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Renal Sodium Retention in Patients with Decreased Effective Circulating Volume In patients with a decreased extracellular volume, such

as diarrhea and vomiting, and in edema-forming states with a decreased effective circulating volume, such as liver disease with ascites and CHF, the pathophysiology of the sodium and water retention is very similar. In these patients there is activation of the renin angiotensin aldosterone system, catecholamines, and also there is the non osmotic release of ADH. Below I will discuss the renal response to decreased ECV and also the mechanisms of sodium retention. 1) Maintaining Renal Function the kidney attempts to maintain renal function in the setting of decreased renal perfusion by a combination of factors including maintaining renal blood flow and increasing filtration fraction (GFR/renal plasma flow). The high concentrations of catecholamines and angiotensin II increase afferent arterial resistance(. The kidney counteracts the local effects of these vasoconstrictors by increasing prostaglandin synthesis, PGE2 dilates the afferent arteriolar somewhat opposing this vasoconstriction and therefore helping to maintain renal plasma flow. As a result any patient who gets NSAIDS included the new Cox 2 inhibitors would no longer have this vasodilatory affect of the prostaglandins and have unopposed vasoconstriction leading to a decrease in renal plasma flow and GFR. The angiotensin II and catecholamines constrict the efferent arterioles so that proximal to the constriction there is an increase in hydrostatic pressure. This increases filtration fraction (GFR/renal plasma flow) but the GFR does not go to normal. In patients with a decreased ECV, ACE inhibitors decrease this efferent arteriolar resistance so that at the level of the kidney this would cause a decrease in GFR. However, in heart failure the expected increase in cardiac output and renal plasma flow after the ACE inhibition helps counteract the effect on the efferent artery so that GFR does not usually decrease or decreases slightly. 2) 1. Sodium Homeostasis increased sodium reabsorption is due to the following factors: As a result of the increased hydrostatic pressure in the glomerulus, there is an increase in the filtration fraction, which leads to an increased oncotic pressure at the end of the glomerulus compared to baseline. This increased oncotic pressure at the level of the peritubular capillaries results in an increase in proximal tubular reabsorption as a result of starling forces. If the normal filtration fraction was 20 percent, then the albumin concentration of 4 g/100 cc would at the end of the glomerulus be concentrated to 4 g/80 cc as a result of the filtration of 20 percent. This would increase the albumin concentration to 5 g/100 cc at the end of the glomerulus. If the filtration fraction increased to 30 percent, the albumin concentration would increase from 4 g/100 cc to 4g/ 70 cc at the end of glomerulus, i.e. a concentration of 5.7 g/100 cc. Since albumin is the main component of the oncotic pressure this increase in the peritubular capillaries would favor increased reabsorption above baseline. Increase in angiotensin II levels which directly stimulates proximal tubular reabsorption. Increase in SNS activity which directly stimulates proximal tubular reabsorption. Increased aldosterone levels will increase reabsorption in the collecting duct.

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As a result, patients with a decreased ECV are characterized by urinary sodium concentration is typically less than 20 mq/L.

ACUTE KIDNEY INJURY

Medical Knowledge 1. 2. 3. 4. 5. 6. 7. 8. Define the role of prostaglandins and ACE in the maintenance of GFR and the effect of NSAIDS and ACE inhibitors on intrarenal hemodynamics. Define the tests used to measure renal function (BUN, Cr, creatinine clearance) and their limitations. Define acute, acute on chronic, anuric, oliguric and non-oliguric renal failure. Describe the broad categories of causes of renal failure (pre-renal, post-renal and intrarenal) and the most common illnesses in each category. Describe the appropriate initial evaluation of the patient presenting with acute kidney injury. Differentiate between pre-renal, post-renal, and intrarenal causes of acute kidney injury using the history, exam, serum and urine electrolytes and urinalysis. Describe the appropriate management of pre-renal, post-renal and renal failure. To know the differential diagnosis for a decline in kidney function in a patient with CHF who is being diuresed.

ACUTE: Pre renal- decreased flow to the glomerulus (not necessarily low CO) (BUN/Cr >20; FeNa <<1% - b/c kidney is retaining salt) Low kidney perfusion, sepsis, renal artery stenosis, cocaine will vasoconstric decreased. Hyaline and granular casts- precipitation due to low flow---BLAND URINE Renal

Glomerulus (nephrotic/nephritic) Acute Interstitial nephritis (drugs) o Prolonged pre-renal (most common cause) o Pyelonephritis Acute tubular necrosis FeNa is greater than 2%. URINALYSIS- red cells, white cells, white cell casts eosinophils STERILE PYURIA (culture shows nothing) o Peripheral eosin o Ischemic ATN- muddy brown urine casts ATN but low fractional excretion Contrast induced nephropathy, rhabdomyolysis, interstitial nephritis

Post Renal Intra (stones) and extra ureter (mass).

FENa = UNa x Pcr/ PNa x Ucr x 100

Acute/Chronic and acute on chronic. Pre renal or post. What meds? Affect kidney? Pathologies? Affect kidney? When patient is on diuretics; look at the urea levels in order to assess kidney function; not FeNa (its affected by the diuretics). Hydrochlorothiazides under 30 GFR doesnt work. Strategy if interpretatring AKI- 1 write own everything that supports either pre, renal or post renal. 2. What diseasesdoes the patient have and how do they affect the kidney. 3. Consider drugscan you adjust dosages 4. Consider obstruction (not everyone has two functional kidneys)

ACUTE KIDNEY INJURY PROBLEM 1 A 75 y/o man with a history of type 2 diabetes and hypertension. Two weeks PTA(prior to admission) he began noticing shortness of breath, at first only with exertion, but in the last week had been short of breath at rest. He has not had any chest pain. He comes to the ED at 4 AM on the day of admission because of increasing dyspnea. He is currently taking HCTZ, metformin, glyburide, atorvastatin, and lisinopril. He has diabetic nephropathy with creatinine 6 months ago 1.2 mg/dL. On exam his BP is 160/98, P 120, R 40, T 100.6. He is in marked respiratory distress. He has crackles 1/2 way up bilaterally and there is dullness the R lung base. He has an intermittent S3, JVP 8cm. His liver is 3 cm below the R costal margin and is smooth and nontender. He has 2+ edema of his feet and ankles. The remainder of his exam is unremarkable. His laboratory studies show the following: Na K C1 CO2 Glucose ABG 2 liters pH 7.48 ECG LBBB 132 mEq/L 3.2 mEq/L 99 mEq/L 24 mEq/L 220 mg/dL pO2 80 BUN 50 mg/dL Creat 2.0 mg/dL U/A 2+ protein, no cells Urine Na 10 mEq/L Urine Cr 200 mg/dL pCO2 30 (low) HCO3 24 mEq/L (normal)

Remember the CHADS criteria; review. CO2 + H2O H2CO3 H+ + HCO3 Clearance = amount excrerted/ plasma concentration 1. Interpret ABG Acute respiratory alkalosis. Secondary to pulmonary edema o Bicarb goes down a little, in chronic it goes up a little (due to mass action) Hyponatremia; hypokalemic Alkalemia- Respiratory alkalosis with no compensation with AG of 12. Delta-delta= is the Why do you think his BUN and creatinine are elevated and the BUN/Cr ratio is 25 (usually about 10)? Pre-renal azotemia from decreased ECV (clinically in heart failure), low fractional excretion of sodium, increased BUN/Cr, relatively benign urine BUN/Cr ratio elevatedBUN is reabsorbed o In heart failure there is increased urea reabsorption o Urea is not regulated, will do whatever it takes to reach a new steady state goes up until you are getting rid of what you are taking o In order to adapt for increased R, you need to increased filtered load o Urea follows water (increased reabsorption of sodium) o Creatinine is not regulated o Urea clearance goes down more than the creatinine clearance BUN/Cr ratio sucks as an independent measure to determine if it is renal/pre-renal If in heart failure and not increased---patient must not be eating 3. Decreased ECV which leads to an increase in both; but a higher increase in BUN; one that has a higher 1:20 ratio. When looking at renal: acute, chronic, acute on chronic. Pre renal, renal, post renal. Muddy casts with ischemia ATN. Acute on chronic Clearance urea=amt exc urea/Purea. P urea=amt exc urea/clearance urea. In CHF clearance is down because you have decreased reabsorption. Not eating low ratio due to not taking protein. Bleeding, sepsis, person on steroidssteroids break down protein---get more protein, high protein diet high BUN/Cr Do ratio, and if you think its pre renal consistent. IF its not consistent; either liver failure or isnt eating. Last thing you look at is the BUN/Cr ratio. Amt Exc Urea=Purea x GFR- R+S (tubular secretion). o P urea x GFR = filtered load In CHF increased reabsorption. With urea, not regulated so itll be get rid of no matter what. By increasing filtered load. All substances not regulated will be get rid of; as much as you produce.

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What is his fractional excretion of Na and interpret the results? Kidney could have precipitated it. LBBB, possible past MI. By looking at echo can see the wall kinetic abnormality. Underlying: 1) Previous MI, chronic HTN, idiopathic cardiomyopathy. Precipitators; renal failure in the setting of CHF, incompliance with meds, another LBBB o He is fluid overloaded, could have had a new MI o Dreaded medication NSAIDs

Urine Na*Pcr= 0.1% Ucr*PNa Less than 1-pre renal. 4. Is it consistent with his clinical presentation? Yes this is consistent with the clinical presentation of prerenal azotemia given th If it werent you would do the fractional secretion of urea. FE=amt exc/filtered load. Cuz its not going to be affected by diuretics. How would you treat him? Lasix---continuous drip or IV bolus Renal insufficiency- give higher dose Once you exceed threshold- diuresis Blunted response to diuresis- put on furosemide and thiazide and aldo antagonist ---let any amount of sodium that gets by loop of henle will be excreted --- TRIPLE THERAPY Document they are losing weight 6. NO fluidsonly time you do this is in rhabdomyalisis with no kidney problems. No; no fluids. Remember that 3-4L can be stored in the interstitia

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What would you do with his current medications while in the hospital? STOP them, except for lisinopril (ACE inhibitor) HCTZ doesnt work if GFR is less than 30 Metformin has to be stopped b/c renal insufficiency Start the insulin; sliding; then long acting like gargine. Dont treat less than 140.

7. How would you treat his diabetes? Kept the treatment for diabetes. But stop the metformin.

An echocardiogram reveals ejection fraction 35% with septal wall akinesis. Three days later his respiratory status is much improved and his edema has cleared. It is decided to start him on a beta blocker. ALL PATIENTS with reduced EF should be on a beta blocker 8. Why was a beta blocker not started on admission? Start beta blocker carvedalol! Start when no longer on clinical heart failure---usually started on discharge---follow patients weights, start at very low dose Temporarily the heart failure gets worse, diurese them---until get on max dose they can tolerate It wasnt started in order maintain (not decrease) sympathetic drive during the exacerbation. If person comes in with long standing beta blocker- keep them.

Pt comes back in with pulmonary edema Keep him on it, otherwise may lose remodeling effect 9. If he needs an angiogram, what medication would you administer before the angiogram to decrease contrast induced nephropathy? 1200mg PO, BID; day prior and day of of N-acetylcysteine / not Na bicarb (cuz its contra indicated). Not N-awant to stabilize; thats it. Mucomist

PROBLEM 2 A 70-year-old man with coronary artery disease and atherosclerotic peripheral vascular disease is hospitalized because of abdominal pain. He has had hypertension for 20 years and hypercholesterolemia for 8 years, both of which are well controlled by metoprolol, HCTZ and atorvastatin. On physical examination, his pulse rate is 112/min and regular, and blood pressure is 90/64 mm Hg. His chest is clear. No cardiac murmurs or gallops are heard. His abdomen is diffusely tender. There is no lower extremity edema. Rectal examination shows a boggy but normal-sized prostate gland, good tone, and a stool specimen that is positive for occult blood. Blood urea nitrogen is 29 mg/dL, and serum creatinine is 1.4 mg/dL. Urinalysis shows a specific gravity of 1.018, trace protein, and no glucose or ketones. Microscopic examination of the urine is normal. The patient undergoes emergency arteriography for intestinal ischemia and subsequently has a right hemicolectomy. Due to ischemic bowel he is administered cefotaxime and metronidazole. On the second postoperative day, his blood pressure is 130/80 mm Hg, but 12-hour urine output is 135 mL. He

is not orthostatic and examination is normal. Blood urea nitrogen is 68 mg/dL, and serum creatinine is 4.1 mg/dL. Urinalysis reveals a specific gravity of 1.009. Microscopic examination shows granular casts and rare tubular cells. Na 140 mEq/L (135 145 mEq/L) C1 105 mEq/L (95 105 mEq/L) FENa = 0.5%. prerenal 1. 2. K 5 mEq/L 3.5 5.0 mEq/L) HCO3 16 mEq/L (24 28 mEq/L)

What are the possibilities for the acute kidney injury? Intrepret FENa. Ischemia/hypoperfusion. Thrombus, emboli. Sepsis- (due to the peripheral vasodilation renal clamps down). Contrast is also another guy that can lower the FeNa. Atheroemboli = cholesterol Emboli high eisinophelia.

The patient is followed and over the next 4 days his Cr values are 4.8 mg/dL, 5.3 mg/dL, 5.6 mg/dL and 5.6 mg/dL. Explain why the rise in creatinine was less each day. His GFR has reached a steady state. PCreatine x GFR = constant cuz its unregulated.

PROBLEM 3 An 82-year-old man with diabetes mellitus, stage 3 chronic kidney disease and ischemic cardiomyopathy with ejection fraction 20% is admitted to the hospital in obvious heart failure. He is taking insulin glargine 20 units at night, lisinopril 10mg, carvedilol 3.25 mg 2XD and furosemide 40mg a day. He also has an implantable defibrillator. On admission his BP 140/80 mm Hg, HR 80/minute, R 18 T 37 Exam is positive for JVD 10 cm, crackles 1/3 up his chest, S3 gallop, 2/6 holosystolic murmur at the apex with radiation to axilla 2+ edema (functional mitral regurg due to the stretched annulus; remember to anticipate this so report it!) Labs: Creatinine 2.0 mg/dL (0.16 1.2 mg/dL), BUN 40 mg/dL (10 20 mg/dL) rest normal After admission he is diuresed with intravenous furosemide 40 mg every 8 hours. Two days later he still has crackles 1/3 up his chest, 2+ edema but his creatinine has increased to 2.6 mg/dL with BUN 50 mg/dL. 1. 2. What is the likely diagnosis to explain his decline in renal function? This is the cardiorenal syndrome. o Deterioration of renal function in the setting of heart failure---nobody knows why Acute kidney failure secondary to hypoperfusion due to CHF exacerbation.

What are your therapeutic options? Patient is in pulmonary edema- need to fix this---get rid of the fluid even if renal function deteriorates more Furosemide Dialysis if necessary

\ PROBLEM 4 A 46-year-old male with a history of type 2 diabetes is seen for fever and redness of his leg. He recently moved to Farmington and this is his first visit. The patient was diagnosed as having diabetes 10 years ago and was initially treated with oral agents. Most recently he has been on glyburide 10 mg once a day. He is not compliant with diet and exercise and the most recent hemoglobin AC was 12.1%. He takes enalapril 10 mg daily for hypertension. He also has diabetic neuropathy manifested by pain, mainly at night. No baseline creatinines. About 10 days ago while checking his feet, he noticed areas of redness on the first metatarsal head. He did not contact his physician and continued to attempt to keep the area clean but began noticing purulent drainage. Eight days ago he took some of his childs TMP/SMX with no improvement. Two days ago he noticed a gradual increase in redness of his leg and swelling of the ankle with an ulceration. During these two weeks his glucose has been 300-350 with polyuria and polydypsia. He has frequently needed to take regular insulin but still has poor control. He smokes one pack of cigarettes per day for the last 20 years but does not drink alcohol. Today he also noted a diffuse rash. On physical exam BP 100/70 Pulse 100 lying BP 90/60 P 130 sitting Temp 38.9 Respiratory rate 20 HEENT retina shows proliferative changes Heart S1 S2 normal without S3 No JVD Lungs clear Extremities: Decreased peripheral pulses. Skin diffuse maculopapular rash. Large ulceration 4 by 4 cm and on his right metatarsal head with purulent foul smelling drainage with redness half-way up the calf. Neurological exam reveals a severe peripheral neuropathy with absent pain, pressure and touch on both lower extremities to the level of the calf. Groin reveals 2 + pulses with 2 by 2 lymph node in the right inguinal area. Labs: WBC 18.6 with 70% polys Hematocrit 40 Creatinine 4.0

10% bands platelets 230,000 BUN 100

12% eosinophils K 5.2 mEq/L

8% lymphocytes

Urinalysis

4 + protein

15-20 WBCs no organisms seen

Foot ulcer treated with Bactrim, diabetes- polyuria pol,ydipsia, rash, ortostatic, increased WBC and eosinophils What is the differential diagnosis for the renal failure? Acute, chronic or acute on chronic Acute on chronic o o Acute o Interstitial nephritis- Bactrim. o Eosinophil in blood, WBC in urine 4+ protein- chronic HTN, diabetic neorphaty- chronic

Sepsis pre-renal

Volume depletion secondary to osmotic diuresis- polyuria, polydipsia, uncontrolled glucose ACE inhibitor- prevents kidney from compensating from LOW FLOW state o o Worsens pre-renal Stop ace inhib

Acute: Septic shockhypoperfusion (due to orthostatic-decreased ECV). Polyuria/dipsia uncontrolled glucose. ACEI- this is where ACE worsens prerenal state (think NSAIDS) Chronic-Diabetic nephropathy (protein in urine) Hypertensive heart disease. Remember: Pre, renal, post. And also chronic, acute and acute on chronic.

PROBLEM 5 A 35 y/o man with no past history is admitted in renal failure. He and some friends had been drinking heavily at a party. An acquaintance offered him some cocaine and, having heard about it but never tried it, he decided to try some. The neighbors called the police because of the noise. When they arrived he became belligerent and combative and needed restraints to bring him to the station. After being booked on disorderly conduct, he could not find anyone to bail him out, so he spent the night in jail. The next morning he was released but felt poorly and came to the ED to be checked out. His BP 110/70, P 80, R 14 not orthostatic. The only thing you find on exam is multiple bruises. You order some lab studies and find the following: BUN 18, Cr 2.3, U/A shows 3+ blood but no RBCs. UA: either hemoglobin or rhabdo Myoglobin is picked up on the dipstick as blood 1. What is the most likely cause of his renal failure? Rhabdo; dipstick positive; but no red cells. Drug induced kidney injury

The patient is given fluids but after 2 L of normal saline, urine output is only 10cc and urinalysis tubular cells. 2. What would you do regarding the treatment of low urine output? Bladder scan /renal ultrasound catheter. Do NOTHING FLUID RESTRICTION No furosemide; this is bite the bullet! No foleyBelow are his values for the first 3days. Day Weight Cr BUN 1 70 Kg. 2.3 mg/dL 18 mg/dL 2 71 Kg 4.2 mg/dL 45 mg/dL 3 71 kg 5.0 mg/dL 55 mg/dL

K HCO3 Urine output/day 3.

4.2 mEq/L 25 mEq/L 100cc

5.6 mEq/L 22 mEq/L 150cc

4.8 mEq/L 20 mEq/L 200cc

How would you treat his increased K on day 2? Kayexalate; can hurt the intestine. o Wont be able to get rid of K+ b/c of renal failure Changing the sodium for potassium.

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Why the decreasing bicarbonate and would you treat it? Possible PT ischemia decreased ammoniogenesis. Not making ammonia No cells in Prox tubutal to make ammonia Do nothing --- can give bicarb

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When would you dialyze this patient? Fluid overload; dialize when they have high K, pulm edema, no response to furosemide. Just treat the complications. Iatrogenic complication vanco- remember to dose based on renal function (not just Cr). BUN of around 120- potassium (look at patient~7-8), severe academia and pulmonary edema unresponsive to furosemide.

PROBLEM 6 A 27 y/o woman with no significant past medical history comes to your office because for the past 6 weeks she has been experiencing fatigue, feverishness, malaise and diffuse arthralgias. She has been taking Advil for the symptoms but they arent getting any better. Your exam is unremarkable except for a temp of 100.9 and a Gr 2/6 blowing systolic murmur at the apex without radiation. You draw some routine labs and the lab calls you that night to tell you your patient has a Hct of 30, BUN of 56 and a Cr 4.2. 1. What is the differential diagnosis of her renal failure? Lupus (systemic complaint; systemic disease) Infectious (mono, subacute endocarditis, rheumatic) NSAIDS use. Autoimmune hemolysis? What tests would you order? BNP, ANA, mono-spot, Echo, indirect/direct bilirubin, coombs, LDH, CK, U/A

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PROBLEM 7 A 72 year old man with a history of diabetic nephropathy presents to the emergency room with weakness. He has a 20 year history of diabetes with his baseline creatinine being 2.3 mg/dL. He is currently on glipizide 5 mg daily. He also has coronary artery disease with a myocardial infarction 6 years ago where he had angioplasty and a stent. His ejection fraction is 25% and currently treated with lisinopril (20 mg daily), carvedilol (6.25 mg 2xd) furosemide (40 mg 2Xd), ASA (81 mg), and atorvastatin (40 mg daily). He also has an implantable defibrillator. His baseline dyspnea is about a block without any orthopnea or PND. About two weeks ago he had an episode of bronchitis and was treated with a 10 day course of trimethoprim-sulfamethoxazole (80/400 mg 2xd). Physical exam Blood pressure 100/70 mm Hg, pulse 90/min, respirations 24/minute and afebrile. Exam was remarkable for JVD 5 mm Hg. Lungs: clear. Heart: PMI laterally displaced, S3 gallop at apex, 2/6 holosystolic murmur with radiation to axilla. Extremities: no edema. Labs Sodium 138 mEq/L Potassium 7.2 mEq/L Chloride 107 mEq/L Bicarbonate 17 mEq/L Creatinine 2.6 mg/dL BUN 48 mg/dL Glucose 110 mg/dL An electrocardiogram showed peaked T waves.

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What is the differential for the increased potassium? Diabetes, betablockers- minimal effect Bactrim (blocks Na channels!), blocks ENAC

o o

Acts like amiloride Remember to not give Bactrim with pts with CKD.

ACEi, heart failure low Na delivery, academia, cell lysis, diabetics (type 4 RTA) hyporenin hypoaldo o Ace inhibitor---aldo becomes even lower---get hyperkalemia May not be filtering much because significant decrease in GFR Decreased secretion: o Lisinopril Tubular secretion impaired Increased Cr: o What meds are they on? Change in dosage? o What diseases? Affect on kidney? o Obstruction?

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How would you treat the increased K? Calcium glutarate, beta agonists, insulin, kayexalate, diuretics, bicarb. IV calcium chloride hemodialysis.