hyperkalemia in CKD

1. MANAGEMENT OF HYPERKALEMIA IN
CKD
Dr.SatchiA.Surendran
Post Graduate
General Medicine
13/02/2017

2. Hyperkalemia-Numbers of
Interest
 Potassium >5.5mEq/L
 10% of Hospitalised patients
 1% with severe hyperkalemia – High
Mortality
In CKD/ESRD patients*
 40-50% prevalence
 1.9 – 5% of deaths in ESRD
*Arch Intern Med. 2009;169(12):1156-1162

4. Mortality Risk
The study concludes,
The risk of hyperkalemia increases with CKD.
Further more, the Odds Ratio for Mortality at 1
day of the event is also higher with
hyperkalemic events in CKD.
Hence, this signifies the importance of
Hyperkalemia as a concern to patient safety in
CKD.

5. Causes
 Pseudohyperkalemia
 Increased Intra to extra cellular shift
 Decreased Excretion

6. Pseudohyperkalemia – to be
ruled out

7. Cellular Shift

8. Inadequate Excretion
 Inhibition of RAAS
ACE Inhb/ARBs/ENaC Inhb/Aldo Inhb.
 Hyoreninemic Hypoaldosteronism
Diabetic Nephropathy,Tubulo Interstitial
Diseases
 Primary Adrenal Insufficiency
Autoimmune, Drugs (Heparin), Infections,
Infiltrative,Congenital

10. Advanced Renal Disease
 Preservation of normokalemia results from
Upto 15ml/min GFR:
An adaptive increase in K+ excretion by remnant
nephrons
Below 15 ml/min GFR:
Increased colonic excretion.
Three times more colonic excretion of K+ is
documented in CKD patientsVs Normal
Individuals

11. Role of Diet in CKD
An impaired GFR combined with a frequently
high dietary K+ intake relative to residual
renal function
If potassium intake is normal, CKD does not
produce significant hyperkalemia until the GFR
is
 < 5 ml/min*
Electrolyte & Blood Pressure 2005; 3:71-78.

12. CKD Sub Groups with High
Risk of Hyperkalemia
 DM
 KidneyTransplant Recipients
 On RAAS InhibitorTherapy *
 Metabolic Acidosis
 Anemia requiring Blood transfusion
 Acute kindney Injury
 CardioVascular Co-morbidity *
*Drug Induced Hyperkalemia

13. Drug induced Hyperkalemia
In an observational retrospective study of
nondialyzed patients with serum potassium
of 6.5 mmol/L or greater on admission or
during hospital stay, more than 60% were
taking at least one drug known to cause or
worsen hyperkalemia.

14. CKD + ACE Inhibitors –
Patient Profile at risk
 Advanced Age > 80Years
 Diabetes
 Heartfailure
 Increased starting dose of ACE I (>10mg//day)
 Concomitant use of K+ Supplements
 Current use of ARBs/Potassium Sparing
Diuretics
 Higher Base line Potassium – Higher the risk

15. Management Principles
 Clinical management for hyperkalemia in
patients with CKD requires
 Exclusion of pseudohyperkalemia
 Assessment of the urgency for treatment, and
 Appropriate acute and chronic therapy

16. PseudoHyperkalemia
 Important to avoid unnecessary treatment
The most common cause of
pseudohyperkalemia is hemolysis, which is
usually
 Easily noted due to a pink tinge to the plasma
resulting from release of hemoglobin from
damaged red blood cells
 Alternatively, an excessively tight tourniquet
surrounding an exercising extremity (e.g., opening
and closing a hand) can increase plasma K+ by > 2
mEq/L)
 Excessive numbers of either leukocytes > 70,000/cm3, or platelets
> 1,000,000/cm3 also can lead to pseudohyperkalemia

17. Pseudohyperkalemia
 When the serum K+ is >0.3 mEq/L as compared with a
simultaneous plasma K+ ,
 Pseudohyperkalemia should be diagnosed
 Plasma K+ can be measured by obtaining a heparinized blood
specimen
 If pseudohyperkalemia exists,
 All further K+ levels should be measured using plasma

18. ECG Manifestations of True
Hyperkalemia
 ECGs
 Considered to be sensitive indicators of the
presence of hyperkalemia
 ECG abnormalities consistent with hyperkalemia in
the hospitalized hyperkalemia patients were
observed in only 14% of episodes
 Serum K+ levels > 8 mEq/L are almost invariably
associated with ECG abnormalities

19. ECG Correlation

20. Clinical Manifestations
 Minor ECG abnormalities (tall-peakedT waves)
may be the first indication of hyperkalemia but
 By the time serious changes occur, the patient
usually complains of muscle weakness,
paresthesia, and lethargy
 Severe hyperkalemia
 Can cause bilateral flaccid paralysis of
extremities, and weakness of respiratory
muscles
 However unlike hypokalemia, complete paralysis is
uncommon.

21. Acute Vs Chronic
Hyperkalemia
ACUTE CHRONIC
Singular Event; Requires no Ongoing
Management
>1 event /year; requires ongoing
management
Caused by abnormal net release of K+
from cells (metabolic
acidosis/trauma/hemolytic states)
Caused by impairment of K+ excretory
process

22. Acute Management
 Acute reduction of serum K+ is required
at levels exceeding 7.0 mEq/L, because
of the risk of cardiac arrest
 For acute therapy of hyperkalemia in an
urgent situation, regardless of the
underlying cause, following treatments
have been recommended

23. Calcium Gluconate IV
 Emergency treatment should be started
by the administration of calcium (10-30
mL of 10% calcium gluconate over 10
min intravenously)
 Intravenous infusion of calcium is the
most rapid and effective way to
antagonize the myocardial toxic effects
of hyperkalemia

24. Dextrose Insulin Infusion
 Furthermore, intravenous glucose (50
mL dextrose 50 %, preferably by central
venous infusion) should be given
followed by or combined with 10 units of
short-acting regular insulin, because
 Combined administration of glucose and
insulin results in a greater decline in serum
K+ levels
 Intravenous insulin rapidly stimulates
uptake of K+ into cells, primarily the
muscle and liver

25. Beta Agonists
 β2-adrenergic agonists,
 which also induce cellular K+ uptake,
are useful for the acute therapy of
hyperkalemia
 A direct comparison between
 Intravenous (0.5 mg) and nebulized (10
mg) albuterol (salbutamol) in ESRD
patients revealed a similar potassium-
lowering

26. Beta Agonists
 However, 20-40% of ESRD patients are
refractory to the K+ -lowering effect of
albuterol and
 Not possible to predict non-responders
 Combined use of
 β2-adrenergic agonists with glucose
and insulin
 will maximize the reduction in serum K+

27. Dialysis for Refractory/
Severe Hyperkalemia
 Hemodialysis is the most rapid method
of K+ removal
 Removal rates of K+ can approximate 35
mEq/hr with a dialysate bath potassium
concentration of 1-2 mEq/L
 A glucose free dialysate is preferable to
minimize a glucose-induced shift of K+ into
cell, lessening the removal of K+

28. Dialysis
 Peritoneal dialysis and chronic
hemodiafiltration are effective in chronic
hyperkalemia, but
 Do not remove K+ fast enough to be recommended
for use in acute, severe hyperkalemia
 Although dialysis is the most rapid method
available to treat most cases of hyperkalemia,
 other modes of treatment should not be delayed
while waiting to institute dialysis

29. Chronic Hyperkalemia
 To find modifiable causes of hyperkalemia in
CKD patients
 Common modifiable causes are
 Concomitant medications and
 Excessive dietary intake
 A careful history on the dietary habit and the
medication is necessary

30. Treatment Strategies
(1)to avoid or replace drugs that cause
hyperkalemia;
(2) to prescribe a low-potassium diet and
avoid constipation, and
(3) to enhance potassium excretion by
residual functioning nephrons or to
remove it more efficiently by dialysis
and/or by the gastrointestinal tract

31. Diuretic Therapy
 Chronic treatment of hyperkalemia in CKD
 Promoting diuresis with a loop diuretic can control chronic, mild
hyperkalemia

32. Diuretic Therapy
 Thiazide and loop diuretics increase the delivery
of sodium to the distal tubule, thereby increasing
urinary potassium excretion
 This may be useful in CKD, especially in
patients treated with an ACE inhibitor or ARB
 Thiazides effective in GFR >30ml/mt ;Loop
diuretics instituted for lower levels.

33. Cation Exchange Resins
 Either after acute hyperkalemia has been corrected
or in chronic management of less severe
hyperkalemia in CKD patients, the more slowly
acting
 Cation exchange resin may be given orally or rectally
(e.g. sodium/calcium polystyrene sulfonate 15-30 g,
with an equal amount of sorbitol to prevent fecal
impaction)
 Cation exchange resin may be given in order to
prevent a further increase in serum K+

34. Potassium binding resins in
hyperkalemia
 In hyperkalemic patients, oral SPS mixed in
water significantly decreases serum
potassium within 24 hours
CJASN ePress. Published on August 26, 2010

35. Potassium binding resins in
hyperkalemia
 SPS/sorbitol-associated colonic necrosis is
most commonly seen in patients
 who have received enemas in the setting of recent
abdominal surgery, bowel injury, or intestinal
dysfunction
 It is a rare event,
 on the order of 0.2 to 0.3%, almost exclusively
present in patients at risk
CJASN ePress. Published on August 26, 2010

36. Potassium binding resins in
hyperkalemia
 SPS ion-exchange resins are the only agents,
 other than dialysis and diuretics,
 Available to increase K+ excretion in
hyperkalemia, and
 when used appropriately,
 they appear to be
 Clinically effective and reasonably safe

37. Chronic Hyperkalemia Summary
 Either asymptomatic and mild hyperkalemia or
chronic hyperkalemia in CKD patients is common

38. Conclusions
 Hyperkalemia is common and life threatening
complication of CKD
 The effective and rapid diagnosis and management
of acute and chronic hyperkalemia is clinically
relevant and can be life-saving

39. Conclusions
 In treatment of moderate to severe hyperkalemia,
the combination of medications with different
therapeutic approaches is usually effective, and
often methods of blood purification can be avoided.
 In patients with severe hyperkalemia and major ECG
abnormalities, conservative efforts should be
initiated immediately to stabilize the patient, but
management should include rapid facilitation of
renal replacement treatment

40. THANKYOU