P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

Subjective

HPI: FG, 53 yo woman, presents to the clinic with gastroenteritis-like symptoms (vomiting, mild diarrhea, tired) that began 3 days ago. Patient acknowledges self- treatment with ibuprofen (600 mg QID x 2 days) to alleviate cramping pain. Initial assessment at the clinic led to an ER referral and subsequent admission for inpatient management of ARF.

PMH:  CRF Stage 3  DM (Insulin dependent, poorly controlled A1C 8.6%)  HTN (SBP 132-145 mmHg baseline)  Obesity (BMI currently 32 kg/m².) Date of initial diagnosis of these conditions is unavailable.

SH: Smokes an unspecified amount for an unknown duration. Employment and family data are unavailable. Use of recreational drugs and alcohol are also unavailable. Exercise and dietary status are unavailable.

FH: Unavailable

Objective Allergies:  NKDA Medications:  Insulin regular 6 u SQ 30 min before breakfast  Insulin glargine 8 u SQ QPM  Exenatide 10mcg SQ BID  Atenolol 50 mg PO BID  Diltiazem SR 240mg PO Daily  Lisinopril 5mg PO Daily  Naproxen 500mg 1-2 PO BID  Ibuprofen 600mg QID PRN x 2 days  Tums 1 tablet (sig not available)  TUMS 1 tablet QD

Vitals:BP 118/65 mmHg HR 94 bpm RR 15 resp/min Temp 37.5oC

ECG: slightly prolonged PR intervals, marginal widening of QRS and peaked T waves

ABG: pH: 7.34, pCO2 34 mmHg, pO2 95 mmHg, HCO3 17 mEq/L.

Urine Studies: (current) UNa+ 20 mEq/L

1 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

Protein 300 mg/g creatinine urineosm 650 mOsm/kg Ucr 220 mg/dL Casts (type unspecified) on light microscopy Urine ouput ~ 15ml/hr for the first 6 hours after admission (oliguria).

Labs from 2 Labs on months prior: admission: BUN (mg/dl) 40 BUN (mg/dl) 89 Scr (mg/dl) 2.3 Scr (mg/dl) 5.9 Na (mEq/L) 142 Na (mEq/L) 152 K (mEq/L) 4.8 K (mEq/L) 6.9 HCO3 (mEq/L) 20 CO2 (mEq/L) 19 Glucose (mg/dl) 67 Glucose (mg/dl) 177 Ca (mg/dl) 7.7 Ca (mg/dl) 7.7 PO4 (mg/dl) 9.6 PO4 (mg/dl) 10.3 Salb (g/dl) 3.6 Salb (g/dl) 3.5 WBC 6.1 WBC 13.0 Hct (%) 34 Hct (%) 33 HA1C (%) 8.6% HA1C(%) N/A

CrCl(current): [(140 - 53) x (61.36kg + 0.4 x (86.36kg - 61.36kg)) x .85] ÷ [(72*5.9mg/dl)] = 12.42 ml/min BUN:Scr(current): 89÷5.9= 15.08

Potassium(mEq/L): 6.9 (~4 hours ago)

Physical Examination General: feels tired, achy Wt 190# Ht 5’7” ROS: non contributory Pulm: dullness in LL base CV: RRR, no murmurs, S3 gallop Abd: obese, no tender, no masses Ext: no CCE; 2+ pulses throughout Neuro: CN intact, DTR 2+, decreased pinprick test (toes) HEENT: PERRLA, arteriolar narrowing, no hemorrhages, exudates, or papilledema

2 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

1. ARF

Assessment: FG presented to the clinic with GI complaints. She has a history of CRF, moderately controlled HTN, and insulin-dependent diabetes. Preliminary lab results indicate acute changes and patient was admitted to manage ARF. Laboratory panel and urine studies indicate prerenal azotemia, most likely due to patient’s increased NSAID use (600 mg QID for past 2 days). While BUN/Scr ratio is 15:1 (down from 17:1 two months ago), calculated FeNa measures 0.35% (prerenal@<1%). Ucr:Scr ratio is marginal at 37:1 (prerenal@>40:1). UNA is also borderline at 20 mEq/L (prerenal@<20 mEq/L).Urine osmolality @ 650 mOsm/kg also indicates prerenal azotemia (prerenal@>500 mOsm/kg) as do the presence of hyaline casts in urine sample upon light microscopy. Absence of muddy-brown casts, eosinophils, and red blood cell casts in urine sample preclude intrarenal azotemia from ATN, AIN, and GN, respectively. Similary, intrarenal azotemia values for calculated FeNa (>1-2%), Ucr:Scr ratio (<20:1), BUN/Scr ratio (10-15:1), and UNA (>40mEQ/L) are not demonstrated by this patient. Serum osmolality is calculated at 346 mOsm/kg, indicating hypertonia (>280 mOsm/kg). Calculated water deficit, using a desired serum Na concentration of 142 mEq/L, is 3.65 L and does not include water lost to urine output (data available for only 6 hours) or insensible water loss to fever as patient is afebrile. Patient also demonstrates mild metabolic acidosis as indicated by low HCO3 (17 mEq/L). Immediate concerns for FG are to relieve prerenal azotemia by discontinuing NSAID use and increasing perfusion of kidneys, and to increase intravascular volume to increase blood pressure. Choices for treatment include IV administration of one- half the water deficit (1800 ml) in NS given of 24 hours. The metabolic acidosis should correct with fluid support and cessation of vomiting. D5W is not recommended as it will increase volume in ICF and interstitium as well as intravascular.

Plan: -Discontinue NSAID (Ibuprofen and Naproxen) use -Administer 1800 ml NS IV over 24 hours -Monitor urine output over 24 hours to assess resolution of oliguria -Run additional laboratory panel following completion of NS infusion to monitor kidney serum markers (BUN, Scr, Na) -Run additional urine study following NS infusion to assess urine Na, osmolality, creatinine, protein, and presence of casts. -Monitor BP every 2 to 4 hours (as dictated by automated BP system for inpatients) -Following new laboratory and urine analysis, reassess kidney function status of FG

3 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

2. Hyperphosphatemia Assessment: FG appears tired from her illness. According her baseline Scr and labs reported from two months ago, FG’s Crcl is 34.49 ml/min. She is at stage III renal failure (NKF K/ DOQI). Her serum phosphate is 10.3 mg/dL, above the goal of 2.7-4.6 mg/dL. The patient’s serum calcium is low 7.7 mg/dL (goal: 8.4-9.5 mg/dL). Her double product is high 79.31 mg/dL (goal: < 55 mg 2/dL 2 to reduce the risk of metastatic calcifications). The treatment goal is to lower serum phosphate. Treatment options include calcium phosphate binders, aluminum phosphate binders, and sevelamer. Calcium containing binders (including TUMS) should be withheld when serum PO4 > 7 mg/dL. Her serum phosphate is not controlled with TUMS, aluminum containing binders can be used to lower her serum phosphate faster. The patient will start Alu-tab 500 mg 1-3 tabs with meals. Due to aluminum toxicities, it cannot be used long term. Patient will need to switch to calcium containing binders or sevelamer 4 weeks after started Alu-tab or if serum phosphate < 6 mg/dL. The patient will start calcium acetate (Phoslo 667 mg) 2- 3 tabs with meal when aluminum phosphate binder is terminated. Serum calcium and phosphate will be reevaluated every month. The patient’s iPTH and Fe status will be evaluated and then reevaluate every three months to guide therapies with the goal of preventing bone disease and metastatic calcifications. The patient needs to restrict dietary phosphorus to 800 to 1,000 mg/day (K/DOQI).

Plan: Order serum iPTH and Fe. D/c TUMS and start Alu-tab 500 mg 1-3 tabs with meals for 4 weeks then switch to Calcium acetate (Phoslo 667 mg) 2-3 tabs with meals. D/c Alu-tab when serum phosphate < 6 mg/dL. We discussed the potential for aluminum toxicities (neurotoxicity, dialysis encephalopathy, bone disease include microcytic amemia). Patient instructed to report symptoms if severe. Monitor PO4 and Ca daily until discharge. Monthly for follow-up monitoring of PO4 and Ca is recommended. Fe and iPTH will be reevaluated every three months. Dietary phosphorus should be restricted to 800 to 1,000 mg/day (K/DOQI). FG seems tired from her illness. According the recent labs reported upon admission, FG’s Crcl is 12.42ml/min. She is at stage V renal failure (NKF K/ DOQI). Her serum phosphate is 10.3 mg/dL, above the goal of3.5-5.5 mg/dL. The patient’s serum calcium is low 7.7 mg/dL (goal: 8.4-9.5 mg/dL). Her double product is high 79.31 mg/dL (goal: < 55 mg2/dL2 to reduce the risk of metastatic calcifications). The treatment goal is to lower serum phosphate. Treatment options include calcium phosphate binders, aluminum phosphate binders, and sevelamer. Calcium containing binders (including TUMS) should be withheld when serum PO4 > 7 mg/dL. Her serum phosphate is not controlled with TUMS, aluminum containing binders can be used to lower her serum phosphate faster. The patient will start Alu-tab 500 mg 1-3 tabs with meals. Due to aluminum toxicities, it cannot be used long term. Patient will need to switch to calcium containing binders or sevelamer 4 weeks after started Alu-tab or when serum phosphate < 6 mg/dL. The patient will start calcium acetate (Phoslo 667 mg) 2- 3 tabs with meal when aluminum phosphate binder is terminated. Serum calcium and phosphate will be reevaluated every month. The patient’s iPTH and Fe status will be determined and then every three months to guide therapies with the

4 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams goal of preventing bone disease and metastatic calcifications. The patient needs to restrict dietary phosphorus to 800 to 1,000 mg/day (K/DOQI).

Plan: Discontinuing TUMS and order serum iPTH and Fe. Start Alu-tab 500 mg 1-3 tabs with meals for 4 weeks or when serum phosphate < 6 mg/dL. Calcium acetate (Phoslo 667 mg) will be used when aluminum phosphate binder is terminated. We discussed the potential for aluminum toxicities (neurotoxicity, dialysis encephalopathy, bone disease include microcytic amemia). Patient instructed to report symptoms if severe. Monitor PO4 and Ca daily until discharge. Monthly for follow-up monitoring of PO4 and Ca is recommended. Fe and iPTH will be reevaluated every three months. Dietary phosphorus should be restricted to 800 to 1,000 mg/day (K/DOQI).

5 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

3. Hyperkalemia Assessment: It is well known and documented that hyperkalemia can cause cardiac arrhythmias, and this high serum potassium is often diagnosed by observing in changes in the ECG. Although this electrolyte imbalance is one of the most dangerous, it can be easily treated. The ECG for FG shows peaked T waves with marginal widening of QRS. Most clinicians agree that the treatment of hyperkalemia should be initiated when potassium levels are greater than 6.5 mEq/L, regardless of ECG changes. Since FG has both ECG changes and a sufficiently high potassium level, treatment of FG’s hyperkalemia is indicated. The treatment of hyperkalemia will be carried out in three phases: 1) antagonism of the myocardium at the cellular level, 2) promote the redistribution of potassium by stimulating influx of potassium into the cells, and 3) continued control of hyperkalemia by removing potassium from the body. Calcium gluconate will be given to antagonize the effect of hyperkalemia on the myocardium. Although FG has a high calcium/phosphate double product, averting arrhythmias trumps the concern over a rise in serum calcium and this can be rectified subsequent to the management of hyperkalemia. Additionally, although the serum potassium levels have not reached the indicated threshold of 7.0 Meq/L for calcium administration, it should still be given due to the recent and continued rise in FG’s potassium levels. To promote potassium influx, insulin will be given, which drives the Na/K ATPase pump, forcing potassium into the cells and subsequently lowering serum potassium levels. Continued control of hyperkalemia will be obtained with kayexalate. Although, in a number of patients, furosemide would be an option, FG has a water deficit and for this reason treatment with diuretics is not indicated at this time.

Plan: Calcium gluconate, 4.65 mEq/10 mL infused over 5 to 15 minutes (central line, administer now, monitor ECG) Insulin 10 U IV in 500 mL D10W (peripheral line, administer 15 minutes after calcium infusion, monitor hypoglycemia, serum potassium) Kayexalate, 10 grams BID (administer at 3 hours, monitor hypokalemia, hypernatremia, constipation)

6 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

4. Proteinuria Assessment: The patient has pre-renal ARF, induced by excessive NSAID use. In ARF, proteinuria is more pronounced in intrinsic, rather than pre-renal ARF. This suggests that the proteinuria may be due to CRF. The patient is Stage 3 CKD based on previous laboratory results, and should be treated for chronic proteinuria as soon as ARF episode is resolved, including, but not limited to hypotension, hyperkalemia, hypernatremia and hyperphosphatemia.

Current lab results indicate the patient is borderline micro/macroalbuminuria at 300mg/gm protein/creatinine. This finding is consistent with the patient’s DM and Stage 3 CKD. The primary treatment goal, in accordance with KDOQI guidelines, is BP management. ACE Inhibitors are recommended by KDOQI guidelines and should be optimized first due to the dual benefit of BP control and their inhibition of TGF-beta secretion in the renal tubules in response to proteinuria. ARB should not be added until Lisinopril therapy has been optimized.

Poor glycemic control (A1C 8.6%) is a contributing factor, but less so than BP. Smoking is also a contributing factor and should be addressed. Dietary protein restrictions are not indicated for GFR>25ml/min.

Plan: Initially, patient’s Lisinopril dose should be increased to 10mg PO QD, and subsequently titrated to BP <130/80mmHg or 20mg or patient tolerance. FG should be checked for Hyperkalemia, GFR, and proteinuria in 3 days at the clinic. Lisinopril dose adjustments should be considered in two weeks. Future considerations should include adding an ARB. Patient should self monitor for hypotension and signs of hyperkalemia (muscle weakenss, GI Upset).

Patient’s readiness to begin a smoking cessation program should be assessed. Patient should be educated that smoking is a major contributing factor to CKD progression. If the patient is ready to consider quitting, then treatment options should be considered.

7 of 8 P765 Group SOAP Note Due: 8 Feb 08

Monday Lab Group D: Tyler Treyharne, Adam Vuong, TJ White, Jeff Wilemsen, Ted Williams

5. Hypertension

Assessment: After reviewing this patient it is evident that they are suffering from acute renal failure. However, in terms of the patients blood pressure which is currently 118/65(which would be great for this patient) this is not the primary issue at hand. The patient is hypovolemic and needs fluid replacement and remission of current acute condition before any further steps can be made to decrease the patients normal blood pressure of 132-145mmHg systolic. FG’s blood pressure with her current condition of CKD and Diabetes Mellitus should be targeted at 130/80mmHG and is not being controlled under the current regimen of Atenolol, Diltiazem, and Lisinopril. The patient should get off anything that could be contributing to acute renal failure which in this case would be the Ibuprofen, Naproxen, and low dose of Ace Inhibitor the patient is taking until these symptoms have passed. Once patient’s ARF has been stabilized, then we can look at other options to decrease her blood pressure to goal (130/80 according to JNC-7/KDOQI guidelines), by. These options would include pushing her Lisinopril dose. to 10- 20mg to help further decrease her BP or even pushing her dose of Atenolol to 100mg BID to assist in achieving her goal blood pressure. However,Iincreasing the ACE inhibitor would be advised since this can also provide more kidney protection and also prevent further proteinuria from occurring. The emphasis of a healthy diet (DASH) with low salt intake, stopping smoking, as well as regular exercise should be emphasized in this patient as well.

Plan: The plan for controlling this patients blood pressure once they are stabilized from their acute kidney failure would be as follows: Currently discontinue any NSAIDS (Naproxen, Ibuprofen) or her Lisinopril which can contribute to acute renal failure until she is stabilized. Once the patient is stabilized we will push tPush the Lisinopril (indicated in diabetics and well as for kidney protection in those with CKD) dose to 10-20mg(gang???)mg in attempt to reduce her blood pressure below 130/80mmHG. and to provide added kidney protection. We will follow up with the patient in 2 weeks to assess Lisinopril therapy. At that time if this is not enough or insufficient we could then look to push her B-Blocker. There should also be a major emphasis in this patient to discontinue smoking, consider implementing a DASH diet into their lifestyle as well as exercising 30min 5X a week if possible. These lifestyle modifications as well as push in Lisinopril could be enough to drop her average BP to goal of 130/85 as stated by the JNC-7 and KDOQI guidelines.

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