Het is echter wel schadelijk om overmatig te alcohol te drinken, zeker als u een infectie heeft. Dit komt de infectie eerder verergerd door het gebruik van alcohol antibiotica kopen Doorgaans worden ze voorgeschreven bij bacteriële infecties die om de één of andere reden niet uit zichzelf over gaan; ze doden dan de bacteriën.
Nd130979xj
Nephrol Dial Transplant (1997) 13: 2402–2406
Continuing Nephrological Education (CNE)Iatrogenic hyperkalaemia—points to consider in diagnosis and management
Kostas C. Siamopoulos, Moses Elisaf and Kostas Katopodis
Department of Internal Medicine, Division of Nephrology, University Hospital of Ioannina, Greece
Introduction
6.1 mmol/l ) and renal impairment (serum creatinine160 mmol/l, creatinine clearance 60 ml/min). Labor-atory investigation established the diagnosis of hypo-
Hyperkalaemia is a potentially life-threatening electro-
reninaemic hypoaldosteronism secondary to chronic
lyte abnormality. In normal subjects it is rare because
interstitial nephritis of unknown origin. A low-
the homeostatic mechanisms to maintain normokalae-
potassium diet plus small doses of frusemide were
mia are highly effective. In particular, the capacity of
introduced and the patient was discharged. A few days
renal potassium excretion is very high under normal
later he developed a urinary tract infection due to E
circumstances [1–4]. Consequently, hyperkalaemia is
coli and co-trimoxazole in conventional doses (1600 mg
practically always associated with impaired urinary
of sulphamethoxazole+320 mg of trimethoprim) was
potassium excretion [5], but in patients with acute or
administered. Five days later the patient was referred
chronic renal failure high potassium intake can
to our hospital with profound muscle weakness,
further contribute to the development of hyperkalae-
nausea, and constipation. Laboratory investigation on
the patient’s admission showed severe hyperkalaemia
We describe three cases of iatrogenic hyperkalaemia
(serum potassium 7.8 mmol/l ) with ECG changes
secondary to drug therapy. The cases illustrate the
(peaked narrow T waves and a shortened QT interval ).
wide spectrum of causes and preconditioning circum-
Hyperkalaemia was accompanied by low potas-
stances. Based on these cases we discuss the appropriate
sium excretion (urine potassium 19 mmol/l, FEK+ 9%,
clinical management of this problem.
TTKG 2.4). Additionally, a normal anion gap hyper-chloraemic metabolic acidosis with an arterial pH of
Case report 1
7.29, a pCO2 of 32 mmHg, a serum chloride level of
112 mmol/l, a serum bicarbonate of 15 mmol/l, a urine
A 71-year-old man was admitted to our hospital
anion gap of 23 mmol/l, and a urine pH of 5.1 was
for evaluation of hyperkalaemia (serum potassium
found. There was also evidence of a low urea excretion( FE
7.2%) in the face of the serum urea levels
Table 1. Causes of hyperkalaemia
(6.6 mmol/l ). Co-trimoxazole was discontinued andhyperkalaemia was appropriately treated. Serum
1. Increased (oral/intravenous) potassium intake
potassium levels were then stabilized at 5.5–6 mmol/l.
2. Increased potassium release from cellsCase report 2
Insulin deficiency, hyperglycaemia and hyperosmolalityb-Adrenergic blockers
A 73-year-old woman with a history of hypertension,
Increased tissue catabolismSevere exercise
non-insulin-dependent diabetes mellitus and hyperlipi-
daemia was admitted because of malaise, diffuse muscle
Drugs: digitalis overdose, succinylcholine, arginine
pain and marked weakness. She had been given quinap-
3. Reduced urinary potassium excretion
ril, amlodipine, gliclazide, and long-acting bezafibrate.
On physical examination all muscle groups were
extremely tender and she could not raise her limbs.
Selective impairment of potassium excretionHypoaldosteronism
Laboratory investigation on patient’s admission wereas follows: haematocrit 34%, white blood cell count8000/ml, platelet count 200 000/ml, serum glucose
Correspondence and offprint requests to: Kostas C. Siamopoulos MSc
19.9 mmol/l, creatinine 186 mmol/l, urea 42.5 mmol/l,
MD FRSH, Professor of Medicine/Nephrology, Division of
potassium 6.5 mmol/l, uric acid 512 mmol/l, sodium
Nephrology, University Hospital of Ioannina, GR 455 50Ioannina, Greece.
140 mmol/l, chloride 100 mmol/l, SGOT 860 IU
1998 European Renal Association–European Dialysis and Transplant Association
Iatrogenic hyperkalaemia—points to consider in diagnosis and management
(normal values 5–40 IU/l ), SGPT 335 IU/l (normal
increasing in recent years. In practically all patients
values 5–40 IU/l ), CK 22 000 IU/l (normal values
with sustained elevation of serum potassium concentra-
40–190 IU/l ), LDH 4280 IU (normal values 225–450
tion predisposing conditions can be found, which inter-
IU/l ), and aldolase 730 IU (normal values 0–8 IU/l ).
fere with potassium homeostasis and especially with
pCO2 renal potassium excretion. Examples include renal
34.5 mmHg, and bicarbonate 16 mmol/l. The serum
insufficiency (even of mild degree) or hypoaldosteron-
anion gap was 24 mmol/l. The patient’s urine was
ism ( Table 2) and this is also illustrated by our patients
brown, cloudy, and strongly positive for blood. The
[6–8]. It is of interest that typically the patients were
urinalysis contained scarce granular casts, 14–20 white
elderly: In elderly subjects age-specific changes of renal
cells and 15–20 red cells per high-power field. Fibrate
function increase the risk of hyperkalaemia, particu-
was discontinued, hyperkalaemia was properly treated,
larly when other potassium-regulatory systems have
and vigorous intravenous fluid therapy to correct the
hypovolaemia was administered. Treatment was fol-
The first case illustrates that conventional doses of
lowed by a progressive decrease in serum creatinine,
trimethoprim may cause hyperkalaemia when addi-
potassium and muscle enzymes towards normal
tional predisposing conditions are present, i.e. in this
values. On the patient’s discharge 10 days later,
case advanced age with hyporeninaemic hypoaldos-
muscle enzymes were normal, serum potassium was
teronism [13–16 ]. Trimethoprim inhibits amiloride-
4.5 mmol/l, serum creatinine 132 mmol/l, and creatinine
sensitive sodium channels in the distal nephron and
dose-dependently reduces the transepithelial voltagewhich facilitates potassium secretion [17,18]. It hasbeen reported that even low doses of trimethoprim can
Case report 3
significantly decrease net transepithelial sodium trans-port and thus lower potassium excretion [18]. In so-
A 74-year-old patient was referred to our hospital with
called renal tubular acidosis type IV, associated with
acute weakness, fatigue, flatulence and vomiting. He
hyporeninaemic hypoaldosteronism and hyperkalae-
was hypertensive and was receiving quinapril 20 mg
mia, tubular pH is typically low. This increases the
once daily and a combination of frusemide plus amilor-
concentration of the charged protonated species of
ide (40 mg+5 mg) once daily. A mild impairment in
trimethoprim, which blocks epithelial sodium channels
renal function had been diagnosed (serum creatinine
most effectively. Thus, the antikaliuretic effect of trime-
160 mmol/l ) 3 years before, as well as osteoporosis for
thoprim is further increased [19]. Finally, nausea, as
which he was administered vitamin D and calcium.
in our patient, reduces protein intake; low urea excre-
revealed urea 71.4 mmol/l, creatinine 336 mmol/l,
to a low flow rate and delivery of tubular fluid to the
glucose 9.2 mmol/l, sodium 130 mmol/l, potassium
cortical collecting duct. This may have further contrib-
uted to a lower rate of potassium excretion in our
patient and may have further exacerbated the impact
of trimethoprim-mediated blockage of sodium channels
12 mmol/l, arterial pH 7.30, and pCO
Creatinine clearance was 20 ml/min. Urinalysis showed
Table 2. Causes of hypoaldosteronism
that the urine sediment contained 18–20 red cells and5–6 white cells per high-power field. Urine pH was
Associated with decreased activity of the renin–angiotensin system
5.5. There were ECG changes suggestive of hyperkalae-
mia (peaked narrow T waves and a shortened QT
Hyporeninaemic hypoaldosteronism (diabetes mellitus most
interval ). Both kidneys were of small size with
Non-steroidal anti-inflammatory drugs (with possible exception
increased echogenicity by ultrasonic examination.
haemodialysis sessions were carried out and the
hyperkalaemia was corrected. A progressive clinical
and laboratory improvement was achieved and he
was discharged 5 days later when laboratory evalua-
(a) low cortisol levels: primary adrenal insufficiency, congenital
tion revealed urea 24 mmol/l, creatinine 168 mmol/l,
potassium 4.8 mmol/l, sodium 146 mmol/l, calcium
(b) normal cortisol levels: heparin, post-removal of
2.37 mmol/l, and arterial pH 7.35. A calcium-channel
blocker was then given for blood pressure control.
hypoaldosteronism (in cases of severe illness)
Aldosterone resistance with normal or increasedDiscussion
Potassium-sparing diureticsTrimethoprimCyclosporin
These cases illustrate the wide spectrum of causes and
Pseudohypoaldosteronism (hereditary or acquired resistance to
clinical manifestations of drug-induced hyperkalaemia.
The incidence of this electrolyte abnormality has been
Table 3. Drug-induced rhabdomyolysis
angiotensin II in the circulation and perhaps also inthe adrenal zona glomerulosa [33], and decrease both
angiotensin II and potassium-mediated aldosterone
release [33,34]. In patients with normal renal function,
serum potassium rarely increases by more than
0.5 mmol/l [35]. In patients with diminished renal
function, as in our patient, the rise in potassium
concentration may be more marked, since the incre-
ment is inversely related to GFR [26 ], particularly
in patients with hyporeninaemic hypoaldosteronism
(e.g. in diabetic nephropathy), in patients on beta-
adrenergic blockers or in patients with potassium-
sparing diuretics, as in our case [6,26,27,36–38]. The
combination of potassium-sparing diuretics and ACE
inhibitors should be avoided and the effects of potas-
sium supplements on serum potassium concentrations
must be closely monitored in elderly patients on ACE
Table 4 summarizes the great number of drugs with
reports on drug-induced hyperkalaemia.
on potassium excretion [20]. As to the management of
kalaemia following a potassium load, severe exercise,
such patients, it should be mentioned, that the antikali-
or in the presence of hypoaldosteronism or renal failure
uretic effects of trimethoprim are minimized by raising
[39–42]. They alter transcellular partitioning of potas-
urine pH [19], as well as by manoeuvres that increase
sium and reduce the activity of the renin–aldosterone
distal delivery of sodium, e.g. administration of
system [5,39]. Central adrenergic inhibitors, e.g. cloni-
dine, or beta-1-selective blockers, e.g. atenolol, inter-
Drug-induced hyperkalaemia can also be caused by
fere less with potassium homeostasis [43–45]. Non-
drug-induced rhabdomyolysis, as illustrated by the
steroidal anti-inflammatory drugs lower plasma renin.
second patient. Table 3 summarizes that, especially in
As a consequence, plasma potassium concentration
the elderly patient [22,23], a number of drugs, alone
rises moderately, by approximately 0.2 mmol/l in sub-
or in combination, can cause muscle damage, deteriora-
jects with normal renal function, but may rise by more
tion of renal function, and hyperkalaemia. Under
than 1 mmol/l when renal function is impaired or when
normal circumstances, the renal tubular cell will
potassium homeostasis is strained, e.g. administration
respond to an increase in serum potassium concentra-
of potassium-sparing diuretics or non-cardioselective
tion by augmenting potassium secretion. If tissue
beta blockers [46–48]. Prolonged heparin administra-
destruction is intense, the ability of the kidney to
tion may cause hyperkalaemia via inhibition of adrenal
excrete the potassium may be overwhelmed, so that
18-hydroxylase [49–53]; the risk of hyperkalaemia is
hyperkalaemia ensues [24,25]. The risk is further
exacerbated by administration of ACE inhibitors or
aggravated, if rhabdomyolysis-induced renal failure
presence of long-standing diabetes mellitus [49,52–55].
occurs. In this circumstance, hyperkalaemia may
An interesting condition, recently reported, is selective
became life threatening. In our case, administration ofACE inhibitors and the resulting relative hypoaldos-
Table 4. Mechanisms of drug-induced hyperkalaemia
teronism, may have also interfered with potassiumexcretion [26,27], illustrating that not infrequently
1. Increased potassium release from cells
several predisposing factors can be found in such
complex situations. Hypolipidaemic drugs, e.g. fibrates
and statins, may cause myolysis [28–30], specifically
Insulin antagonists (somatostatin, diazoxide)Arginine hydrochloride
when long-acting bezafibrate preparations are adminis-
tered to elderly patients with reduced renal function
without appropriate modification of the dose of the
2. Decreased activity of the renin–angiotensin axis
drug [24,29,31,32]. Our case illustrates the necessity,
particularly in the elderly patient, of adjusting the dose
b-Adrenergic blockersNon-steroidal anti-inflammatory drugs
to the renal function and to monitor CK levels as the
first sign of impending muscle damage [24].
3. Inhibition of potassium secretion
The third case illustrates that simultaneous adminis-
tration of drugs with known hyperkalaemic potential
may cause a dangerous increase in serum potassium
concentration, again particularly in elderly patients
with even minor reduction in renal function [6–8].
ACE inhibitors reduce conversion of angiotensin I to
Iatrogenic hyperkalaemia—points to consider in diagnosis and management
hypoaldosteronism in critically hypoxic patients which
aldosteronism. Kidney Int 1980; 17: 118–134
predisposes to heparin-induced hyperkalaemia [12,56 ].
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17. Choi MJ, Fernandez PC, Patnaik A et al. Trimethoprim-induced
emia has been reported after prolonged use of pentami-
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dine to treat HIV-associated Pneumocystis carinii. Like
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