advanced concepts: chronic kidney disease management
TRANSCRIPT
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Advanced Concepts: Chronic Kidney Disease Management
Mary E. Krebs, MD, FAAFP
Activity DisclaimerThe material presented here is being made available by the American Academy of Family Physicians
for educational purposes only. Please note that medical information is constantly changing; the
information contained in this activity was accurate at the time of publication. This material is not
intended to represent the only, nor necessarily best, methods or procedures appropriate for the
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Physicians may care to check specific details such as drug doses and contraindications, etc., in
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does not necessarily imply the endorsement by the AAFP.
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Disclosure Statement
It is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflicts of interest. If conflicts are identified, they are resolved prior to confirmation of participation. Only participants who have no conflict of interest or who agree to an identified resolution process prior to their participation were involved in this CME activity.
All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.
Learning Objectives
1. Screen all patients for renal disease.2. Manage complications of renal disease.3. Prescribe medications appropriately in patients
with renal disease.
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Who to Screen?
U.S. Preventive Services Task Force found insufficient evidence recommend screening for chronic kidney disease in the general population
American College of Physicians recommends against screening asymptomatic adults without risk factors.
Who to Screen?
Patients with diabetes or hypertension be screened annually for CKD.
Consider screening patients with other risk factors, including cardiovascular disease, older age, history of low birth weight, obesity, and a family history of CKD.
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How to Screen?
Serum creatinine
Estimation of GFR using a serum creatinine-based equation
Cystatin C
Measurement of the urine albumin/creatinine ratio
Urinalysis
GFR
Cockcroft-Gault equation to estimate GFR is used to determine dosing adjustments for medications.
All other purposes: Chronic Kidney Disease Epidemiology Collaboration equation (http://www.kidney.org/professionals/kdoqi/gfr_calculator.cfm) Improved accuracy in persons with near-normal estimated GFR
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Cystatin C
Cystatin C is a small protein that is expressed in all nucleated cells, produced at a constant rate, and freely filtered by the glomerulus.
Endogenous marker of renal function.
Cystatin C–based GFR equations may be superior to creatinine-based formulas in obese CKD patients, especially those with a BMI≥35 and in obese women.
Cystatin C
Consider checking Cystatin C in adults with GFR 45–59 who do not have markers of kidney damage if confirmation of CKD is required.
If GFR from cystatin C is also <60, the diagnosis of CKD is confirmed. If GFR from cystatin C is ≥60 ml/min/1.73 m2, the diagnosis of CKD is not confirmed.
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Urine Albumin/Creatinine Ratio
Initial proteinuria evaluation using the spot urine albumin/creatinine ratio obtained from an early morning sample
24-hour urine collections are no longer recommended as an initial diagnostic tool because of the potential for inadequate collection, inconvenience to patients, and the lack of diagnostic advantage over the urine albumin/creatinine ratio.
Urinalysis
Urinalysis has a high sensitivity for heavy proteinuria (greater than 300 mg per 24 hours, as estimated from the spot urine protein/creatinine ratio) but may not detect clinically significant lower levels (30 to 300 mg).
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Stages of Chronic Kidney Disease
Stage 1 with normal or high GFR (GFR > 90 mL/min)
Stage 2 Mild CKD (GFR = 60-89 mL/min)
Stage 3A Moderate CKD (GFR = 45-59 mL/min)
Stage 3B Moderate CKD (GFR = 30-44 mL/min)
Stage 4 Severe CKD (GFR = 15-29 mL/min)
Stage 5 End Stage CKD (GFR <15 mL/min)
AES Question
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Question 1
58 y/o F with HTN and BMI 38 presents to your office. You screen her for CKD. Her GFR is 58. Her urinalysis and urine albumin/creatinine ratio are both normal. What is next step?
A. Full evaluation for cause of renal diseaseB. Refer to nephrologyC. Check Cystatin CD. Check 24 hour urine
Management of CKD
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Dietary Recommendations
Dietary sodium restriction to reduce proteinuria and to improve blood pressure control should be considered. Studies vary, but limiting intake to about 2,000 mg per day is generally accepted.
Limiting dietary protein intake to 0.6-0.8g/kg/day to decrease CKD progression when the eGFR is below 60 increases malnutrition risk, which requires close monitoring.
Lifestyle
Physical activity compatible with cardiovascular health and tolerance (aiming for at least 30 minutes 5 times per week)
Healthy weight
Avoid tobacco
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HTN in Non-Diabetic Patients
Non-dialysis and urine albumin excretion <30 mg/day should treated to a goal ≤140/90
Non-dialysis and urine albumin excretion of >30 mg/day should be treated to a goal of ≤130/80.
ACE-I or ARB should be used in non-diabetic adults, not on dialysis and urine albumin excretion of >30mg/day in whom treatment with BP-lowering drugs is indicated.
Blood Pressure Management
One meta-analysis suggests reduced mortality in CKD when systolic blood pressure is maintained below 140 mm Hg.
ACE inhibitors or ARBs should be used to treat patients who have CKD with albuminuria and diabetes mellitus.
For CKD with albuminuria but no diabetes, an ACE inhibitor is recommended because of a 31% reduction in end-stage renal disease.
No other antihypertensive medications reduce CKD progression.
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HTN in Patients with CKD and DM
DM and non-dialysis with urine albumin excretion <30mg/day should be treated to goal of <140/90
DM and non-dialysis with urine albumin excretion >30mg/day should be treated to goal of <130/80
HTN in Elderly
Individualize treatment
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Blood Pressure After Kidney TransplantGoal <130/80
ACE or ARB When No HTN
Nondiabetic kidney disease + a random urine total protein-to-creatinine ratio greater than 200 mg/g
Diabetic kidney disease should be treated with an ACE inhibitor or an ARB, regardless of the presence of hypertension.
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AES Question
Question 262 y/o M with stage 3B diabetic renal disease. He denies complaints. He does not have a history of HTN. His medications are: long-acting insulin, mealtime insulin, levothyroxine, and albuterol. He was previously on lisinopril which he stopped due to a cough. BP today is 128/72. What is the best choice in regard to his medication?
A. Continue current medication. B. Start enalapril.C. Start a phosphate binder.D. Start losartan.
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Diabetes
Target HbA1c) of ~7.0% to prevent or delay progression of the microvascular complications of diabetes, including diabetic kidney disease.
Can modify if risk of hypoglycemia or limited life expectancy
Vaccines in CKD
Annual influenza vaccine, unless contraindicated. GFR <30 and those at high risk of pneumococcal infection (e.g., nephrotic
syndrome, diabetes, or those receiving immunosuppression): polyvalent pneumococcal vaccine unless contraindicated. Adults with CKD who have received pneumococcal vaccination are offered
revaccination within 5 years. All adults who are at high risk of progression of CKD and have GFR <30:
hepatitis B vaccine and the response confirmed by appropriate serological testing.
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Complications of CKD
Cardiovascular Disease
All patients with CKD are at increased risk for cardiovascular disease.
Patients with CKD are more likely to die of cardiovascular causes than develop ESRD.
Level of care for ischemic heart disease and heart failure offered to patients with CKD should be the same as non-CKD patients.
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Cardiovascular Disease
Patients with CKD should be regularly examined for signs of peripheral arterial disease and be considered for usual approaches to therapy.
Patients with CKD at risk for atherosclerotic events be offered treatment with antiplatelet agents unless the risk of bleeding outweighs the benefits.
CKD and heart failure: any escalation in therapy and/or clinical deterioration should prompt monitoring of GFR and potassium.
Interpreting Labs in Heart Disease
GFR<60: BNP/NT-proBNP should be interpreted with caution and in relation to GFR with respect to diagnosis of heart failure and assessment of volume status.
GFR<60: troponin be interpreted with caution with respect to diagnosis of acute coronary syndrome.
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Metabolic Acidosis
When CKD is complicated by metabolic acidosis, sodium bicarbonate supplementation can slow progression to end-stage renal disease.
CKD and bicarbonate <22 mmol/l: treat with oral bicarbonate to maintain serum bicarbonate within the normal range, unless contraindicated.
Urate-lowering therapy does not slow CKD progression.
Hyperphosphatemia
Calcium acetate as the first-line phosphate binder to control serum phosphate in addition to dietary management.
Consider calcium carbonate if calcium acetate is not tolerated or patients find it unpalatable.
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Hyperphosphatemia
Stage 4 or 5, not on dialysis and taking a calcium-based binder: Consider switching to a non-calcium-based binder if calcium-based
phosphate binders are not tolerated Consider either combining with, or switching to, a non-calcium-based
binder if hypercalcemia develops or if low PTH
Stage 5 CKD on dialysis and remain hyperphosphatemicdespite adherence to the maximum recommended or tolerated dose of calcium-based phosphate binder, consider either combining with, or switching to, a non-calcium-based binder.
Hyperphosphatemia
Stage 5 CKD on dialysis and taking a calcium-based binder, if serum phosphate is controlled by the current diet and phosphate binder regimen but elevated calcium or low PTH Consider either combining with, or switching to, sevelamer
hydrochloride or lanthanum carbonate.
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AES Question
Question 3
70 y/o M with stage 4 CKD, not on dialysis with elevated phosphorus. You decide to start a phosphate binder. What is the best first-line choice?
A. N-acetyl cysteineB. Calcium acetateC. Calcium carbonateD. Magnesium sulfate
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AES Question
Question 4The same 70 y/o M with stage 4 CKD, not on dialysis with elevated phosphorus returns for follow up. His phosphorus is still elevated. Careful questioning reveals that he stopped taking calcium acetate due to a bad taste. You decide to start a phosphate binder. What is the best first-line choice?
A. Continue calcium acetateB. Change to calcium carbonateC. Change to sevelamer hydrochlorideD. Change to lanthanum carbonate.
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Metabolic Acidosis
When CKD is complicated by metabolic acidosis, sodium bicarbonate supplementation can slow progression to end-stage renal disease.
Urate-lowering therapy does not slow CKD progression.
Evaluation of CKD: Mineral and Bone DisordersPatients with GFR>45 can be screened for osteoporosis using
the same strategy as the general population.
GFR<45: densitometry is not recommended because fracture risk prediction is less accurate.
GFR<30: do not prescribe bisphosphonate without a strong clinical rationale.
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Evaluation of CKD: Mineral and Bone Disorders Patients with GFR<45 should have annual check of: serum calcium phosphorus 25-hydroxyvitamin D parathyroid hormone alkaline phosphatase
GFR <45: maintain serum phosphate concentrations in the normal range according to local laboratory reference values.GFR <45: the optimal PTH level is not known. If elevated PTH,
evaluate for hyperphosphatemia, hypocalcemia, and vitamin D deficiency.
Anemia
Anemia is often associated with iron deficiency.
Intravenous iron replacement is most efficient, oral replacement is optimal when taken every other day. Erythropoiesis-stimulating agents should not be used when hemoglobin is 10 or more.
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Anemia Screening
GFR ≥60: when clinically indicated
GFR 30–59: at least annually
GFR <30: at least twice per year
Dialysis dependent: at least every 3 months
Anemia Diagnosis
CKD and age >15 years when the hemoglobin is <13.0 g/dl in males and <12.0 g/dl in females.
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Evaluation of Anemia
CBC with differential
Absolute reticulocyte count
Serum ferritin level
Serum transferrin saturation (TSAT)
Serum vitamin B12 and folate levels
Other tests as indicated
Anemia Monitoring
For CKD patients with anemia not being treated with an erythropoiesis-stimulating agent (ESA), check hemoglobin: At least every 3 months in patients with CKD 3–5ND and CKD 5PD At least monthly in patients with CKD 5HD When otherwise clinically indicated
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Anemia Treatment with Iron
Not on iron or ESA therapy, consider IV iron or 1–3 month trial of oral iron therapy if not on dialysis and: An increase in Hb concentration without starting ESA treatment is
desired and TSAT is ≤30% and ferritin is ≤500 ng/ml
On ESA therapy who are not receiving iron supplementation, consider IV iron or 1–3 month trial of oral iron therapy if not on dialysis and: An increase in Hb concentration or a decrease in ESA dose is desired
and TSAT is ≤30% and ferritin is ≤500 ng/ml
Anemia Treatment with Iron
Non-dialysis patients who require iron supplementation, select the route of iron administration based on the severity of iron deficiency, availability of venous access, response to prior oral iron therapy, side effects with prior oral or IV iron therapy, patient compliance, and cost.
Subsequent iron administration based on Hb responses to recent iron therapy, ongoing blood losses, iron status tests (TSAT and ferritin), Hb concentration, ESA responsiveness and ESA dose in ESA treated patients, trends in each parameter, and the patient’s clinical status.
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Erythropoiesis Stimulating Agent (ESA) InitiationAddress all correctable causes of anemia (including iron
deficiency and inflammatory states) prior to initiation of ESA therapy.
Extreme caution with active malignancy (in particular when cure is the anticipated outcome), a history of stroke, or a history of malignancy.
Do not start ESA if hemoglobin ≥10.0 g/dl
Erythropoiesis Stimulating Agent (ESA) InitiationNon-dialysis patients with hemoglobin <10.0 g/dl: individualized
decision.
Dialysis patients: ESA therapy when the hemoglobin is between 9.0–10.0 g/dl
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ESA Hyporesponsiveness
ESA hyporesponsiveness if no increase in hemoglobin from baseline after the first month of ESA treatment on appropriate weight-based dosing.
Do not increase ESA dose beyond double the initial weight-based dose.
Acquired ESA Hyporesponsiveness
Acquired ESA hyporesponsiveness if after treatment with stable doses of ESA, they require 2 increases in ESA doses up to 50% beyond the dose at which they had been stable in an effort to maintain a stable Hb concentration.
Do not increase ESA dose beyond double the dose at which they had been stable.
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ESA Hyporesponsiveness
Evaluate patients with either initial or acquired ESA hyporesponsiveness and treat for specific causes of poor ESA response.
Anemia Monitoring on ESA
Initiation phase: check hemoglobin at least monthly.
Non-dialysis maintenance: check hemoglobin at least every 3 months.
Dialysis maintenance: check hemoglobin at least monthly.
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ESA Maintenance
Recommendation: do not use ESA to maintain hemoglobin above 11.5 g/dl
Some patients may have improvements in quality of life at Hb concentration above 11.5 g/dl and will be prepared to accept the risks.
In all adult patients, do not use ESA to intentionally increase the hemoglobin concentration above 13 g/dl.
AES Question
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Question 5The same 70 y/o M with stage 4 CKD, not on dialysis returns for follow up. He c/o mild fatigue. His hemoglobin is 10.1, transferrin saturation is 20% and ferritin is 320ng/m. He had a negative colonoscopy 4 months ago, and you determine his CKD is the cause of his anemia. What do you recommend?
A. MonitorB. Oral ironC. ErythropoetinD. Blood transfusion
AES Question
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Question 6The same 70 y/o M with stage 4 CKD, not on dialysis returns for follow up. His fatigue is unchanged and he states he has taken his iron consistently. His hemoglobin had initially improves slightly, but then over four months, slowly trends down to 8.9. Repeat testing confirms a hemoglobin of 8.9. There are no other causes of anemia. What do you recommend?
A. Start erythropoietin and recheck hemoglobin in one weekB. Start erythropoietin and recheck hemoglobin in one monthC. Blood transfusionD. Continue iron
Evaluation for Pure Red Cell Aplasia (PRCA) Investigate for possible antibody-mediated PRCA when a
patient receiving ESA therapy for more than 8 weeks develops: Sudden rapid decrease in hemoglobin at the rate of 0.5-1.0/week OR
requirement of transfusions at the rate of approximately 1-2/week, AND Normal platelet and white cell counts, AND Absolute reticulocyte count <10,000/µl
Stop ESA therapy if antibody-mediated PRCA.
Peginesatide can be used to treat antibody-mediated PRCA.
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Use of Red Cell Transfusion in Chronic Anemia Avoiding red cell transfusions when possible due to risks.
If eligible for organ transplantation, avoid red cell transfusions to minimize the risk
of allosensitization when possible.
The benefits of red cell transfusions may outweigh the risks in patients in whom: ESA therapy is ineffective (e.g., hemoglobinopathies, bone marrow failure, ESA
resistance)
The risks of ESA therapy may outweigh its benefits (e.g., previous or current malignancy,
previous stroke)
Transfusion for non-acute anemia should not be based on any arbitrary
hemoglobin threshold, but based on symptoms.
Contrast-Induced Renal Injury
Contrast-induced nephropathy is an increase in serum creatinine greater than 25 percent from baseline or an absolute increase greater than 0.5 within the first few days after receipt of intravenous contrast.
Patients with CKD and a GFR less than 60 are at high risk of contrast-induced nephropathy, and preventive measures should be considered.
Consider alternative imaging without contrast if the perceived risks of an intravenous contrast study outweigh the benefits.
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Contrast-Induced Renal Injury
Consider alternative imaging without contrast if the perceived risks of an intravenous contrast study outweigh the benefits.
Efforts to minimize the risk of contrast-induced nephropathy include avoidance of dehydration and nonsteroidal anti-inflammatory agents, and use of the lowest possible doses of contrast agents.
Isotonic intravenous hydration with sodium bicarbonate or saline has been shown to prevent contrast-induced nephropathy.
Contrast-Induced Renal Injury
N-acetylcysteine has conflicting evidence.
Given the relatively low cost and favorable safety profile of N-acetylcysteine, some experts recommend giving 1,200 mg orally twice daily on the day before and the day of contrast administration.
Check the serum creatinine level in high-risk patients within this time frame 48-72 hours after dye.
Prophylactic dialysis after contrast media administration does not prevent kidney injury.
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Contrast-Induced Renal Injury
Gadolinium has been associated with acute kidney injury and with nephrogenic systemic fibrosis, a progressive multiorgan system fibrosing disease.
The pathogenesis is unknown.
No treatment for this debilitating disease.
Contrast-Induced Renal Injury
Most patients who develop nephrogenic systemic fibrosis from gadolinium were receiving long-term dialysis, with the remainder were patients with a GFR less than 30.
American College of Radiology considers patients with GFR>30 to be at no or extremely low risk of developing nephrogenic systemic fibrosis.
The FDA recommends avoidance of gadolinium in patients with a GFR less than 30, or with acute kidney injury caused by hepatorenal syndrome or in the perioperative liver transplantation period.
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Medications in CKD
Drug Dosing in CKD
Cockcroft-Gault equation to estimate GFR is used to determine dosing adjustments for medications.
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Medications in CKD
GFR <60 and serious current illness that increases the risk of AKI: temporary discontinuation of potentially nephrotoxic and renally excreted drugs such as: RAAS blockers (including ACE-Is, ARBs, aldosterone inhibitors, direct
renin inhibitors) Diuretics NSAIDs Metformin Lithium Digoxin
Drug Dosing in CKD
Thiazide diuretics are not recommended if creatinine >2.5 mg or GFR<30.
Potassium-sparing diuretics and aldosterone blockers should be used with caution in CKD because of the rise in serum potassium that typically accompanies renal dysfunction.
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Drug Dosing in CKD: HTN Medications
Hydrophilic beta blockers are eliminated renally and dosing adjustments are needed in patients with chronic kidney failure. Atenolol Bisoprolol Nadolol Acebutolol
Beta blockers metabolized by the liver so no adjustment: Metoprolol tartrate Metoprolol succinate Propranolol Labetalol
Antibiotics in CKD
High levels of injectable penicillin G may be associated with neuromuscular toxicity, myoclonus, seizures, or coma.
Imipenem/cilastatin can accumulate in patients with CKD, causing seizures if doses are not reduced. Consider meropenem.
Tetracyclines, with the exception of doxycycline, have an antianabolic effect that may significantly worsen the uremic state in patients with severe disease.
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Antibiotics in CKD
Most quinolones should be renally dosed.
Nitrofurantoin has a toxic metabolite that can accumulate in patients with chronic kidney disease, causing peripheral neuritis.
Aminoglycosides should be avoided in CKD when possible.
Pain Medications in CKD
Patients with stage 5 kidney disease are more likely to experience adverse effects from opioid use.
Metabolites of meperidine, morphine, tramadol, and codeine can accumulate in patients with chronic kidney disease, causing CNS and respiratory adverse effects. These agents are not recommended in patients with stage 4 or 5 disease.
A 50 to 75 percent dose reduction for morphine and codeine is recommended in patients with a GFR<50.
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Pain Medications in CKD
Acetaminophen can be used safely in patients with renal impairment.
Extended-release tramadol should be avoided in patients with chronic kidney disease.
ACE and ARB
ACE inhibitors and ARBs inhibit the renin-angiotensin-aldosterone system, causing efferent arteriolar dilation. This can cause an acute decline in GFR >15% from baseline with proportional elevations in serum creatinine within the first week of initiating therapy. This most commonly occurs in patients with congestive heart
failure, taking diuretics or NSAIDs, and in high dose ACE inhibitors or ARBs. ACE inhibitors and ARBs can be continued safely if the rise in
creatinine <30%. Typically, the level will return to baseline in four to six weeks.
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ACE and ARB
Evidence suggests a reduction of adverse renal outcomes even in advanced stages.
ACE inhibitors and ARBs cause increases in potassium. May be continued if serum potassium is 5.5 mEq per L or less.
Combinations of ACE inhibitors and ARBs should not be used.
ARBs are an appropriate alternative for ACE inhibitor–induced cough, but not appropriate after angioedema.
AES Question
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Question 762 y/o F with stage 3 CKD, not on dialysis presents with BP of 158/86.Her creatinine is 1.7. Her potassium is 4.2. You start lisinopril. She returns in one month. Her BP is 134/78. Her creatinine is 2.0. Her potassium is 5.1. What do you recommend?
A. Continue lisinopril.B. Stop lisinopril and start amlodipine.C. Stop lisinopril and start metoprolol.D. Increase lisinopril.
Medications in CKD
Where precision is required for dosing (due to narrow therapeutic or toxic range) and/or estimates may be unreliable (e.g., due to low muscle mass), consider dosing based upon cystatin C or direct measurement of GFR.
Patients with CKD should seek medical or pharmacist advice before using OTC medicines or nutritional protein supplements.
Patients with CKD should not using herbal remedies.
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Medications and CKD
All people taking potentially nephrotoxic agents such as lithium and calcineurin inhibitors should have their GFR, electrolytes and drug levels regularly monitored.
Patients with CKD should not be denied therapies for other conditions such as cancer but there should be appropriate dose adjustment of cytotoxic drugs according to knowledge of GFR.
CKD and Diabetes
Metformin can be started above an eGFR of 45 and safely continued until eGFR drops to 30.
Consider SGLT-2 inhibitors and GLP-1 receptor agonists to reduce CKD progression.
Sulfonylureas should be avoided in patients with stages 3-5 CKD.
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CKD and Bowel PrepDo not to use oral phosphate-containing bowel preparations in people with a GFR <60 or in those known to be at risk of phosphate nephropathy.
When to Consider Referral
AKI or abrupt sustained fall in GFR GFR <30
A consistent finding of significant albuminuria (≥300 mg/)
Progression of CKD
Urinary red cell casts, red blood cells (RBCs) >20 per high power field sustained and not readily explained
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When to Consider Referral
CKD and hypertension refractory to treatment with 4 or more antihypertensive agents
Persistent abnormalities of serum potassium
Recurrent or extensive nephrolithiasis
Hereditary kidney disease
Practice RecommendationsScreen patients with risk factors for CKD.
Manage complications of renal disease, including anemia and hyperphosphatemia.
Choose appropriate medications and dosages for patients with CKD.
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References Gaitande D. Chronic Kidney Disease: Detection and Evaluation. Am Fam
Physician. 2017 Dec 15;96(12):776-783. Chronic Kidney Disease: Evaluation and Treatment Guidelines from the VA/DoD. Am Fam
Physician. 2020 Sep 15;102(6):378-379. Hyperphosphataemia in chronic kidney disease.
https://www.guidelinecentral.com/summaries/hyperphosphataemia-in-chronic-kidney-disease-management-of-hyperphosphataemia-in-patients-with-stage-4-or-5-chronic-kidney-disease/#section-society
KDIGO clinical practice guideline for anemia in chronic kidney disease. https://www.guidelinecentral.com/summaries/kdigo-clinical-practice-guideline-for-anemia-in-chronic-kidney-disease/#section-434
KDIGO clinical practice guideline for the management of blood pressure in chronic kidney disease. https://www.guidelinecentral.com/summaries/kdigo-clinical-practice-guideline-for-the-management-of-blood-pressure-in-chronic-kidney-disease/#section-427
Munar M. Drug Dosing Adjustments in Patients with Chronic Kidney Disease. Am Fam Physician. 2007 May 15;75(10):1487-1496.
Answers
1. C2. D3. B4. B5. B6. B7. A
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