1 Management of Hyperkalemia in Ckd Patients

7/30/2019 1 Management of Hyperkalemia in Ckd Patients

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Management ofHyperkalemia in CKD

patientsDr


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Overview

Introduction

Hyperkalemia in CKD

Incidence

Significance

Causes

Management Summary and conclusions


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Introduction

CKD

Common disease

Affecting a growing number of populationacross globe

May be associated with a variety of

electrolyte disturbances

Such as hyperkalemia

Arch Intern Med. 2009;169(12):1156-1162


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Introduction

CKD - Hyperkalemia

Great concern to nephrologists

because of Possible implications for patient safety

related to the potential for associated

adverse cardiac outcomes

Arch Intern Med. 2009;169(12):1156-1162


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Hyperkalemia in CKD

Hyperkalemia is usually defined as

Plasma potassium (K+ ) > 5.0 mEq/L,

even though exact cut-off is arbitrary The incidence of hyperkalemia in

hospitalized patients varies from

1.4% to 10% depending on the arbitrary

level of potassium

Electrolyte & Blood Pressure 2005; 3:71-78.


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Hyperkalemia in CKD

Hyperkalemia

Prevalence in ESRD

5% to 10% Contributes to 1.9% to 5% of deaths

among patients with ESRD

Electrolyte & Blood Pressure 2005; 3:71-78.ESRD: End stage renal disease


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Hyperkalemia in CKD: Incidence

Arch Intern Med. 2009;169(12):1156-1162


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Hyperkalemia in CKD: Significance

CKD - Hyperkalemia

One study determined the incidence of hyperkalemiain CKD and whether it is associated with excessmortality

Results:

Of the 66 259 hyperkalemic events (3.2% of records),more occurred as inpatient events (n=34 937 [52.7%])than as outpatient events (n=31 322 [47.3%]).

The adjusted rate of hyperkalemia was higher inpatients with CKD than in those without CKD amongindividuals treated with RAAS blockers (7.67 vs 2.30per 100 patient-months; P.001) and those withoutRAAS blocker treatment (8.22 vs 1.77 per 100 patientmonths; P.001).

Arch Intern Med. 2009;169(12):1156-1162


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CKD Hyperkalemia Study results continued

The adjusted odds ratio (OR) of death with a

moderate (K+

, 5.5 and 6.0 mEq/L [to convertto mmol/L, multiply by 1.0]) and severe (K+ ,6.0 mEq/L) hyperkalemic event was highestwith no CKD (OR, 10.32 and 31.64,respectively) vs stage 3 (OR, 5.35 and19.52, respectively), stage 4 (OR, 5.73 and

11.56, respectively), or stage 5 (OR, 2.31and 8.02, respectively) CKD, with all P.001vs normokalemia and no CKD.

Arch Intern Med. 2009;169(12):1156-1162


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CKD Hyperkalemia

Study Conclusions

The risk of hyperkalemia is increased withCKD, and its occurrence increases the

odds of mortality within 1 day of the event

These findings underscore the

importance of this metabolic disturbanceas a threat to patient safety in CKD

Arch Intern Med. 2009;169(12):1156-1162


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Hyperkalemia in CKD: Causes

CKD hyperkalemia:

Causes

An impaired GFR combined with afrequently high dietary K+ intake relative

to residual renal function

Arch Intern Med. 2009;169(12):1156-1162


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Pediatr NephrolPublished online 22 December 2010


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If potassium intake is normal, CKD

does not produce significant hyper-

kalemia until the GFR is < 5 ml/min



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CKD hyperkalemia:

Causes Commonly observed extracellular shift of

K+ caused by the metabolic acidosis ofrenal failure

Under almost all conditions,

Hyperkalemia not due to redistributionof potassium is related to impairedrenal potassium excretion

Arch Intern Med. 2009;169(12):1156-1162


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CKD hyperkalemia:

Causes

Most importantly, recommendedtreatment with renin angiotensin-

aldosterone system (RAAS) blockers that

inhibit renal K+ excretion

Arch Intern Med. 2009;169(12):1156-1162


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Am J Kidney Dis 2010;56:387-393.


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Hyperkalemia in CKD

Preservation of normokalemia results from

An adaptive increase in K+ excretion by

remnant nephrons and increased bowel loss

However, hyperkalemia may be an early

feature of renal failure in patients with

(hyperchloremic) metabolic acidosis and

hyporeninemic hypoaldosteronism, which

occur particularly in patients with

Tubulointerstitial disease and diabetes mellitus



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Hyperkalemia in CKD

Clinical management for hyperkalemia

in patients with CKD requires

Exclusion of pseudohyperkalemia,Assessmemt of the urgency for

treatment, and

Appropriate acute and chronic therapy



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Hyperkalemia in CKD

Pseudohyperkalemia Important to avoid unnecessary treatment

The most common cause of pseudohyperkalemiais hemolysis, which is usually

Easily noted due to a pink tinge to the plasmaresulting from release of hemoglobin fromdamaged red blood cells

Alternatively, an excessively tight tourniquetsurrounding an exercising extremity (e.g., openingand closing a hand) can increase plasma K+ by > 2mEq/L)

Excessive numbers of either leukocytes >70,000/cm3, or platelets > 1,000,000/cm3 also canlead to pseudohyperkalemia



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Hyperkalemia in CKD

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 usingplasma



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Hyperkalemia in CKD

Clinical manifestations of hyperkalemia

May be asymptomatic or life-threatening

The main danger of hyperkalemia is a

Cardiac arrhythmia

ECGs

Considered to be sensitive indicators of the presence ofhyperkalemia

ECG abnormalities consistent with hyperkalemia in thehospitalized hyperkalemia patients were observed in

only 14% of episodes Serum K+ levels > 8 mEq/L are almost invariably

associated with ECG abnormalities

However, minimal or atypical ECG changes have beenobserved in some cases of severe hyperkalemia



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Hyperkalemia in CKD

Clinical manifestations of hyperkalemia

Minor ECG abnormalities (tall-peaked T waves) maybe the first indication of hyperkalaemia but

By the time serious changes occur, the patient usuallycomplains of muscle weakness, paresthesia, andlethargy

Severe hyperkalemia

Can cause bilateral flaccid paralysis of extremities,and weakness of repiratory muscles

However unlike hypokalemia, complete paralysis isuncommon.



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Hyperkalemia in CKD: Treatment

Acute / emergency treatment of

hyperkalemia

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 beenrecommended



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hyperkalemia

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 themyocardial toxic effects of hyperkalemia



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Acute / emergency treatment ofhyperkalemia

Furthermore, intravenous glucose (50 mL

dextrose 50 %, preferably by central venousinfusion) should be given followed by orcombined with 10 units of short-actingregular 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



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hyperkalemia

2-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 revealeda similar potassium-lowering



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Acute / emergency treatment ofhyperkalemia

However, 20-40% of ESRD patientsare refractory to the K+ -loweringeffect of albuterol and Not possible to predict non-responders

Combined use of 2-adrenergic agonists with glucose andinsulin

will maximize the reduction in serum K+



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hyperkalemia

When especially used alone, bicarbonate is

probably less effective than either 2-agonistor insulin in the acute treatment of

hyperkalemia

Recent studies show conflicting evidences

whether bicarbonate can act in a synergisticfashion with either insulin or 2 -adrenergic

agonists



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Acute / emergency treatment ofhyperkalemia Dialysis should be considered the primary

method of K+ removal when hyperkalemia ispersistent or severe

Hemodialysis is the most rapid method of K+removal

Removal rates of K+ can approximate 35 mEq/hrwith 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, lesseningthe removal of K+



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Acute / emergency treatment of hyperkalemia

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



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Chronic treatment of hyperkalemia in CKD

Important to determine underlying causes for

hyperkalemia.

One should find modifiable causes of hyperkalemiain CKD patients

Common modifiable causes are

Concomitant medications and

Excessive dietary intake A careful history on the dietary habit and the

medication is necessary



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3 general categories

(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 removeit more efficiently by dialysis and/or by thegastrointestinal tract



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Follow-up should be in 2 weeks if serum K+ >5.1mEq/L for outpatients management of CKD

If mild hyperkalemia develops after medications,

Reduce the dose of medications that interfere K+balance by 50% and

Reassess the serum K+ every 5 to 7 days until serumK+ has returned to baseline

If serum K+ does not return to baseline within 2 to 4

weeks, Discontinue that medications and select an alternate

medication



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Target potassium intake of a low potassium

diet is


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Beside excess potassium dietary intake andconstipation, it is also important to look for

prolonged fasting Overnight fasting in preparation for surgery

in dialysis patients may inducehyperkalemia due to a fall in theconcentration of insulin

This can be avoided by continuous infusionof 10% glucose at 50 mL/h mixed with orwithout regular insulin



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Chronic treatment of hyperkalemia in

CKD Promoting diuresis with a loop diuretic can

control chronic, mild hyperkalemia



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Thiazide and loop diuretics increase thedelivery of sodium to the distal tubule,

thereby increasing urinary potassiumexcretion

This may be a useful side-effect in CKD,especially in patients treated with an ACEinhibitor or ARB

However, most of thiazides are effective inkaliuresis in patients with GFR > approx. 30mL/min/1.73 m2



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Chronic treatment of hyperkalemia in

CKD

An active component of licorice, Glycyrrhetinic acid might be considered

as one of the therapeutic agents for

chronically hyperkalemic patients on

maintenance hemodialysis



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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+



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Potassium binding resins in

hyperkalemia

Hot topic in Nephrology

Recent editorial

Damned If You Do, Damned If YouDont: Potassium Binding Resins in

Hyperkalemia

CJASN ePress. Published on August 26, 2010


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hyperkalemia

SPS resins increase stool potassium

excretion in normokalemic subjects,

but proportionately more potassiumexcreted due to cathartics when the

two are combined

In hyperkalemic patients, oral SPS

mixed in water significantly decreasesserum potassium within 24 hours



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hyperkalemia

SPS/sorbitol-associated colonicnecrosis is most commonly seen inpatients

who have received enemas in thesetting 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



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hyperkalemia

Authors concluded

SPS ion-exchange resins are theonly agents, other than dialysis and diuretics,

Available to increase K+excretionin hyperkalemia, and when used appropriately,

they appear to be Clinically effective and reasonably safe



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Summary: Drugs for hyperkalemia



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Either asymptomatic and mild hyperkalemia

or chronic hyperkalemia in CKD patients is

common



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Conclusions

Hyperkalemia is common and lifethreatening complication of CKD

The effective and rapid diagnosis andmanagement of acute and chronichyperkalemia is clinically relevant and canbe life-saving

In treatment of moderate to severehyperkalemia, the combination of

medications with different therapeuticapproaches is usually effective, and oftenmethods of blood purification can beavoided.


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Conclusions

In patients with severe hyperkalemia and

major ECG abnormalities, conservative

efforts should be initiated immediately to

stabilize the patient, but managementshould include rapid facilitation of renal

replacement treatment


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1 Management of Hyperkalemia in Ckd Patients

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