Post on 31-Dec-2021
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
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
Disclosures
• ConsultingGSK
• Stock
Gilead
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
#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.
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
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
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)
ESA’s globally
Published Feb 2021 SOURCE: https://www.datamintelligence.com/research-report/erythropoietin-stimulating-agents-market
#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….
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
Pre-terminal rhythm with very high K
SOURCE: https://www.slideshare.net/ravirajmenon/hyperkalemia-56833946
K= 9.9 mEq/L
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”
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
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
?
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
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
Bicarb
Blumberg et al, Am J Med, 85, 1988
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
#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
Stones
• Calcium oxalate– 70-80%
• Uric Acid– 10-15%
• Magnesium ammonium phosphate (struvite infection related)– 10-15%
• Cystine– <1%
• Others – <1%
• 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
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.
What stones don’t show up on imaging
• 85% of stones are radio-opaque
– Ca containing
– Cystine
• 15% radiolucent
– Uric acid
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
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).
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
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