HTN for many years, DHP CCB, ACEI, ARB use.
ATN with superimposed acute pulmonary effusion s/p lasix treatment and discharge 1 month ago.
COPD with corpulmonale, with right ventricle systolic dysfunction and moderate TR, LVEF: 60%, no cold limbs. NYHA: I-II
BW gain about 10 kg from 59kg to 67kg within 1 month. Daily water intake: 600c.c
Cr: 1.4-->1.5-->1.7-->2.2-->2.6-->2.8-->2.62(after admission), BUN: from 50 to around 60 in the last two test
acute renal failure, complicated with acute pulmonary effusion, present with major fissure fluid accumulation, cause?
there was no fever, no other medications, no other infection source, no JVE, no murmur. Alb:(2.7), K:3.1 Na: 137
bilateral pitting edema over lower limbs.
How to approach and thinking process?
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Acute renal failure:
以前就知道臨床上會分Pre-renal, renal, post-renal
pre-renal 又可分為hypovolemia or relative hypoperfusion of kidney
前者補補水，後者就要從病人的underlying：CHF, cirrhosis→hepatorenal, Renal stenosis…依據根本原因做治療
drugs: 除了relative hypoperfusion of kidney造成的ischemia影響以外，drugs of NSAID以及ACEI, ARB往往也有可能impair renal perfusion, 或加劇其惡化情形。（因為PGE1會對入球小動脈有擴張作用、而Angiotensin則對出球小動脈有收縮作用。NSAID限制入球小動脈的擴張而ACEI, ARB讓出球小動脈擴張，影響到glomerular capillary perfusion）
postrenal可以從PE, bladder脹不脹先行判斷。Sono是必備的好診斷工具。
複雜的是renal的部份：
依許V的經驗，區分pre-renal以及renal比較準的parameter是FENa, 不過其實臨床上也有很多檢驗值跟實際病情兜不起來的case，故臨床上其實從history大致上就可先行推斷。
一般可以有四個思考方向: vascular, glomeruli, tubular, and interstitial.
Vascular: obstruction(artery or vain), vasculitis.
Tubular: ATN (necrosis), toxin(分為內生性：rhabdomyolysis, hemolysis及外生性： radiocontrast, calcineurin inhibitors, antibiotics (e.g., aminoglycosides), chemotherapy (e.g., cisplatin), antifungals (e.g., amphotericin B), ethylene glycol), infection, or ischemia (pre-renal的惡化版)
Intersitial: AIN (nephritis), 可區分為allergy(antibiotics [beta-lactams, sulfonamides, quinolones, rifampin], nonsteroidal anti-inflammatory drugs, diuretics, other drugs) or infection. (pyelonephritis)
Glomeruli: 十分複雜，可參考harrison chap.277, clinical s/s: hematuria, proteinuria, BP high or normal, general edema.
臨床分類（依時間進程） 對應病理切片renal bx
Acute 2-3days to 1 week Diffuse Glomerular nephritis
RPGN 2wks to 2months Cresent GN
Slowly progression Months to years Focal (segmental ) proliferation <50%
Micorscopic hematuria Mesangial expansion.
懷疑GN可驗ANCA, Anti-GBM, C3，各有各自的ddx→請翻書。
一般C-ANCA: Wegner’s disease, with pathology: pauci-immune study
Anti-GBM: associated with lung: goodpasture’s disease. with pathlogy: linear immunradio study.
C3 decreased: endocarditis, PSGN…, with pathology granular deposit.
Mimic type: HUS, TTP.
BUN and Creatinine
常見BUN increase的原因（會受蛋白質營養、水份影響）：
protein代謝增加：Tigecycline, NSAID. Absorbtion增加：UGIB. 濃度：dehydration.
Creatinine 增加：(多從glomerular濾出貨從tubular secretion)
Baktar, Cimetidine均會 inhibition tubular secretion。
有哪些情況Creatinine會減少：liver function decreased: cirrhosis, muscle wasting, pregnant.
----------so the intervention for this patient--------
1. We use Lasix po initially, but change to 100mg Q8h in the afternoon due to no much U/O.
2. Consult CV for help evaluation due to the sign of right heart failure: subtle JVE, Ascites, bilteral lower limb pitting edema.
3. arragned Chest once diagnosed tapping.
----------and the other day-----------------------------
1. U/O: 470 cc. BP: 107/60 mmHg. Still dyspnea, change O2 from N/C to Ventri 50% a/c to SpO2 drpped to 89% in night.
2. Cardiologist add dobutamine, run 5ug/kg/min and arragned Thailium scan see if necessary to do Cath. --> treat as right heart failure. And followed Bun/Cr being prone to pre-renal ARF.
3. Consult CM, for immediate pig-tail insertion for s/s relieved and monitor the amount of pleural effusion. (may caused by lymph drainage due to pre-load overload in Right HF) yellowish 1000cc. transudate.
4. keep observation...
