Module 5: Additional Complications of CKD - PowerPoint Presentation

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Module 5: Additional Complications of CKDHyperkalemia, Metabolic Acidosis, Malnutrition, Depression & Acute Kidney Injury

Andrew

Narva

, MD, FASN &

Amy Barton

Pai

, PharmD, MHI, FASN, FCCP, FNKF

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Andrew Narva, MD, FASNNo financial disclosures/conflicts of interest

Amy Barton

Pai, PharmD, MHI, FASN, FCCP, FNKFDisclosure: Consultant for Keryx

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Faculty Disclosure Information

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About NKDEP

This professional development opportunity was created by the National Kidney Disease Education Program (NKDEP), an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. With the goal of reducing the burden of chronic kidney disease (CKD), especially among communities most impacted by the disease, NKDEP works in collaboration with a range of government, nonprofit, and health care organizations to:

raise awareness among people at risk for CKD about the need for testing;

educate people with CKD about how to manage their disease;provide information, training, and tools to help health care providers better detect and treat CKD; andsupport health system change to facilitate effective CKD detection and management.To learn more about NKDEP, please visit: http://www.nkdep.nih.gov. For additional materials from NIDDK, please visit: http://www.niddk.nih.gov.

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Meet our Presenters

Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF

Dr. Barton Pai is Chair of the National Kidney Disease Education Program’s Pharmacy Working Group

Dr. Amy Barton Pai, Pharm.D., MHI, FASN, FCCP, FNKF is Associate Professor of Clinical Pharmacy at the University of Michigan College of Pharmacy.  She obtained her Bachelor of Science in Pharmacy from Albany College of Pharmacy in 1996 and then completed a Pharmacy Practice Residency at St. Peter’s Hospital in Albany, New York. She received her Doctor of Pharmacy from Albany College of Pharmacy in 1999. From 1999-2001 she was a Nephrology Research Fellow at the University of Illinois at Chicago. Dr. Pai was on faculty at the University of New Mexico College of Pharmacy and School of Medicine from 2001 to 2008 and at Albany College of Pharmacy and Health Sciences from 2008 to 2016. She earned a Master's degree in Healthcare Innovation in 2018.

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Andrew S. Narva, M.D., F.A.C.P.

Dr. Narva is the Director of the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health. Prior to joining the NKDEP in 2006, he served as Director of the Kidney Disease Program for the Indian Health Service (IHS). Dr. Narva continues to serve as the Chief Clinical Consultant for Nephrology for IHS and to provide care for patients at Zuni Pueblo through a telemedicine clinic. Dr. Narva is a member of the American Board of Internal Medicine Nephrology Subspecialty Board. He has served as a member of the Eighth Joint National Committee (JNC 8) Expert Panel, the National Quality Forum Renal Steering Committee, the Kidney Disease Outcomes Quality Initiative Work Group on Diabetes in Chronic Kidney Disease, and the Medical Review Board of End Stage Renal Disease Network 15.

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Meet our Presenters

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After this module, you will be able to:

Recognize hyperkalemia, metabolic acidosis, malnutrition, depression & acute kidney injury (AKI) as important complications of CKD.

Evaluate patient clinical data to identify appropriate treatments for hyperkalemia and metabolic acidosis.

Identify laboratory data that is used to assess and monitor metabolic acidosis, malnutrition and AKI in CKD.

Describe important implications of depression in CKD patients.

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HYPERKALEMIA

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Serum potassium may increase as eGFR decreases

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Reference: Adapted from USRDS

Annual Data Report (NIDDK, 2009)

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Serum potassium levels affect muscle and cardiac function

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Hypokalemia

Cardiac arrhythmiasMuscle weaknessGlucose intolerance

Hyperkalemia

Cardiac arrhythmias

Muscle weakness

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Hyperkalemia is potentially life threatening

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Susceptibility

to hyperkalemia depends on serum calcium and other factors determining transmembrane potential.Cardiac arrhythmias and cardiac arrest are possible if severe hyperkalemia is not recognized and treated.

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Potassium Balance

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About 85% of dietary potassium is absorbed.

Proximal tubules reabsorb 70–80% of potassium. Potassium secretion occurs in distal tubule and collecting duct and may be an “adaptation” to high intake. A small amount may be excreted in the feces.Gennari & Segal,

Kidney

Int

2002; 62(1):1–9.

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Renin-angiotensin-aldosterone system (RAAS)

affects potassium excretion

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Activation of RAAS increases potassium excretion via aldosterone.

Medications that inhibit RAAS increase risk for hyperkalemia.

Palmer,

N

Engl

J Med

2004; 351(6): 585-592

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Medication-induced hyperkalemia is a concern in CKD

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Medication

Mechanism

Beta-blockers (non-selective)

Decreased Na

+

/K

+

-ATPase pump activity and renin release

Digoxin intoxication

Decreased Na

+

/K

+

-ATPase pump activity and renin release

ACE inhibitors

Blockade of angiotensin II synthesis and decreased aldosterone secretion

ARBs

Competitive binding of the angiotensin II receptor and decreased aldosterone synthesis

NSAIDs

Decreased prostaglandin-mediated renin release

Calcineurin inhibitors

Decreased aldosterone synthesis and Na

+

/K

+

-ATPase pump activity

Aldosterone antagonists

Blockade of mineralocorticoid receptors

Potassium-sparing diuretics/trimethoprim

Blockade of luminal sodium channels

Ben Salem, C. Drug

Saf

. 2014 37:677-692

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Potassium-rich fruits & vegetables

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Fruits

Vegetables•Apricots (fresh)•Bananas•Cantaloupe•Dates•Nectarines•Kiwi•Prunes/prune juice

•

Oranges/orange juice

•Raisins

•Acorn and

butternut squash

•Avocado

•

Baked beans

•Beet and other greens

•

Broccoli (cooked)

•Brussels sprouts (cooked)

•Chard

•Chile peppers

•

Mushrooms (cooked)

•

Potatoes

•

Pumpkin

•

Spinach (cooked)

•Split peas, lentils, beans

•

Sweet potatoes, yams

•

Vegetable juice

•

Tomatoes

/tomato juice/tomato sauce

https://www.niddk.nih.gov/health-information/health-communication-programs/nkdep/a-z/nutrition-potassium/Pages/nutrition-potassium.aspx

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Potassium restriction is not indicated in the absence of hyperkalemia

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Specific level of eGFR does not determine need for potassium restriction.

Restrict dietary potassium to help achieve and maintain safe level.Level of potassium restriction should be individualized.

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Question

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A patient with an eGFR of 35 mL/min/1.73m

2 presents with a serum potassium of 5.8 mEq/L. His medications include labetalol 100 mg BID, lisinopril 40 mg once daily and acetaminophen 500 mg every 4 hours for osteoarthritis. He was started on Bactrim DS 5 days ago. Which of following is not likely contributing to his hyperkalemia?labetalollisinoprilacetaminophenBactrim DS

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Answer

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Answer: C

The answers A B and D are incorrect because non-selective beta-blockers, ACE inhibitors and trimethoprim can all induce hyperkalemia via renin, aldosterone or luminal sodium channel mechanisms. Acetaminophen does not decrease prostaglandins and does not decrease renin release.A patient with an eGFR of 35 mL/min/1.73m2 presents with a serum potassium of 5.8 mEq/L. His medications include labetalol 100 mg BID, lisinopril 40 mg once daily and acetaminophen 500 mg every 4 hours for osteoarthritis. He was started on Bactrim DS 5 days ago. Which of following is not likely contributing to his hyperkalemia?labetalollisinopril

acetaminophen

Bactrim DS

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Potassium shifts between intracellular and extracellular compartments

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98% of potassium is intracellular.

75% in muscles2% is extracellular (65–70 mEq).Transcellular electrical potential generated by sodium-potassium exchange is responsible for voltage gradient across cell membranes.Gradient difference is needed for muscle and nerve function.

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Factors affecting potassium shifts between compartments

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Insulin concentration and hyperglycemia

Insulin moves potassium into cells.Insulin deficiency may lead to hyperkalemia.Acid-base status Metabolic acidosis may drive potassium out of cells, as hydrogen ion is buffered intracellularly.

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Treating hyperglycemia and acidemia

may lower serum potassium

Control hyperglycemia with adequate insulin.Potassium follows glucose into the cells.Treating acidosis may lower serum potassium.Treatment may allow continued use of RAAS inhibitors that lower urine albumin and slow progression. Palmer, N Engl J Med 2004; 351(6):585–592

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Treatments for hyperkalemia 

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Severe hyperkalemia (> 6.0

mEq/L):Intravenous calciumAgents to induce intracellular shift: insulin and glucose, sodium bicarbonate and beta-2 agonist (albuterol)Removal of potassium: Loop diuretics or DialysisMild hyperkalemia (5.5-6.0 mEq/L):Sodium polystyrene sulfonate Patiromer

Sodium zirconium cyclosilicate

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Sodium Polystyrene Sulfonate

Mechanism

of action: Cation exchange resin, exchanges sodium for potassiumDosage:Adult dose: 15g to 60 g (divided into 15g one to four times daily)In CKD: 30 g orally daily for up to 7 daysSide effects: nausea, vomiting, anorexia, constipation, hypomagnesemia, hypocalcemiaFecal impaction has been reported in childrenGI concretions with oral administration has been reported

GI tract ulceration or necrosis leading to intestinal perforation has been reported

http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/011287s022lbl.pdf

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Patiromer

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Mechanism of action: non-absorbable cation exchange polymer that exchanges calcium for potassium

Starting dose: 8.4g once daily (Max 25.2 g daily) Warning: Avoid use in patients with severe GI conditionshttps://www.accessdata.fda.gov/drugsatfda_docs/label/2015/205739s000lbl.pdf

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Sodium Zirconium Cyclosilicate

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Mechanism of action: Cation exchange resin, exchanges sodium/hydrogen for potassium

Dosage:10 g TID for 48 hours, then 10 g once daily Side effects: less gastrointestinal side effects than other agents Can reduce serum potassium within 1 hour with proposed dosing, more rapid than other agentsSodium absorption can be significant (800 mg/dose)

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Considerations for pharmacists

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Drug preparation

All available potassium binding resins are available in available in powder form. Symptoms of hypokalemiaIrritability, confusion, muscle weakness, hyporeflexiaDrug interactionsSPS: antacids, non-absorbable cation-donating antacids and laxatives, digoxin, sorbitol, lithium, thyroxinePatiromer: Other drugs should be taken 3 hours before or after

patiromer

. 

Sodium Zirconium Cyclosilicate: Separate other medications by

2 hours

https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/205739s000lbl.pdf

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Summary: Hyperkalemia

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The reference range for serum K level is 3.5–5.0

mEq/LHyperkalemia is potentially life threateningRAAS affects potassium excretionMedication-induced hyperkalemia is a significant concern in CKDHyperkalemia treatment includes: Acute treatment: Insulin + beta agonist + calcium or dialysisChronic treatment:

SPS,

patiromer

, sodium zirconium cyclosilicate

Choice of potassium resins should be based on risk of sodium absorption and gastrointestinal intolerance

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METABOLIC ACIDOSIS

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Serum bicarbonate may decrease as eGFR decreases

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Reference: Adapted from USRDS

Annual Data Report (NIDDK, 2009)

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Serum bicarbonate may decrease as eGFR decreases

Eustace JA et al. Kidney

Int 2004;65:1031-1040Metabolic acidosis is usually defined as serum bicarbonate concentration <22mEq/L.Approximately, 2.3% to 13% of CKD Stage 3 patients are estimated to have metabolic acidosisApproximately, 19% to 37% CKD Stage 4 patients are estimated to have metabolic acidosis

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Metabolic acidosis = excessive hydrogen ions in the blood

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Acid production exceeds acid elimination

CO2 + H2O HCO3 + H+The reference range for serum bicarbonate (HCO3

)

is

21–28

mEq

/L.

Maintaining normal serum HCO

3

may be beneficial.

Bailey JL. Kidney Int. 2005;68(

suppl

96):S15–S23.

de Brito-Ashurst I et al. J Am

Soc

Nephrol

. 2009;20(9):2075–84.

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Kidney tubules help maintain normal

acid-base balance

Tubules reabsorb filtered HCO3 and synthesize HCO3 to neutralize acid load.About 80–85% is reabsorbed within the proximal tubules.

Patients with CKD have fewer functioning nephrons.

Less hydrogen ion (acid) is excreted.

Capacity to reabsorb and synthesize HCO

3

is reduced.

Condition may lead to chronic metabolic acidosis.

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Chronic metabolic acidosis

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Accelerates muscle degradation

Reduces albumin synthesis

Exacerbates pre-existing bone disease

May impair glucose tolerance due to interference with insulin actions

May accelerate CKD progression

May stimulate inflammation

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Interventions for chronic metabolic acidosis

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Adequate, not excessive, intake of animal protein

Supplemental base may be prescribed to balance the acid

Sodium bicarbonate may be prescribed,

650 mg tablet has 179 mg sodium

Re-emphasize dietary salt restriction

May require higher dose of diuretic

Kraut &

Madias

,

Nat Rev

Nephrol

2010; 6(5):274–285

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Sodium Bicarbonate

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Contraindication

:

Any medication or disease state that would induce hypochloremia (example. NG suction or severe vomiting) 

Chronic

metabolic

acidosis

dose:

initial, 650 mg orally 3 times daily or calculated bicarbonate requirement; increase to maintain serum bicarbonate level at 22-24

mEq

/L

Side effects:

Flatulence/feeling of fullness

Fluid retention

Metabolic alkalosis

Kraut &

Madias

, Am J Kidney Dis. 2016 Feb;67(2):307-17

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Summary: Metabolic acidosis

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Animal protein may increase acid load.

Reducing protein intake may improve serum HCO3.Supplemental base may be prescribed to treat metabolic acidosis. Sodium bicarbonate will increase daily sodium intake. Review salt restriction, if prescribed.Treatment may improve serum albumin levels by improving nutritional status.

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Serum albumin is a marker for nutritional status and inflammation

HYPOALBUMINEMIA

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Serum albumin

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Maintains oncotic pressure and blood volume

Acts as bufferBinds:Calcium, magnesiumHormonesVitamins (e.g., A, riboflavin, B6, C, and folate)Medications (e.g., furosemide) Serum albumin is a marker for nutritional status and inflammation

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Changes in drug binding to albumin in CKD

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Metabolic acidosis changes protein confirmation, reduces binding, and increases free drug plasma concentration

Uremic toxins compete for binding to albuminReduced albumin increases the volume of distribution of water soluble drugs (third spacing)

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Serum albumin at dialysis initiation is an independent risk factor for mortality

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Serum albumin ≥ 4.0 g/

dL at initiation of dialysis is associated with reduced mortality risk. Only 11% of incident dialysis patients had serum albumin ≥ 4.0 g/dL (1999–2005).Reference: Kaysen et al.

J Renal

Nutr

2008; 18(4):323–331.

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Hypoalbuminemia in CKD is multi-factorial

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Inflammation

Acute or chronic, e.g., foot ulcer, infected toothAlbuminuriaMetabolic acidosisInsulin resistanceReduced appetite particularly for foods high in protein

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Low serum albumin in CKD is

associated with inflammation

Reference: Eustace et al. Kidney Int 2004; 65(3):1031–1040.

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Summary: Hypoalbuminemia in CKD

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Reduce inflammation, treat infections

Serum albumin ≥ 4.0 g/dL at initiation of dialysis associated with lower risk of mortalityControl blood pressure and use ACE inhibitor to reduce proteinuriaProvide adequate protein and caloriesTreat metabolic acidosisEating less protein may reduce acid loadMay be treated with sodium bicarbonate

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DEPRESSION

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Depression is Common in CKD

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Bautovich

 A, et al. Australian & New Zealand Journal of Psychiatry 2014; 48(6): 530–541 

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Assessing Depression in CKD is Complex

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Medications used to treat patients with CKD might also cause depression or have side effects that mimic its symptomatology

ClonidinePropranololUremia—which is common in advanced CKD—results in symptoms that may overlap with those of depression (e.g., weight change, sleep disturbances, decreased appetite)Cukor D, et al. Psychosocial Aspects of Chronic Disease: ESRD as a Paradigmatic Illness 2007; 18(12):3042-55; Kimmel PL. Depression in patients with chronic renal disease: What we know and what we need to know 2002; 53(4):951-6.

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Social and Lifestyle Factors Influence the

Relationship between CKD and Depression

DepressionPhysical activityDiet

Adherence

CKD

Socioeconomic Status

Cukor D, et al. JASN 2007; 18(12):3042-55;

Bautovich

A, et al.

Australian & New Zealand Journal of Psychiatry

2014; 48(6): 530–541; Norton J, et al. JASN 2016; 27:2576–95

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Biopsychosocial consequences of CKD and depression

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Biological consequences

: Increased inflammation and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis as a consequence of depression and often reported in those with CKDBarrier to healthy behaviors: Depression is a barrier to maintaining medical, dialysis and diet regimens. CKD is associated with a sedentary lifestyle, which is an independent risk factor for depressionCukor D, et al. JASN 2007; 18(12):3042-55; Bautovich

A, et al.

Australian & New Zealand Journal of Psychiatry

2014; 48(6): 530–541

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Biopsychosocial consequences of CKD and depression

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Symptom burden:

CKD patients have increased fatigue and sleep disturbance which all increase the risk of subsequent depressionLoss: Those with CKD report loss of role, identity, body image and employment, which all increase the risk of depressionBautovich A, et al. Australian & New Zealand Journal of Psychiatry 2014; 48(6): 530–541

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Negative outcomes are associated with depression in CKD

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Higher all-cause mortality

Increased risk for hospitalization and length of stayBarrier to adherence to medical and nutritional regimensReduced quality of lifePalmer S, et al. Kidney Int. 2013; 84:179–191; Lopes AA, et al. Kidney Int. 2002; 62: 199–207.Hedayati SS et al. JAMA 2010;303:1946–1953; Chilcot J, et al.

Sem

Dial. 2010;23: 74–82

Kimmel PL, et al. Kidney Int. 2000; 57: 2093–2098

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Summary

Depression is a very common but complex problem

among people with CKD Depression has been associated with higher rates of mortality, increased hospitalization, reducedtreatment adherence and lower QOL.Screening and treatment of depression in those with CKD should be prioritized along with evidence-based pharmacotherapy

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ACUTE KIDNEY INJURY (AKI)

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Community-acquired acute kidney injury (CA-AKI)

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Rapid decline of kidney function in the outpatient setting

Most commonly hemodynamically mediatedOutcomes are similar to patients who develop hospital-acquired AKIEarly patient-reported symptoms can include fatigue, reduced urine output and edemaCA-AKI may be more insidious, subtle signs/symptoms may be more important to glean from patient interviewMehta RL et al . Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury,” Critical Care. 2007;11 (2):R31

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CA-AKI is common and preventable

Drug induced AKI accounts for 18% of AKI hospital admissions from the outpatient setting.

Most cases are hemodynamically-mediatedThere is a 3-8 fold age-dependent increase in the frequency of CA-AKI in patients >60 years oldHistory of AKI is a strong risk factor for both new-onset CKD and accelerated progression of existing CKDCoca SG et al. Acute kidney injury in the elderly: predisposition to chronic kidney disease and vice versa. Nephron Clin

Pract

. 2011;119

Suppl

1:c19-24.,

Feest

TJ et al. Incidence of severe acute renal failure in adults: results of a community-based study. BMJ 306:481–483, 1993

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Who is at highest risk for CA-AKI?

Patients with:

existing CKD are at highest riskdiabetes and/or hypertensionrenin-dependent comorbid conditions which are acquired with age (e.g. congestive heart failure, renal artery disease, severe liver disease) comorbid conditions that require the use of drugs that affect renal hemodynamics (ACE Inhibitors, ARBS, diuretics, NSAIDs)

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Hemodynamically-mediated AKI

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This video details the hemodynamic effects of

RAASi, and NSAIDs with concurrent illnessRenal HemodynamicsPlease also see this separate CE program focused on NSAID-induced AKI

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NSAIDs and CA-AKI

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In a retrospective study of Medicaid enrolled patients, use of NSAIDs increased the risk of and AKI hospitalization by 58% (relative risk [RR] = 1.58; 95% CI = 1.34-1.86), and higher doses of ibuprofen (the most commonly used NSAID) were associated with a higher risk of developing AKI

The most relevant risk factors for AKI associated with NSAIDs from observational data are preexisting CKD, older age (ie, >65 years), concomitant use of diuretics and RAAS inhibitors, and recent initiation of an NSAID.Pai AB et al . Need for a Judicious Use of Nonsteroidal Anti-inflammatory Drugs to Avoid Community-Acquired Acute Kidney Injury. Ann Pharmacother. 2018;

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“Triple whammy”

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Loboz

KK, Shenfield GM. Br J Clin Pharmacol 2005; 59(2): 239–243.ACEI/ARB

Diuretics

Non-steroidal anti-inflammatory drugs (NSAID)

ACEI/ARB decreases angiotensin II

Dilate the efferent arteriole

Lowers glomerular perfusion pressure and glomerular filtration rate (GFR)

Lead to volume depletion

GFR cannot be maintained due to insufficient hemodynamics

Combination with ACEI/ARB and NSAID increases risk of AKI

Inhibit renal vasodilatory prostaglandins

Constricts the afferent arteriole

Lowers glomerular perfusion pressure and GFR

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Case

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The patient is a 60-year-old (110 kg) male who presents to urgent care with confusion, shortness of breath and edema. His past medical history includes hypertension, diabetes and back pain. His wife states that he had been taking naproxen multiple times per day for back pain that developed a couple weeks before admission. He stated he has not made much urine for the past few days. Today his labs reveal BUN 77 mg/dl, and

SCr 3.9 mg/dL (baseline 1.2 mg/dL), potassium 5.9 mEq/L. Home medications: Lisinopril 40mg once daily, Hydrochlorothiazide 50mg once daily, Humulin 70/30, Naproxen 220 mg 2 tablets q12h PRN

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Question

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Which of the following is most likely the cause of acute kidney injury in this patient?

Humulin + LisinoprilLisinopril + Humulin + HydrochlorothiazideLisinopril + Naproxen + HydrochlorothiazideHumulin + Naproxen

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Answer

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Answer: D

Concurrent use of ACEI/ARB, NSAID and diuretic has been associated with risk of community acquired acute kidney injury. Which of the following is most likely the cause of acute kidney injury in this patient?Humulin + LisinoprilLisinopril + Humulin + HydrochlorothiazideLisinopril + Naproxen + HydrochlorothiazideHumulin + Naproxen

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What are “Sick Day Rules”?

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https://

www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2018/01/Think-Kidneys-Sick-Day-Guidance-2018.pdfDehydration can be a significant risk for people taking certain medicines. Health care professionals can provide advice to patients who are at increased risk of AKI (e.g. patients with CKD / heart failure) that certain drugs should be temporarily discontinued during acute intercurrent illnesses(vomiting, diarrhea and fever), particularly where there is disturbed fluid balance.

This is commonly described as ‘sick day rules’

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https://

ihub.scot

/media/1290/20170814-medicines-sick-day-rules-card-v2-0-print.pdf

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https://

ihub.scot

/media/1290/20170814-medicines-sick-day-rules-card-v2-0-print.pdf

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Summary

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Community-acquired AKI is becoming better defined and the prevalence rate may be higher than previously described.

The majority of CA-AKI cases are hemodynamically mediated and can be prevented.CA-AKI is associated with long-term consequences on kidney function and clinical outcomes.Use of ACEI, ARBs, diuretics and NSAIDs concomitantly has been associated with increase risk of CA-AKI in high risk patients

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