2014.11.27 MGR 오심, 구토로 내원한 57세 남자 신장 내과 R3 김민제 Prof. 임천규

History Chief complaint Present illness Vomiting onset : 4일전 Cb. infarction, HTN으로 본원 NR (Prof. 박기정), DM으로 본원 IE (Prof. 우정택), DM CKD로 본원 IN (Prof. 임천규) follow up 하며, 약물 치료중인 환자. 2주전 부터 오심 증상 발생하였으나, 별다른 치료 없이 지내던 중, 4일전 부터 vomiting 발생 및 악화되어 응급실 내원함

Past Medical History DM / HTN / TBc / Hepatitis (+/+/-/-) DM (+) : 2012년 진단 HTN (+) : 1998년 진단 Cb. Infarction (+) : 2012년 진단 DM CKD (+) : 2012년 진단 Op Hx (-) Medication (+) : repaglinide 100mg TID, insulin glargine 14U aspirine 100mg QD, valsartan 160mg QD rosuvastatin 10mg QD

Personal History Family History Alcohol (-) Smoking (+) : 30PY(ex-smoker, 2년전 stop) Family History Cancer Hx (-) DM DM

Review of System 1. General Genealized weakness (+) : 약 2주 전부터 증상 지속됨 Weight change (-) Edema (-) Fever (-) 2. Skin Rash (-) Pigmentation(-) Itching(-) Jaundice (-) 3. Head/Neck Headache (-) Pain (-) Sorethroat (-) Hoarseness(-) 4. Eyes Pain(-) Visual disturbance (-) 5. Respiratory Cough(-) Sputum (-) Dyspnea (-) Hemoptysis (-)

Review of System 6. Cardiac Chest pain (-) Palpitation (-) DOE (-) Orthopnea(-) 7. Gastrointestinal A/N/V/D/C(-/+/+/-/-) : 2주 전부터 발생하여 Nausea Grade II 4일 전부터식사와 상관없는, non projectile, 3 ~ 4 회 / day Abd. distension (-) Hematemesis (-) Hematochezia (-) Abd. Pain (-) 8. Genitourinary Dysuria (-) Frequency (-) Urgency (-) Oliguria (-) 9. Nerve system Fainting (-) Dizziness (-) Sensory/Motor weakness (-/-)

Physical Examination Height : 171.0cm Weight : 65.0 kg BMI : 22.2 kg/m2 Vital Sign : 120/80 mmHg - 76/min - 16/min – 36.5℃ 1. General appearance Alert consciousness Chronically ill looking appearance 2. Thorax Symmetric chest expansion Clear breathing sound without rale/wheezing Regular Heart Beat without murmur 3. Abdomen Soft / obese abdomen Normoactive bowel sound Tenderness(-) / Rebound Tenderness(-) Shifting dullness(-) Fluid wave(-)

Physical Examination 4. Back/Extremities Generalized edema (-) Pretibial pitting edema (-/-) Back pain(-) CVA tenderrness(-) 5. Neurology Motor V V Sensory 100 100 V V 100 100

Initial Lab Finding 1. CBC/DC 2. Chemistry 3. ABGA (room air) 4,800/mm² - 9.6 g/dl – 29.4 % - 232K (seg 73.0%) PT (INR) 0.97 aPTT 31.7 2. Chemistry TB 0.21 mg/dL Prot/Alb 5.9/3.6 g/dL AST/ALT 11/12 IU/L Glucose 235 mg/dL BUN/Cr 111/9.4 mg/dL Na/K/Cl 136/6.0/106 mmol/L LD/CK 351/75 U/L Uric acid 8.3 mg/dL Ca/P/Mg/ 8.3/5.9/3.0 mg/dL CRP <0.3 mg/dL HbA1c 7.3 % CK/CK-MB/TnI 75/3.6/0.01 TG/total/LDL 85/192/66 mg/dL 3. ABGA (room air) pH 7.303 - pCo2 29.3 mmHg - po2 108.4 mmHg - HCo3- 15.4 mmol/L so2 95.6% 4. U/A RBC 0~1 /HPF WBC 0~1 /HPF pH 5.5 SG 1.014 Blood (-) Protein (+++) Glucose (++++) Leukocytes (-) Nitrite (-) Total cholesterol : 192 mg/Dl L.D.L cholesterol : 84 mg/DL TG : 243 mg/DL Metabolic acidosis with High anion gap Na – (HCO3 + Cl) = 14.6

Previous K level & kidney function 9.4 28.6 6.0 5.7 18.7 5.1 5.0 15.7 4.8 5.0 4.2 3.6 12.5 2.5 6.94 Figure 1.

Chest X-ray (2014 / 11 / 13) Inactive Tbc, RUL. Calcific nodules, left retrocardiac space. Others - unremarkable.

Simpel abdomen (2014 / 11 / 13) Small bowel gas가 약간 증가하였으며 mild distention된 loops이 있음. Liver, spleen, kidneys등 복부장기의 크기, 모양, 위치에 이상소견 없음. Abnormal calcific density 없음. 양측 psoas shadow 도 정상적으로 유지되어 있음. Ascite or mass 없음. Bony structure에 이상소견 없음.

EKG (2014 / 11 / 13) .Normal sinus rhythm` (73 Beats per min) .Normal ECG

Initial problem list #1. Vomiting #2. Elevated serum Cr c Hyperkalemia c Metabolic acidosis #3. DM with retinopathy, nephropathy #4. HTN #5. Old cerebral infarction

Initial problem list #1. Vomiting #2. Elevated serum Cr c Hyperkalemia c Metabolic acidosis #3. DM with retinopathy, nephropathy #4. HTN #5. Old cerebral infarction Acute on DM CKD Hyperkalemia Metabolic acidosis DM with retinopathy

Initial assessment & plan #1. Acute on DM CKD Diagnostic plan) Urine Chemistry (FENa, FEUrea), Urinanalysis Abdomen & pelvis US, Kidney doppler Therapeutic plan) 유발원인 제거(dehydration, medication 중단) Fluid infusion, acetylcysteine, antibiotics if needed Foely catheter insertion 등 obstruction 해소

Initial assessment & plan #2. DM with retinopathy Diagnostic plan) Fasting serum plasma glucose, HbA1c 합병증 검사 microvascular : 안저, 신경 (Touch pressure, 자율신경, 신경전도, 인지역치검사) macrovascular : ABI, CAVI Therapeutic plan) 식사/운동 요법 경구 혈당강하제, 인슐린 요법 신경병증 치료제 (eg. Gabapentin, Thioctacid), 항혈소판제(eg. Aspirin) 필요시, 안저 광응고술

AKI AKI 원인에 대하여 살펴보면 크게 신전성, 신성, 신후성으로 나뉠 수 있습니다. 우선 Urinary tract obstruction 과 관련하여 신후성원인이 있는데, 환자는 급성 요폐가 발생하지 않았으며, 이로인해 발생할 수 있는 급성 복통, 하복부 팽만감등을 호소하지 않아 가능성이 낮습니다. Glomerularnephritis, vasculitis 의 가능성도 낮습니다. 대혈관과 연관되어 renovascular obstruction 이 가능한데, 이경우는 Atrial fibrillation, Arterial thrombosis, Nephrotic syndrome, Pulmonary embolism 등의 병력 과같은 thrombogenic condition 과 연관되어 있으며, 신실질을 침범하는 질환들은 신성 급성신부전을 일으 킬 수 있습니다. 그밖에 Acute tubular necrosis, Interstitial nephritis, Intratubular obstruction 을 일으 킬수 있는 다음의 원인들이 있으나, 모두 본케이스의 경우에 합당하지 않습니다. Hypovolemia 의 징후, 증상은 환자에게서는 확인되지 않았으며, 환자는 심기능, 간기능 정상이며, Systemic vasodilatation과 renal vasoconstriction 이 일어날 상태도 아닙니다. 마지막으로 신전성의 원인은 renal hypoperfusion 을 일으키는 원인들입니다. 따라서 Renal autoregulatory response impairment 항목에 원인이 있다고 판단됩니다.

Abdomen SONO & Renal doppler Pelvic cavity에 mass 또는 ascites 없음 Right renal length는 9.6 cm, left renal length는 10.6 cm임. BK의 interlobar artery levels에서 얻은 Doppler spectrum의 모양은 정상이며 mean RI는 RK가 0.68, LK가 0.67로 정상범위임. RK와 LK의 main renal arteries와 veins는 patent하며 abnormal spectrum 없음. ====== [Conclusion] ====== Unremarkable abdominal US and renal Doppler US. Renal arterial resistive index Dr Matt A. Morgan and Dr Yuranga Weerakkody et al. The renal arterial resistive index (RI) is a sonographic index to assess for renal arterial disease. It is measured as  RI = (peak systolic velocity - end diastolic velocity ) / peak systolic velocity the normal value is ≈ 0.60  with 0.70 being around the upper limits of normal Technique Measured at arcuate arteries (at the corticomedullary junction) or interlobar arteries (adjacent to medullary pyramids) Reasons for elevated values renal artery stenosis (if measured upstream from the stenosis) ureteric obstruction extreme hypotension very young children perinephric fluid collection Reasons for elevated values in a transplant kidney acute tubular necrosis (ATN) acute or chronic transplant rejection renal vein thrombosis drug toxicity There is thought to be little correlation between the RI and the quantitative extent of renal dysfunction (measured by serum creatinine values) 2

Lab Finding 1. Serology 2. ABGA (room air) 3. Osmol 4. Urine chemistry C3/C4 114/25.7 mg/dL ANA (정성) Non reactive 2. ABGA (room air) pH 7.303 - pCo2 29.3 mmHg - po2 108.4 mmHg - HCo3- 15.4 mmol/L so2 95.6% 3. Osmol Serum 357 mOsm/kg Urine 450 mOsm/kg 4. Urine chemistry Cr/Urea 67/461 mg/dL Na/K/Cl 28/70/49 mmol/L Metabolic acidosis with High anion gap Na – (HCO3 + Cl) = 14.6 Total cholesterol : 192 mg/Dl L.D.L cholesterol : 84 mg/DL TG : 243 mg/DL

SONO (2014.11.13) TTKG : 8.53 Spot K / Cr 역시 41.79 mmol / g

Fundoscopy (2012)

Fundoscopy (2014)

당뇨합병증 검사

ABI, CAVI The ankle-brachial index (ABI) is the ratio of the systolic blood pressure (SBP) measured at the ankle to that measured at the brachial artery. Originally described by Winsor1 in 1950, this index was initially proposed for the noninvasive diagnosis of lower-extremity peripheral artery disease (PAD).2,3 Later, it was shown that the ABI is an indicator of atherosclerosis at other vascular sites and can serve as a prognostic marker for cardiovascular events and functional impairment, even in the absence of symptoms of PAD. Arterial stiffness is a surrogate indicator for the development of cardiovascular disease. The cardio-ankle vascular index (CAVI) is a recently developed clinical metric for evaluating arterial stiffness. ABI 해석 > 1.3 하지동맥 경화도 증가, 팔동맥 협착 1.1 ~ 1.3 정상 < 0.9 하지동맥 협착 < 0.7 하지 동맥 폐색 Circulation 2012, 126:2890~2909

IMT 양측 Carotid artery에서 시행함. 1. 우측 CCA: unremarkable 2. 우측 ICA: unremarkable 3. 우측 ECA: unremarkable 4. 우측 bifurcation: unremarkable 5. 좌측 CCA: unremarkable 6. 좌측 ICA: unremarkable 7. 좌측 ECA: unremarkable 8. 좌측 bifurcation: uniformly echogenic plaque (0.18cm) 9. 우측 CCA IMT:0.51-0.62mm 10. 좌측 CCA IMT:0.62-0.83mm plaque of the Lt. bifurcation rec) clinical correlation

Calcium polystyrene sulfonate 복용 Clinical course eGFR 5.82 9.9 9.4 Calcium polystyrene sulfonate 복용 6.0 5.7 5.1 5.0 4.8 4.2 5.0 (2014.11.13) FENa : 5.2% FEUrea : 58.3% 3.6 4.2 2.5 Eposartan 600mg Valsartan 80 mg Valsartan 160 mg Eposartan 300mg (s BP 160 ~ 170) -> Eposartan 600mg (s BP 100 ~ 110) 이어서 valsartan 80mg 으로 변경함 8월 NR 외래에서 ‘집에서 잴때 110 ~ 140/75 ~85’ 라는 말 듣고 유지함 10월 NR 외래에서 ‘집에서 잴때 s BP 170 까지 올라가기도 해요’ 말 듣고 160mg 으로 증량 --- drugs that interfere with adaptive responses to hypoperfusion may convert compensated renal hypoperfusion into overt prerenal ARF or ATN. Pharmacologic inhibitors of renal prostaglandin biosynthesis [nonsteroidal anti-inflammatory drugs (NSAIDs)] or angiotensin-converting enzyme (ACE) activity (ACE inhibitors) and angiotensin II receptor blockers (ARBs) are major culprits. While NSAIDs do not compromise GFR in healthy individuals, these medications may precipitate prerenal ARF in patients with volume depletion or in those with chronic kidney disease (in whom GFR is maintained, in part, through prostaglandin-mediated hyperfiltration by the remaining functional nephrons). Angiotensin II increases biosynthesis of vasodilator prostaglandins (e.g., prostaglandin E2 and prostacyclin), also resulting in afferent arteriolar vasodilation. In addition, angiotensin II induces preferential constriction of efferent arterioles. As a result, the fraction of plasma flowing through glomerular capillaries that is filtered is increased (filtration fraction), intraglomerular pressure is maintained, and GFR is preserved. - Hemodialysis 계획 - GS consult for AVF OP Eposartan 300mg : 160 ~ 170 Eposartan 600mg : 90 ~ 100 120 / 80 sBP 178

Diagnosis #1. Acute on DM CKD (Stage V) #2. Resolved hyperkalemia d/t ARB after calcium polystyrene sulfonate #3. DM with DM retinopathy, DM autonomic neuropathy #4. Atherosclerotic disease (Lt. carotid bifurcation plaque) #5. HTN #6. Cerebral infarction