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Hyperkalaemia is a common biochemical finding that can allude to preanalytical or truly pathological causes. Here, we present a case of a 41-year-old female patient who has regularly presented with incidences of isolated hyperkalaemia since 2012, with otherwise normal renal function and no other associated symptoms. Investigations into the patient's family history revealed similar biochemical findings in her brother and eldest son. Familial causes of hyperkalaemia were investigated and an eventual diagnosis of pseudo-hypoaldosteronism type 2C was established. This is a rare congenital renal tubular disorder - also known as Gordon syndrome - that can cause a characteristic triad of symptoms that include hyperkalaemia, metabolic acidosis and hypertension. The presence and severity of each of these symptoms is dependent upon the disease-causing mutation that occurs in WNK4, WNK1, CUL3 or KLHL3 genes. These mutations alter the regulation of sodium/chloride co-transporter (NCC) expression on the luminal membrane of the principal cells of the distal convoluted tubule, disrupting normal homeostatic regulation of electrolyte reabsorption and excretion. The resolution for treating this condition is the administration of a thiazide diuretic, which directly counteracts the effects of NCC co-transporter overexpression and consequently aims to resolve the symptoms that arise as a result of this aberrant signalling. The case described here uniquely presents an extremely rare pathogenic variant in the conserved acidic motif of WNK1 resulting in a clear electrolyte phenotype with no hypertension.

Background: The present study was aimed at determining the effect of the tube type used for primary sample collection and the manner of transport prior to assessment (either manual or by pneumatic tube) on the degree of pseudohyperkalaemia in leukaemic patients., Methods: Blood from six leukaemic patients was collected into seven primary sample tubes (Monovette®, Sarstedt): sample A, heparinized blood gas syringe (potassium reference value); sample B, plasma Li-heparin without separator gel; sample C, plasma Li-heparin with separator gel; and sample D, serum with separator gel. The primary sample tubes designated B, C and D were transported to the laboratory manually. Duplicates of the same sample tubes, B(PT), C(PT) and D(PT), were sent to the laboratory by pneumatic tube., Results: In patients with chronic lymphocytic leukaemia (CLL), there was no increase in the concentration of potassium in samples B, C and D when compared to the reference value. Transport of the samples by pneumatic tube led to a pronounced increase in potassium concentration in samples B(PT) and C(PT), whereas there was no increase in sample D(PT) when compared to the reference value. In the patient with chronic myeloid leukaemia (CML), an increase in potassium concentration occurred in sample D and in samples B(PT), C(PT) and D(PT). A similar finding was observed in the patient with acute lymphocytic leukaemia (ALL), furthermore with an extremely high concentration of potassium in samples C and C(PT)., Conclusions: Manual transport of non-coagulable blood (plasma Li-heparin without separator gel) to the laboratory results in the least possible artificial increase in potassium concentration in the sample.

Background: Spurious hyperkalaemia is a relatively common occurrence in samples originating from primary care. Failure to identify spurious hyperkalaemia carries a significant risk of patient mismanagement. We have carried out a retrospective evaluation to review the impact of the use of centrifuges in primary care for biochemistry blood samples on the management of hyperkalaemia., Methods: Serum potassium concentrations in samples received from primary care were reviewed for six months prior to and after the implementation of on-site centrifugation. Samples exhibiting significant hyperkalaemia (serum potassium >6.0 mmol/L) were further investigated to ascertain the degree of patient follow-up., Results: There was a significant decrease in the number of samples exhibiting marked hyperkalaemia following the implementation (2244 versus 524; P < 0.0001). In terms of patient follow-up, we observed a reduction in the number of patients exhibiting pseudohyperkalaemia that previously had led to inappropriate hospital admissions over the same time period (6 cases postimplementation versus 22 cases preimplementation). We also observed an increase in the number of patients exhibiting true hyperkalaemia during the six-month period postimplementation (33 cases postimplementation versus 6 cases preimplementation)., Conclusions: The centrifugation of serum samples in primary care improves the sample quality and the integrity of the potassium results reported. We have also demonstrated evidence of an improvement in patient management and quality of care.

We report a previously healthy man presenting with life-threatening hyperkalaemia and heart failure. The only possible cause was thought to be the long list of herbal medications he was taking, several of which contained significant amounts of cardiac glycosides. Hyperkalaemia is known to be associated with digoxin toxicity and we present this as the likely cause in this case, and emphasize the importance of a thorough drug history in forming a differential diagnosis.

We report a six-week-old boy with genitourinary structural abnormalities who presented with profound hyponatraemia and hyperkalaemia due to transient type 1 pseudohypoaldosteronism (PHA) precipitated by a urinary tract infection (UTI), which responded rapidly to intravenous saline and antibiotics. In infants with structural abnormalities of the urinary tract, we wish to highlight the importance of recognizing type 1 PHA and its association with a UTI since prompt and appropriate treatment rapidly corrects the associated metabolic abnormalities. Conversely, the identification of type 1 PHA in an infant should precipitate a search for a UTI and structural abnormalities of the urinary tract.

Background: To study the detection and prevalence of spurious hyperkalaemia due to potassium ethylenediaminetetra-acetic acid (kEDTA) contamination., Methods: In a one-month prospective study, serum EDTA, zinc, calcium, magnesium concentrations and alkaline phosphatase activity were measured in samples with serum potassium >or=6.0 mmol/L., Results: Twenty-eight out of 117 hyperkalaemic samples were contaminated with EDTA. Only serum zinc values below the reference range had 100% sensitivity for indicating EDTA contamination, but even at an optimal specificity of 89% at least 12 potentially genuine hyperkalaemic samples would be rejected., Conclusion: Spurious hyperkalaemia due to kEDTA contamination is common. Gross kEDTA contamination is obvious by marked unexpected hyperkalaemia, hypocalcaemia, hypomagnesaemia and hypozincaemia. Spurious hyperkalaemia due to low concentrations of kEDTA contamination can only be confidently detected by measurement of serum EDTA.

Background: Pre-analytical problems causing pseudohyperkalaemia have been highlighted previously. These include transit time and temperature effects when sample collection points are geographically widely spread. Similarly, inappropriate phlebotomy technique (in particular, requesting patients to fist clench to facilitate venesection) is a documented cause of pseudohyperkalaemia, but its incidence may be impossible to establish. This study illustrates how primary care population serum potassium data altered when local phlebotomy clinics optimized their technique., Methods: The effect of improving phlebotomy was studied by plotting average monthly primary care population serum potassium data and average percentage of samples with hyperkalaemia (5.2 mmol/L or higher) against mean monthly temperature before and after changes in phlebotomy practice. Only samples from primary care were included between 2002 and 2005 inclusive., Results: Primary care population serum potassium was inversely related to ambient temperature. Following the change in phlebotomy practice, the annual percentage of results above reference range (5.2 mmol/L or higher) was reduced from 9% to 6% and the number of results breaching the upper telephoning threshold (5.8 mmol/L or higher) fell from 0.9% to 0.5%., Conclusions: Ensuring that phlebotomists were trained to avoid facilitating venesection by requesting patients to hand grip (fist clench), was associated with lower mean serum potassium results for the primary care patient population and a reduced incidence of hyperkalaemia. It is likely that the contribution of patient fist clenching during phlebotomy to pseudohyperkalaemia has been underestimated.

The well recognized cardiac effects of severe hyperkalemia include progressive rhythm and conduction disturbances such as bradycardia, spiked and narrow T waves, widening QRS complex, widening and flattening P wave, disappearance of the P wave, and cardiac arrest. Paradoxically, a heart rate greater than 200 beats/min may coexist with hyperkalemia in some cats. This report describes three cats with moderate to severe hyperkalemia and concurrent rapid heart rate. In each cat, the serum potassium (K(+)) concentration was > or =7.5 mEq/dl with a concurrent heart rate > 200 beats/min. In each cat, nine-lead electrocardiograms demonstrate an absence of P waves and a wide-complex tachycardia. Hyperkalemia should be considered in the differential diagnosis when a feline electrocardiogram demonstrates a wide-complex tachycardia without identifiable P waves.

Background: Potassium is usually the most important analyte affected by in vitro haemolysis and the result obtained may falsely indicate or disguise a life-threatening abnormality and so give rise to inappropriate treatment. The purpose of the study was to provide a solution to the problem of reporting potassium on haemolysed samples, taking into account both clinical needs and analytical concerns (inter-individual and inter-sample variability)., Methods: Using a new procedure that mimics the collection process in an actual clinical setting, haemolysed samples were prepared from 41 volunteers with a range of inter-individual factors - haemoglobin 80-173 g/L, red blood cells 2.42-6.77 x 10(12)/L, leucocytes 3.0-306 x 10(9) /L and platelets 31-710 x 10(9)/L - in order to develop a more accurate correction equation using a haemolytic index (HI) corresponding to g Hb/L in plasma., Results: The mean (range) potassium increase was 0.0036 mmol/L (0.0029-0.0053 mmol/L) per unit HI. The following equation was developed to estimate potassium increase per HI, in order to compensate approximately for potassium leakage in haemolysed samples: Corrected K+ = Measured K+ -(HI x 0.004)., Conclusion: The balanced solution is this: instead of reporting the post-haemolysis corrected potassium result a qualitative comment is given, indicating the likely range of the potassium concentration. If the potassium result is in a critically low or high range, it is communicated promptly to the requesting clinician.