additional pearls in nephrology
TRANSCRIPT
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Ajay K. Singh, MB., FRCP
Physician, Renal Division,
Brigham and Women’s Hospital,
Course Director, IRIM
Senior Associate Dean for Postgraduate Medical Education,
Harvard Medical School
Additional Pearls in Nephrology
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Ajay K. Singh Bio
• Attending Nephrologist, Brigham and Women’s Hospital
• Senior Associate Dean for Postgraduate Medical Education, Harvard Medical School
• Research interests: Anemia of CKD and CKDu
• Clinical interests: managing patients with CKD
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Disclosures
• ConsultingGSK
• Stock
Gilead
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Clinical Scenarios In General Nephrology
• #1 CKD-Anemia
– 62-year-old woman with CKD and anemia
• #2 CKD-Hyperkalemia
– A 44-year old patient with CKD who has a K of 7.2
mEq/L
• #3 Kidney Stones
– 37-year-old man presents with 2 hours of excruciating
pain in left groin
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#1 62-year-old woman with CKD and
anemia
62-yo woman with 10-year history of CKD from
diabetes; slowly worsening renal function. Past
medical history of a right CVA stroke. She sees
you in the office. Feels great. Working, exercising,
eating well. Lab data shows BUN 48 mg/dL, Cr 4.2
mg/dL, eGFR 18 ml/min/1.73m2, Hb 9.1 g/dL, Tsat
30%, ferritin 282.
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Anemia in CKD patients
• Causes include
– Iron deficiency (reduced absorption, poor intake)
– Blood loss (frequent blood draws, GI bleeding)
– Relative erythropoeitindeficiency
SOURCE: Babbit and Lin, JASN 2013 https://jasn.asnjournals.org/content/23/10/1631
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Anemia Treatment in Dialysis
and Non-Dialysis Patients
• Don’t need treatment if patient asymptomatic (usually start treatment Hb <10 g/dL)
• Make sure patient is iron replete
• TSAT >20%, Ferritin >100
• Target range - Hb 10-11 g/dL
• Use an ESA (2 ESA’s in US – Epo or Darbepoietin)
• Newer ESA’s – prolyl hydroxlase inhibitors (PHIs) not approved in US currently
• Be cautious with ESA treatment in patients with a history of stroke and/or cancer
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ESAs Currently in Use in the U.S.
Source: Fishbane S et al, 2013http://www.nephrologynews.com/articles/109496-choice-of-erythropoiesis-stimulating-agent-in-esrd
* Methoxy polyethylene glycol epoetin beta. (Micera)
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ESA’s globally
Published Feb 2021 SOURCE: https://www.datamintelligence.com/research-report/erythropoietin-stimulating-agents-market
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#2 A 44-year old patient with CKD who has a K of 7.2 mEq/L
• A 44-year old woman with a history of stage 4 CKD is noted to have a serum K of 7.2 mEq/L. She denies N, V and diarrhea. No new medications
• On physical examination. Wt 72 Kg, BP 141/62 mmHg, heart and lung examination normal, no edema.
• EKG – see next slide….
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ECG Changes of hyperkalemia
Peaked T wavesP wave wide and flatProlonged QRS interval with bizarre QRS morphology, High-grade AV block with slow junctional and ventricular escape rhythms, Conduction block (bundle branch blocks, fascicular blocks)(Development of a sine wave appearance (a pre-terminal rhythm))
http://www.aafp.org/afp/2006/0115/p283.html
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Pre-terminal rhythm with very high K
SOURCE: https://www.slideshare.net/ravirajmenon/hyperkalemia-56833946
K= 9.9 mEq/L
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Causes of Hyperkalemia• Increased intake
– K+ supplements, diet, transfusions, iatrogenic
• Decreased renal excretion– Renal disease, particularly with type IV RTA
– DRUGS (e.g., potassium-sparing diuretics (eg, spironolactone, triamterene, amiloride; NSAIDs)
– Adrenal insufficiency
• Intra → extracellular shifts– Hyperosmolarity
– Insulinopenia
– Metabolic acidemia
– DRUGS (e.g., beta-blockade)
• Artifactual– in vitro hemolysis, leukocytosis, thrombocytosis
– “pseudohyperkalemia”
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Management of Hyperkalemia as an Outpatient
K< 5.5 mEq/L K>6.0 mEq/LK 5.5-6.0 mEq/L
No structural CVD diseaseChronically on high side Hold K raising meds
Recheck
Structural CVD disease
Do EKGHold K raising medsDietTreat with resin
Do EKGHold K raising meds
Treat with resin
Emergency treatment
Do EKGIf EKG changes
Ca gluconateThen Insulin/Dex/resindialysis
No EKG ChangesRecheck KInsulin/dextrose/resinDiet
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Treatment of Hyperkalemia
Mechanism Therapy Dose Onset Duration
Stabilize membrane
potential
Calcium 10% Ca-gluconate,
10 ml over 10 min.
1-3 min. 30-60
min
Cellular K+ uptake Insulin
β2-agonist
10 U R with 50 ml
of D50, if BS<250
nebulized albuterol,
10 mg
30 min.
30 min.
4-6 h
2-4 h
K+ removal Kayexalate
ZS9
Hemodialysis
30-60 g PO
5-10 g PO
hours
hours
Immediate
?
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SOURCE: https://www.medscape.org/viewarticle/880329_2
*Kayexalate SPS= sodium polystyrene sulfonate
8.4 g PO qDay
VeltassaLokelma
10 g PO qDay30-60 g PO qDay
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Kayexalate/SPS Complications
• Ischemic colitis and colonic necrosis- risk in enema form
- often fatal
- risk with sorbitol - but can occur without sorbitol and is associated with intestinal SPS crystals
- post-transplant and post-op patients at risk
• Volume overload
• Reduction in serum calcium
• Iatrogenic hypokalemia
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Bicarb
Blumberg et al, Am J Med, 85, 1988
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Changes in plasma K during IV infusion of
bicarbonate in HD patients
Values= means + SE
*P<0.5, + P<0..01 vs. baseline
Blumberg et al KI, 41: 369-374, 1992
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#3 37-year-old man. After a few twinges
over past 2 months, presents with 2 hours of
excruciating pain in left groin
• A 37-year old man presents with 2 hrs of excruciating pain in the left groin. Started in left flank. Episode of gross hematuria. PMH of rt flank twinges.
• On physical examination. Looks in pain (writhing, sweaty), Wt 72 Kg, BP 155/80 mmHg, HR 105 bpm, afebrile, JVP 8 cm, normal skin turgor, moist mucous membranes, lungs clear, mild tenderness left flank, no guarding, no edema.
• Na 140, K 4.2, Cl 100, BUN 24, Cre 1.1, BG 98 mg/dL. UA SG 1015, pH 5.0, 4+ blood, 1+ leuks, rest neg. SedTNTC RBCs not dysmorphic, ocass WBC
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Stones
• Calcium oxalate– 70-80%
• Uric Acid– 10-15%
• Magnesium ammonium phosphate (struvite infection related)– 10-15%
• Cystine– <1%
• Others – <1%
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• Dehydration
– concentrates stone forming constituents
• Anatomic abnormalities
– promote stasis, infection and/or crystal adhesion
• Changes in urinary pH
– e.g. calcium oxalate less soluble in alkaline urine
• Diet
– high protein / salt intake promotes hypercalciuria
– diet high in oxalate promotes oxaluria
• Medications
– furosemide /ca wasting; acetozolamide /bicarb
Risk Factors for Stone Formation
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Work-up
• Imaging
– Non-Contrast helical CT with Stone protocol is gold
std (detects stones not visible by KUB/IVP and has
significantly better sensitivity/specificity)
– Ultrasound: For patients needing avoidance of
radiation (pregnant, childbearing age)
– IVP: No longer favored due to lower sensitivity,
HIGHER radiation exposure
– KUB: Will miss radiolucent uric acid stones, small
stones, stones with overlying bony structures.
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What stones don’t show up on imaging
• 85% of stones are radio-opaque
– Ca containing
– Cystine
• 15% radiolucent
– Uric acid
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Treatment
• Urologic Intervention?
– X<5mm : most pass spontaneously. Possible observation and pain control
– X>5mm : less than 20% chance of passage and may need urologic intervention
• So when to consult urology?
– If > 5mm
– For ANY size with ….
• Urosepsis, AKI, anuria, unyielding N/V/Pain -> Inpatient consult
• Failed conservative management and stone did not pass spontaneously -> Inpatient or Outpatient consult depending on severity
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Role of Tamsulosin (Flomax)
• Double-blind, placebo-controlled study • N= 3296 patients with distal ureteral stones, 30 centers• Evaluate the efficacy and safety of tamsulosin• Randomly assigned (1:1) into tamsulosin (0.4 mg) or placebo groups for 4 wk• Tamsulosin treated pts had higher stone expulsion (CT confirmed over 28-day period)
rate than placebo (86% vs 79%; p < 0.001) for distal ureteral stones. • Secondary end points: tamsulosin-treated patients shorter time to expulsion
(p < 0.001), required lower use of analgesics vs. placebo (p < 0.001), and significantly relieved renal colic (p < 0.001).
• Subgroup analysis: tamsulosin better for the treatment of large distal ureteral stones (>5 mm).
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Summary
• #1 CKD-Anemia
– 62-year-old woman with CKD and anemia
• #2 CKD-Hyperkalemia
– A 44-year old patient with CKD who has a K of 7.2
mEq/L
• #3 Kidney Stones
– 37-year-old man presents with 2 hours of excruciating
pain in left groin
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References
• N Engl J Med 2000; 342:1581-1589
• Blumberg et al KI, 41: 369-374, 1992
• N Engl J Med 2015; 372:222-231
• MED ARH 2011; 65(4): 213-215
• Am Fam Physician. 2011 Dec 1;84(11):1234-1242.
• Ann Intern Med. 2003;139:137-147
• Nat Rev Dis Primers. 2016 Feb 25, 25;2:16008