflects the improvement of ARF.
(A) Causes of diuresis:
a) Normal RBF and no tubule obstruction.
b) Concentration function of tubule is not recovered
completely. Water and sodium can not be absorbed
normally. The osmolality of urine remains low.
c) Osmotic diuresis.

55. (B) manifestations of diuresis phase:
polyuria，>400 ml/d；
Early stage： Hyperkalemia, Azotemia , Metabolic acidosis
Late stage：dehydration, hypokalemia, hyponatremia, infection.
25% of the deaths in ARF occurs in diuresis phase.

56. 3 Phase of functional recovery
The process of full recovery can take up to a year or more.
50% cases are restored to health.
50% cases become to CRF or die.
Influence factors:
(a) presence or absence of preexisting renal disease
(b) age of patients
(c) length of the oliguria phase

57. (II) Nonoliguric ARF
Some patients may develop an acute loss of renal function without oliguria (urine volume>400 ml/day).
Characters:
higher GFR than oliguria ARF,
character of urine: volume 1280ml/24h,lower osmolality ,low specific gravity ,higher urinary Na+ concentration than normal(lower than oliguric ARF)
fewer complications,
low mortality rate
no or mild hyperkalemia
still high BUN
Nonoliguric oliguric

58. V Treatment principles
(I) Prevention
1) Identify at risk patients, treat the underlying disease；
Avoid nephrotoxic agents
2) Monitor serum electrolytes

59. Treatment principles (II)Treatment Make the patient safe
Volume overload
Hyperkalemia
Control Azotemia
Acidosis
infection
Specific treatments
dialysis

60. Fluid therapy
Fluid therapy needs to be closely monitored to maintain normovolemia.
Fluid intake= insensible fluid loss
+urine volume
+ any ongoing losses
－ metabolic water

61. Treatment of hyperkalemia: sodium bicarbonate
For hyperkalemia
Oliguric renal failure is often complicated by hyperkalemia, increasing the risk in cardiac arrhythmias
Treatment of hyperkalemia:
sodium bicarbonate
insulin + hypertonic glucose
dialysis

62. nutrition For metabolic acidosis provide adequate caloric intake
limit protein intake to control increases in BUN
minimize potassium and phosphorus intake
limit fluid intake
For metabolic acidosis
NaHCO3 may be administered

63. §3 Chronic Renal Failure, CRF
Definition
Etiology
Pathogenesis
Alteration of Metabolism and Function
Prevention & Treatment

64. Dysfunction of excretion and endocrine
I Definition
etiological factors destruct nephron
Dysfunction of excretion and endocrine
waste product , acid-base and electrolyte disorders ， dysfunction of endocrine

65. II Causes of CRF
Renal diseases： chronic glomerulonephritis(NO.1) et al
Vascular disorders：diabetes mellitus、hypertensive disease、Periarteritis nodosa(结节性动脉周围炎）, et al
renal interstitium:chronic pyelonephritis(慢性肾盂肾炎）, Chronic nephritis et al
Urinary tract obstruction：urinary calculus(尿结石）,tumor,prostatic hyperplasia（前列腺增生） et al 65

66. III Clinical Course of CRF
compensatory stage
Renal insufficiency stage
Renal failure stage
Uremia stage 66

67. stage Clinical symptoms Ccr （ml/min） BUN (mmol/L) Cr (umol/L)
compensatory
>50
<9
<178
Primary disease,no specifical symptoms
Renal insufficiency
20～50
9～20
186～442
fatigue，mild anemia ，digestive tract discomfort
Renal failure
10～20
20～28
451～707
anemia，metabolic acidois，hypocalcemia 、hyperphosphorus 、polyuria and nocturia
Uremia
<10
>28.6
>707
Uremic symptoms 67

68. IV Pathogenesis of CRF Intact nephron hypothesis
Glomerular hyperfiltration hypothesis
Renal tubular-renal interstitium hypothesis
Trade-off hypothesis 68

69. Intact nephron hypothesis
causes
Destroy nephron persistently
Progressive reduction in the number of nephrons
Compensatory glomerular
hyperfiltration
Renal compensation insufficiency
Glomerulosclerosis
Renal failure 69

70. Renal tubular-renal interstitium hypothesis
Causes(Urine protein, cytokine,inflammatory factor, complement)
renal tubular epithelial cell apoptosis,necrosis
Renal tubular epithelial cell activated and proliferation
Renal tubular atrophy
Renal function aggravate progressively 70

71. Trade-off hypothesis Decreased GFR
Increased concentration of some solutes
Stimulate release of related regulatory factors (hormones)
Increase the solutes excretion
(good)
Further metabolic disorders
Aggravate the CRF (bad)

72. Decreased GFR
Decreased phosphate excretion
Increased serum concentration of phosphate
Decreased serum ionized calcium
Stimulate release of parathormone (PTH) by parathyroid glands
Increase the phosphate excretion from kidneys (good)
Stimulate calcium release from bone
[P] ,[Ca2+] osteomalacia (bad)

73. V Changes of Function and Metabolism
(I) characteristics of urine ：
1.volume：nocturia
polyuria（>2000ml/d）
oliguria oliguria(<400ml/d)
initial urine flow rate
osmotic diuresis
Renal concentrating function
2.specific gravity：hypotonic urine (early stage)、 isotonic urine(late stage)
3.sediment：Proteinuria(蛋白尿）、hematuria（血尿）、pyuria（脓尿）、casts 73

74. 尿渗透压的变化 正常
低渗尿
等渗尿
尿相对密度 74

75. II azotemia (NPN>28.6mmol/L)
BUN is not parallel to renal function
Plasma creatinine
endogenous creatinine clearance rate
----反应肾功能
Ucr × Vu
CCR=
Pcr 75

76. III acid-base and electrolyte disorders
1Dehydration
(A) due to polyuria, nocturia.
The ability to dilute the urine is preserved with a reduced ability to concentrate the urine.
(B) Diarrhea, vomiting may quickly cause dehydration.
Dehydration will lead to hypovolemia, decreased GFR and further deterioration of renal function.
The water intake should be of sufficient quantity and frequency (day and night) to compensate for the polyuria.

77. 2 Hypervolemia, General edema
Congestive heart failure.
Cause:
excess water intake
fixed urine volume(oliguria)

78. 3. Sodium imbalance
In normal persons sodium excretion may vary from nearly zero to more than 20g/day in response to a variable intake.
Patients with CRF lose the ability to regulate the sodium balance.

79. (A) Sodium deficiency and hyponatremia
Increased loss from kidneys : Osmotic diuresis,renal tubule fluid flow quicky (intact nephron ),
methylguanidine inhibit sodium reabsorption
Vomitting , diarrhoea
(B) Sodium excess (which leads to edema, hypertension)
Oliguria in terminal stage
Taking more

80. 4.Potassium imbalance
(1) Normal serum [K+] : maintained until the stage of renal failure. (GFR=10%~25% )
Causes of normal serum [K+]
(A) increased excretion from renal tubular and collecting duct(aldosterone secretion increase)
(B) increased excretion from intestine.
(2) Hypokalemia
Causes:A) polyuria in early stage
B) vomiting
C) diarrhea
D) restrict intake

81. (3) Hyperkalemia
Causes:A) oliguria in end-stage
B) acidosis
C)acute infection

82. P(>1.6mmol/L) :early stage : compensation（PTH ）
5. Ca P ：
P(>1.6mmol/L) :early stage : compensation（PTH ）
late stage: nephron bone dissolve
Ca(<2.25mmol/L)
P 【Ca】×【P】=40
calcium phosphate
calcitonin
1,25-(OH)2VitD Absorption of intestine Ca
Toxic substance damage intestinal tract
Intake
正常60%-80%磷由尿排出， 82

83. 1) impaired ability of H+ excretion, reduced HCO3- reabsorption.
6. Acidosis
1) impaired ability of H+ excretion, reduced HCO3- reabsorption.
2) impaired ability of NH4 + excretion, reduced HCO3- regeneration.
3)Sodium excretion increase, secondary RAS activation(metabolic acidosis with normal AG)
4) impaired ability of fixed acids excretion ( phosphate, sulfate, organic acids) metabolic acidosis with AG increase
Effects of acidosis
Anorexia, nausea and lethargy (depression of mental activity) may be due in part to the acidosis.
Kussmaul respiration (deep sighing respiration) is for increasing CO2 excretion. 83

84. (IV) Renal hypertension
Fluid and sodium retention(Na+-dependent,75%)
(2) Renin (renin-dependent)
(3) kinin、PGE2 84

85. (v) Hemorrhagic tendency
Toxic substance inhibite the function of platelet
PF3
17%-20%患者出现皮下瘀斑，紫癜，鼻粘膜出血，牙龈出血，胃肠道粘膜出血 85

86. Bleeding Platelet counts are normal.
Platelet function is impaired by uremic toxins.
adhesion
aggregation

87. (VI) Anemia and bleeding(97%)
Concept: normochromic, normocytic anemia, too few red blood cells
1)Primary factors of renal anemia:
(A) Deficient production of RBC
EPO (erythropoietin) is a red blood cell growth factor produced by kidney (90%), which can stimulate the production of RBC in bone marrow.

88. Uremic toxins may inactivate EPO._
EPO is produced by the kidneys
damaged kidneys _
Uremic toxins may inactivate EPO.
blood
Uremic toxins may suppress the response of bone marrow to EPO.
stimulates the production of RBC in bone marrow _

89. (B)Reduced red blood cell survival
The RBC lifespan is shortened by uremic toxins.
Secondary factors of renal anemia:
Iron deficiency
Drug effects
bleeding

90. Symptoms of anemia
Fatigue
Loss of appetite

91. (2)1,25-（OH)2Vit D3 : absorption of intestine Ca
(VII) renal osteodystrophy
(1)P Ca and secondary hyperparathyroidism： high turnover bone disease
(2)1,25-（OH)2Vit D : absorption of intestine Ca
(3) acidosis：bone mineral lysis，decalcification
A)Bone salt leaves the bone to blood for buffering increased [H+]
B)Acidosis decreases the formation of active vit.D3.
C) Acidosis decreases the calcium absorption from the gut.
(4) aluminum poisoning : low turnover bone disease 91

92. Principles of treatment
1 Focus on primary disease treatment
2 alimentary control
Nutritional management
Protein restriction
Salt-restriction diet
3 treat complications
4 dialysis
5 transplantation 92

93. End-stage renal failure
uremia
ARF
CRF
Intoxication
symptom
Toxin
End-stage renal failure 93

94. Uremia toxin
source： Metabolite Ectogenesis toxin Ectogenesis toxin metabolite Normal activity material 94

95. Uremia toxin
common： urea, uric acid,guanidine（methylguanidine 、creatinine ）, amines and phenol，middle molecules、PTH 95

96. change of function and metabolism96

97. 头痛、头昏、烦燥不安、抑郁、嗜睡甚至昏迷， 葡萄糖耐量降低，负氮平衡，高脂血症，代酸
神经系统
头痛、头昏、烦燥不安、抑郁、嗜睡甚至昏迷，
周围神经病变
心血管系统
高血压
心力衰竭
心包炎
血液和免疫 贫血
出血倾向
易感染 代谢
葡萄糖耐量降低，负氮平衡，高脂血症，代酸
尿毒症
消化系统
食欲不振、厌食、恶心、呕吐或腹泻，溃疡性炎症
肌肉骨骼系统
肾性骨病
生长迟缓
内分泌系统
甲低，甲旁亢，垂体-性腺功能失调 皮肤
瘙痒、干燥、脱屑和颜色改变，尿素霜
呼吸系统
库氏呼吸，氨臭，纤维性胸膜炎，肺水肿 97

98. 1、treatment of the primary disease 2、 dialysis therapy
Treatment principle
1、treatment of the primary disease
2、 dialysis therapy
3、 renal transplantation 98