中山醫學大學腎臟科 醫學生 Orientation

2007-12-07 Update (簡易版)

一. Meeting
(1.) Morning meeting : W3, 4 7:30AM 9F 衛教中心 / 會議室
(Clerk/Intern/Resident 請於前一天跟病房 CR 確認 Case,新舊病歷皆需帶)
(2.) Case conference by Dr. 林智廣 : W2 1:00PM 4705 會議室
(請 Resident 跟 Dr. 林 確認預討論 Case)
(3.) Case conference by Dr. 吳勝文 : W2 3:00PM 10F 會議室
(Clerk/Intern 請準備一位 Case , 不一定要是腎臟科的)
(4.) Journal meeting : 每 W4 下午 4: 00PM 10F 會議室
(5.) 腎臟科基礎教學 : 每 W5 下午 4: 00PM 10F 會議室
(6.) 臨床病理討論及教學 : 每月第二個禮拜四 3: 00PM 10F 會議室
(7.) 腎臟科/泌尿科/放射科聯合討論 : 每 W5 8:00 AM 1F 放射科
(7.) Bedside teaching and 門診教學 : as schedule

二. 次分科病房見習課程時間表 :

見附件一

三. 學習重點

(1.) Edema/proteiuria/hematuria/urinalysis 判讀
(2.) Hyper/hyponatremia
(3.) Hyper/hypokalemia
(4.) Metabolic/respiratory acidosis/alkalosis ( ABG 判讀)
(5.) Acute renal failure
(6.) Chronic renal failure (esp diabetic nephropathy)
(7.) Glomerular disease (Nephrotic syndrome and nephritic syndrome)
(8.) Tubular disorders and tubulointerstitial disorders
(9.) Vascular injury to kidney
(10.) Replacement therapy of renal failure
(A.) Dialysis therapy (hemodialysis and peritoneal dialysis )
(B.) Renal transplantation
(11.) Nephrolithiasis
(12.) Urinary tract infection and pyelonephritis
(13.) Urinary tract obstruction
 腎臟內科學習指引綱要

(Part I) Approach to the patient with renal disease

(一) 尿液分析

1.如何判讀 Dipstick 各項結果？(protein, blood, sugar, pH, 比重, ….等)，當

Dipstick protein 與 Sulfosalicylic acid test 兩者有差異時，代表什麼意義？

2.如何分辨 glomerular 或 nonglomerular hematuria？

3.各類 casts 代表的意義如何？

(二) 腎功能評估

4.測定 glomerular filtration rate (GFR)的方法有那幾種？它的意義如何？ 那

些因素會影響 GFR 的測定？

5.血液 BUN / Creatinine 正常比值約多少？那些狀況會造成比值上升或下

降？

(三) 影像學檢查

6.腎臟超音波檢查有那些功用(適用時機)？超音波強度與腎臟大小判讀的意

義如何？

7.Intravenous pyelograply (IVP) 有 那 些 功 用 ？ 那 些 病 人 較 可 能 發 生

contrast-induced nephropathy ?
(四) 腎臟穿刺檢查

8.什麼是腎臟穿刺的適應症和禁忌？它可能造成什麼併發症？

(Part II) 體液、電解質和酸鹼平衡

9.Osmolality 如何估計？如何 Approach hyponatremia 的病人？

10.SIADH 的原因和診斷要點是什麼？如何治療？

11.如何區分 renal loss 或 extrarenal loss 的 hypokalemia？hypokalemia 的治療

準則如何？(如何估計補充量？如何給予？)

12.Hyperkalemia 的 EKG 變化如何？如何緊急處理嚴重病例？

13.Anion gap 是指什麼？正常範圍約多少？如何利用 anion gap 作 metabolic

acidosis 的鑑別診斷？什麼情況才須補充 NaHCO3

14.如何利用 volume status 和 urine chloride level 來作 metabolic alkalosis 鑑別

診斷？

15.Hypercalcemia 常見的原因有那些？intact parathyroid hormone (iPTH)及

PTH-related protein (PTHrP)的診斷意義如何？

16.Hypophosphatemia 對全身各器官產生那些危害？(例如中樞神經、神經肌

肉、血液、腎臟等)
(Part III) Clinical Nephrology

(一) 腎衰竭

17.如何利用 FeNa 和 urinary indices 來作急性腎衰竭的鑑別診斷？

18.那些狀況會使慢性腎衰竭病人產生急性惡化，須儘早矯治？

19.那些措施可減緩 GFR 下降的速度？

20.需要接受緊急透析的適應症(indications)有那些？

21.Hemodialysis (HD)與 continuous ambulatory peritoneal dialysis (CAPD)各有

何優缺點？兩種透析式各有何併發症？

22.CAPD 腹膜炎如何診斷？其治療原則如何？

23.尿毒症病人發生 congestive heart failure 或 pulmonary edema 時如何診斷和

治療？

24.那些常用藥物在腎臟衰竭病人身上須減量？

25.腎臟移植術前如何準備(HLA typing, Donor 的選擇)?

26.腎臟移植的抗排斥藥物治療的種類和機轉如何?
(二) 腎絲球病變

27.Nephrotic syndrome (腎病症候群)的定義如何？請列舉其常見的發生原

因？(依原發性或繼發性來區分)

28.那些腎絲球腎炎其血清補體有下降現象？

29.IgA nephropathy 的臨床和病理特徵如何？那些因素表示預後較差？

30.糖尿病腎病變的 stage 如何區分？那些措施可減緩它的 progression？

31.Lupus nephritis 的 WHO 分類如何？那個分類預後最差？

(三) 腎間質小管病變、腎血管病變等

32.急性腎小管間質炎的臨床特點如何？導致此病的常見藥物有那些？

33.Complicated urinary tract infections 有那些特色？

34.Autosomal dominant polycystic kidney disease(ADPKD)會造成那些併發

症？影響其預後的因素有那些？

35.對 懷 疑 患 有 繼 發 性 高 血 壓 病 人 需 要 安 排 那 些 檢 查 ？ 利 用 captopril

screening test 診斷 renal artery stenosis 的 criteria 如何？

四. 病房工作要點

(1.) 住院常規
(A.) CBC, BUN, Cre, Na, K, GPT, Ac sugar (or DC, Alb, TP, Ca, P, UA, .)
(B.) Urinalysis
(C.) Chest X-ray ( or KUB)
(D.) 12 lead ECG
(E.) Record body weight or urine output or input
(F.) Inspect and review the necessity of current drugs and the correlation
with diagnosis every day
(G.) Set therapeutic goal and preparation for discharge

(2.)個別疾病常規
(A.) Acute renal failure
--- survey medical history, drug history, family history, …..
--- Exclude post-renal etiology by physical exam, KUB, urinary
catheterization or renal echo
--- Check FENa, urine-osmo or urine-Na to differentiate pre-renal and
intrinsic etiology
--- correct precipitated factors and keep adequate urine output by
diuretics if needed ( hydration may be needed but cautiously in
oligouric or anuric patient
(B.) Chronic renal failure or end stage renal stage
--- collect 24-H urine for Ccr and daily urine protein
--- check HbsAg, anti-HCV, anti-HIV, VDRL, intact-PTH, ferritin, Fe,
TIBC, Mg, Ca, P, ABG ( esp for dialysis)
--- renal echo
--- EPO for anemia after correction of iron deficiency if existence
--- CaCO3/VitD3(Macolol or Alfarol) for hypocalcemia and Ulcerin for
hyperphosphotemia
(C.) Electrolyte imbalance
--- collect serum/urine biochemistry (serum/urine osmolarity, Na, K, Cl,
24 hour urine K, or ABG) before therapy as possible according to
individual disease
--- follow electrolyte daily till stabilization or normalization
(D.) Nephrotic syndrome or glomerulonephritis
--- collect 24-H urine for Ccr and daily urine protein
--- check ANA, C3, C4, IgG/A/M, HbsAg, anti-HCV, anti-HIV, Alb, TP,
TG/Chol(NPO at least 8 hours), or ANCA if needed
--- perform serum/urine electrophoresis and immunoelectrophoresis
(E.) Work-up for renal biopsy
(a.) Prepare for renal biopsy
--- check coagulation status including platelet, PT, APTT, and
bleeding time
--- survey any absolute or relative contraindication for renal biopsy
--- explain the risk/配合事項 to the patient and family
--- DDAVP 4amp IVD or analgesic( ex Demerol IM ) before biopsy
if needed
(b.) Post biopsy
--- bed rest and wound compression strictly and check vital sign as
order
--- follow urinalysis and renal echo the next day
(F.) Renal transplantation
--- Three combined therapy : Tacrolimus(FK506)/cyclosporine,
Mycophenolate(Cellcept), and steroid ; (+ Baktar)
--- check body weight and urine output daily
--- check Cre level and drug level ( FK506 and C2 level) if deteriorated
renal function, drug interaction, or adjustment of dosage of
immunosuppressive drugs
--- survey precipitated factors of deteriorated graft kidney function
--- Rescue therapy : MTP and ATG
五. 醫學生需注意 / 完成事項
(1.) 依照 resident 分配完成 primary care patient 的 general history, progress
note…
(2.) 完成 morning meeting, Bedside teaching and 門診教學記錄
(3.) 查房及 meeting 要準時出現,且查房時要主動向 attending 報告病人情況
/data
(4.) 請實習醫師詳實記錄 Special chart 上的 Lab data results，包括門診及急
診 data
(5.) 幫忙通知下一梯醫學生提前找 ward CR 報到
 Classification and Major Causes of Acute Renal Failure (ARF)

PRERENAL ARF
I. Hypovolemia
A. Hemorrhage, burns, dehydration
B. Gastrointestinal fluid loss: vomiting, surgical drainage, diarrhea
C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoadrenalism
D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, severe
hypoalbuminemia
II. Low cardiac output
A. Diseases of myocardium, valves, and pericardium; arrhythmias; tamponade
B. Other: pulmonary hypertension, massive pulmonary embolus, positive pressure
mechanical ventilation
III. Altered renal systemic vascular resistance ratio
A. Systemic vasodilatation: sepsis, antihypertensives, afterload reducers, anesthesia,
anaphylaxis
B. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrine, cyclosporine,
tacrolimus, amphotericin B
C. Cirrhosis with ascites (hepatorenal syndrome)
IV. Renal hypoperfusion with impairment of renal autoregulatory responses
Cyclooxygenase inhibitors, angiotensin-converting enzyme inhibitors
V. Hyperviscosity syndrome (rare)
Multiple myeloma, macroglobulinemia, polycythemia
INTRINSIC RENAL ARF
I. Renovascular obstruction (bilateral or unilateral in the setting of one functioning kidney)
A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissecting
aneurysm, vasculitis
B. Renal vein obstruction: thrombosis, compression
II. Disease of glomeruli or renal microvasculature
A. Glomerulonephritis and vasculitis
B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, disseminated
intravascular coagulation, toxemia of pregnancy, accelerated hypertension, radiation
nephritis, systemic lupus erythematosus, scleroderma
III. Acute tubular necrosis
A. Ischemia: as for prerenal ARF (hypovolemia, low cardiac output, renal vasoconstriction,
systemic vasodilatation), obstetric complications (abruptio placentae, postpartum
hemorrhage)
B. Toxins
1. Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminoglycosides),
chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylene glycol), acetaminophen,
illegal abortifacients
2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (e.g.,
myeloma)
IV. Interstitial nephritis
A. Allergic: antibiotics (e.g., β-lactams, sulfonamides, trimethoprim, rifampicin),
nonsteroidal anti-inflammatory agents, diuretics, captopril
B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g.,
cytomegalovirus), fungal (e.g., candidiasis)
C. Infiltration: lymphoma, leukemia, sarcoidosis
D. Idiopathic
V. Intratubular deposition and obstruction
Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphonamides
VI. Renal allograft rejection
POSTRENAL ARF (OBSTRUCTION)
I. Ureteric
Calculi, blood clot, sloughed papillae, cancer, external compression (e.g., retroperitoneal
fibrosis)
II. Bladder neck
Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot
III. Urethra
Stricture, congenital valve, phimosis
 Urine Diagnostic Indices in Differentiation of Prerenal versus Intrinsic Renal ARF

Typical Findings in ARF

Diagnostic Index Prerenal Intrinsic Renal

Fractional excretion of sodium (%)a <1 >1

Urine sodium concentration (mmol/L) <10 >20

Urine creatinine to plasma creatinine ratio >40 <20
Urine urea nitrogen to plasma urea nitrogen ratio>8 <3
Urine specific gravity >1.020 ~1.010
Urine osmolality (mosmol/kg H2O) >500 ~300
Plasma BUN/creatinine ratio >20 <10–15
a
Renal failure index <1 >1

Urinary sediment Hyaline castsMuddy brown granular casts

 Stages of Chronic Kidney Disease CKD

StageDescription GFR, mL/min per 1.73 m2

At increased risk 90 (with CRD risk factors)

1 Kidney damage with normal or increased GFR90
2 Kidney damage with mildly decreased GFR 60–89
3 Moderately decreased GFR 30–59
4 Severely decreased GFR 15–29
5 Renal failure <15 (or dialysis)

Note: GFR, glomerular filtration rate.

Source: Adapted from Levey, with permission

Summary of Clinical Presentations That may Suggest Given Major Categories of Causes
of Chronic Renal Disease

Cause Clinical Presentation

Diabetic kidney History of diabetes, proteinuria, retinopathy

disease
Hypertension Elevated blood pressure, normal urinalysis, family history.
Nondiabetic Nephritic or nephrotic presentations
glomerular disease
Cystic kidney Urinary tract symptoms, abnormal urinary sediment, radiologic
disease imaging abnormalities
Tubulointerstitial History of urinary tract infections and reflux, chronic medication and
disease drug exposure, abnormalities in urinary tract imaging, tubular
syndromes including urine-concentrating defect, abnormal urinalysis
 Maintenance Immunosuppressive Drugs

Agent Pharmacology Mechanisms Side Effects

Glucocorticoids Increased bioavailability Binds cytosolic Hypertension, glucose

with hypoalbuminemia and receptors and heat intolerance,
liver disease; shock proteins. dyslipidemia,
prednisone/prednisolone Blocks transcription osteoporosis
generally used of IL-1,-2,-3,-6,
TNF-α, and IFN-γ
Cyclosporine Lipid-soluble polypeptide, Trimolecular Nephrotoxicity,
(CsA) variable absorption, complex with hypertension,
microemulsion more cyclophilin and dyslipidemia, glucose
predictable calcineurin → block intolerance,
in cytokine (e.g., hirsutism/hyperplasia of
IL-2) production; gums
however, stimulates
TGF-β production
Tacrolimus Macrolide, well absorbed Trimolecular Similar to CsA, but
(FK506) complex with hirsutism/hyperplasia of
FKBP-12 and gums unusual, and
calcineurin → block diabetes more likely
in cytokine (e.g.,
IL-2) production;
may stimulate
TGF-β production
Azathioprine Mercaptopurine analogue Hepatic metabolites Marrow suppression
inhibit purine (WBC > RBC >
synthesis platelets)
Mycophenolate Metabolized to Inhibits purine Diarrhea/cramps;
mofetil (MMF) mycophenolic acid synthesis via inosine dose-related liver and
monophosphate marrow suppression is
dehydrogenase uncommon
Sirolimus Macrolide, poor oral Complexes with
bioavailability FKBP-12 and then blocks
p70 S6 kinase in the IL-2
receptor pathway for
proliferation
 The Most Common Opportunistic Infections in the Renal Transplant Recipient

Peritransplant (<1 month)

Wound infections
Herpesvirus
Oral candidiasis
Urinary tract infection
Early (1–6 months)
Pneumocystis carinii
Cytomegalovirus
Legionella
Listeria
Hepatitis B
Hepatitis C
Late (>6 months)
Aspergillus
Nocardia
BK virus (polyoma)
Herpes zoster
Hepatitis B
Hepatitis C