Profound Hypokalemia Research Articles

Hypokalemia-Induced Rhabdomyolysis by Primary Aldosteronism Coexistent With Sporadic Inclusion Body Myositis.

We describes a patient with hypokalemia-induced rhabdomyolysis due to primary aldosteronism (PA), who suffered from slowly progressive muscle weakness after laparoscopic adrenalectomy, and was later diagnosed with coexisting sporadic inclusion body myositis (sIBM). A 54-year-old Asian male presented with severe muscle weakness of both lower extremities. Laboratory findings showed profound hypokalemia, and extreme elevation of the serum creatine phosphokinase levels, suggestive of hypokalemia-induced rhabdomyolysis. Further evaluation strongly suggested PA by an aldosterone-producing adenoma, which was successfully removed surgically. However, muscle weakness slowly progressed one year after the operation and a muscle biopsy demonstrated findings consistent with sIBM. This case is the first report of hypokalemia-induced rhabdomyolysis by PA coexistent with sIBM, to the best of our knowledge.

Large negative U waves associated with hypokalemia

Negative U waves in the electrocardiogram are highly specific indicators of hypertensive, valvular or ischemic heart disease. Hypokalemia, on the other hand, is usually associated with large positive U waves. In this report we present a case where a routine preoperative electrocardiogram showed large negative U waves in the chest leads. Thorough cardiac evaluation ruled out any of the listed structural or functional abnormalities. At the time of the recording, the patient had profound hypokalemia. After normalization of the serum potassium, the large negative U waves resolved. To our knowledge, this is the first reported case of negative U waves in hypokalemia. We offer a possible explanation for this unusual finding.

Nephrocalcinosis in primary Sjogren's syndrome

A 29-year-old woman presented with a known nephrocalcinosis that had developed nine years earlier. Her past medical history was remarkable for a cardiac arrest secondary to a profound hypokalaemia (1.7 mEq/L) in the post-operative period following a complicated appendicular peritonitis at 19 years of age. Her on-going treatment included potassium citrate supplementation and increased fluid intake to induce hyperdiuresis. There was no relevant family history. On admission, pertinent laboratory data were as follows: hypokalaemia (3.4 mEq/L), normal anion gap hyperchloraemic metabolic acidosis (plasma 21 mEq/L), inappropriately high urine pH (7.0), positive urinary anion gap (þ21 mEq/L), tubular proteinuria 0.5 g per 24 h and chronic kidney disease (serum creatinine, 1.4 mg/dL. CKD Epi MDRD creatinine clearance, 72 mL/min). A urine pH of >5.3 in the presence of metabolic acidosis suggests distal renal tubular acidosis. On bicarbonate loading, was <5%, with a low (urinary–blood) DpCO2 (13 mmHg), suggesting defective H+ secretion by alpha-intercalated cells. A CT scan imaging (Figure 1A) and plain X-ray of the abdomen (Figure 1B) showed macroscopic bilateral nephrocalcinosis. Biochemical analysis of the kidney stone revealed a calcium phosphate stone type suggestive of distal renal tubular acidosis (dRTA). She had polyclonal hypergammaglobulinaemia and positive antinuclear antibodies (1/1600) of anti-Ro/SS-A type. Accessory salivary gland biopsy showed Grade 2 inflammatory infiltrates on the Chisholm–Mason scale. The kidney biopsy revealed mild inflammatory cell infiltrates, with interstitial fibrosis. Fig. 1. (A) Bilateral macroscopic nephrocalcinosis. (B) Plain X-ray. Distal RTA is the most common cause of nephrocalcinosis due to hypercalciuria without hypercalcaemia. The reported prevalence of nephrocalcinosis in patients with dRTA ranges from 60 to 80%. Distal renal tubular acidosis (dRTA) related to Sjogren's syndrome occurred in up to 33%. Primary Sjogren's syndrome may manifest itself as dRTA-associated nephrocalcinosis by autoantibodies directed against the A-type intercalated cells in the collecting tubules leading to a defect in hydrogen ion secretion.

Prolonged Coma after Single, Unintentional Overdose of Insulin: Concurring Factors Leading to a Persistent Neurological Condition

We refer the case of a 62-year old female diabetic patient, under insulin therapy since twelve year. She was found unconscious from her husband and the emergency team assisting the patient on site found a newly opened insulin vial of 10 ml half empty. Supposedly she had injected almost five ml of insulin glargine, with a total of 500 UI of insulin, and the plasma glucose value of 29 mg/dl supported the overdose diagnosis. The patient was emergently admitted in an intensive care unit with profound hypoglycemia and hypokalemia, and in deep coma. Dextrose bolus and continuous infusions normalized her glycemic levels only after three days of uninterrupted perfusions, with the patient remaining in coma for another two days after glycemia normalization. Discharged with a paraparetic gait as neurological sequelae, she improved considerably within the next month from the event. The reason of overdose was not clearly formulated, but a tricyclic antidepressant was added on in the therapy after psychiatric consultancy was obtained.

Acute Intermitent porphyria and early hematin treatment before confirming the diagnosis

The term porphyria refers to a heterogeneous group of metabolic diseases resulting from variable catalytic defects of the enzymes involved in the heme biosynthesis pathway. Acute intermittent porphyria (AIP) is an autosomal dominant disorder resulting from a partial deficiency of porphobilinogen (PBG) deaminase. A 21-year-old woman presented to us with the complaints of abdominal pain and vomiting. Her father and sister are diagnosed as acute intermittent porfiria. The laboratory findings showed profound hyponatremia, hypokalemia and high values of creatine kinase. AIP was suspected because of family history and clinic of patient. Our initial management consisted of continuous infusion of 10% glucose and 3% NaCI solution. We decided to start hematin treatment because of no clinical response with current therapy. After the hematin treatment she had regained consciousness, the abdominal pain subsided. The hyponatremia and elevation of creatine kinase was corrected. The analysis of PBG in 24-h urine confirmed the diagnosis of AIP.

Acute Kidney Injury Secondary to Exposure to Insecticides Used for Bedbug (Cimex lectularis) Control

Bedbug (Cimex lectularis) infestation is becoming a worldwide epidemic due to the emergence of insecticide-resistant strains. Pyrethroids are approved by the US Environmental Protection Agency for use against bedbugs and are considered minimally toxic to humans, with known respiratory, neurologic, and gastrointestinal effects. We present the first reported case of pyrethroid-induced toxic acute tubular necrosis (ATN). A 66-year-old healthy woman receiving no prior nephrotoxic medications presented with extreme weakness, decreased urine output, and acute kidney injury. She had administered multiple applications of a bedbug spray (permethrin) and a fogger (pyrethrin), exceeding the manufacturer's recommended amounts. She was found to have severe nonoliguric acute kidney injury associated with profound hypokalemia. Kidney biopsy revealed toxic ATN with extensive tubular degenerative changes and cytoplasmic vacuolization. With conservative management, serum creatinine level decreased from 13.0 mg/dL (estimated glomerular filtration rate, 3 mL/min/1.73 m(2)) to 1.67 mg/dL (estimated glomerular filtration rate, 37 mL/min/1.73 m(2)) within 6 weeks. Literature review uncovered no prior report of pyrethroid insecticide-induced ATN in humans, although there are reports of ATN with similar tubular vacuolization in rats exposed to this agent. Bedbug insecticides containing pyrethroids should be used with caution due to the potential development of toxic ATN after prolonged exposure.

The PI3K/AKT/mTOR Signaling Pathway Is Overactivated in Primary Aldosteronism

BackgroundTo date, the available non-invasive remedies for primary aldosteronism are not satisfactory in clinical practice. The phosphoinositide 3-kinase (PI3Ks)/protein kinase B (PKB or AKT)/mammalian target of rapamycin (mTOR) signaling pathway is essential for tumorigenesis and metastasis in many types of human tumors, including renal cancer, adrenal carcinoma and pheochromocytoma. The possibility that this pathway is also necessary for the pathogenesis of primary aldosteronism has not yet been explored. To answer this question, we investigated the activity of the PI3K/AKT/mTOR signaling pathway in normal adrenal glands (NAGs), primary aldosteronism (PA) patients and NCI-H295R cells.Methodology/Principal FindingsBetween January 2005 and December 2011, we retrospectively reviewed the records of 45 patients with PA. We compared clinical characteristics (age, gender and biochemical data) and the expression of phospho-AKT (p-AKT), phospho-mTOR (p-mTOR), phospho-S6 (p-S6) and vascular endothelial growth factor (VEGF) by immunohistochemical staining and western blotting, analyzing 30 aldosterone-producing adenomas (APAs), 15 idiopathic hyperaldosteronism (IHA) tissues and 12 NAGs following nephrectomy for renal tumors (control group). Compared with the control group, most of the PA patients presented with polydipsia, polyuria, resistant hypertension, profound hypokalemia, hyperaldosteronemia and decreased plasma renin activity. Compared with normal zona glomerulosa, the levels of p-AKT, p-mTOR, p-S6 and VEGF were significantly upregulated in APA and IHA. No significant differences were found between APA and IHA in the expression of these proteins. Additionally, positive correlations existed between the plasma aldosterone levels and the expression of p-AKT and p-mTOR. In vitro studies showed that mTOR inhibitor rapamycin could inhibit cell proliferation in NCI-H295R cells in a dose- and time-dependent manner. Furthermore, this inhibitor also decreased aldosterone secretion.ConclusionsOur data suggest that the PI3K/AKT/mTOR signaling pathway, which was overactivated in APA and IHA compared with normal zona glomerulosa, may mediate aldosterone hypersecretion and participate in the development of PA.

Paralysie périodique thyréotoxique hypokaliémique : quatre observations et revue de la littérature

PurposePeriodic thyrotoxic hypokalemic paralysis (TPP) is a neuromuscular complication of hyperthyroidism. It is more common in young Asian males than in Caucasian and African patients. We report four new cases and review the literature. Case reportsFour consecutive patients were diagnosed with TPP. They were all men with a median age of 34.5 years at presentation. Two patients originated from the Philippines, one was African and one was Caucasian ethnic background. They all presented with a paresis or flaccid paralysis, without respiratory failure. Previous similar episodes in their past medical history, the presence of profound hypokalemia (mean serum potassium level of 2 mmol/L) and the presence of clinical and biological signs of hyperthyroidism led to the diagnosis of TPP. All four patients were diagnosed with Graves’ disease. Outcome was favourable in all four patients with the symptomatic treatment of TPP and treatment of Graves’ disease. ConclusionTPP is a severe condition, due to a dysfunction of the Na+-K+ ATPase pump. Initial management relies on β-blocker treatment and careful potassium supplementation. Then, medical or surgical etiological treatment of the thyrotoxicosis is essential to prevent a recurrence. The disease is probably underdiagnosed: it must be suspected when a profound hypokaliema resolves very quickly (<12hours); hyperthyroidism should always be included in the differential diagnosis of a paresis associated with hypokalemia.

Xylitol

Xylitol is a prevalent sugar substitute found in a wide variety of foods, particularly those labeled as “low carb.” It is found in many medicines and dental products both for its antibacterial activity and to increase palatability. Originally, this toxin was recognized as a problem in dogs following sugarless gum ingestions. Xylitol is generally nontoxic to mammals except for dogs. In the dog, xylitol induces marked increases in insulin production and occasionally hepatopathy. The clinical syndrome is manifested with signs consistent with profound hypoglycemia, hypokalemia, hypophosphatemia, and acute hepatic failure. Treatment relies upon administration of intravenous glucose, hepatic support, and general supportive care.

Rifampin-associated tubulointersititial nephritis and Fanconi syndrome presenting as hypokalemic paralysis

BackgroundRifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin.Case presentationA 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and β2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient’s clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria.ConclusionThis case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin.

Hypokalemic paralysis in a girl with dental and renal calculi: Questions

A 15-year-old Chinese girl presented to the emergency department with muscle paralysis of bilateral lower extremities over the course of 1 day. She had a 2-year history of polyuria, nocturia, and rampant dental caries and calculi. She denied vomiting, diarrhea, or use of alcohol, laxatives, or diuretics, and her family history was unremarkable. Her pulse rate was 90/min, blood pressure 112/72 mmHg, and body temperature 36.4 °C. Physical examination revealed severe dental caries and calculi (Fig. 1a) with dry oral mucosa. Her thyroid gland was not enlarged. Neurologic examination disclosed symmetric flaccid paralysis with areflexia of both lower extremities. The remainder of the physical examination was unremarkable. The most striking biochemical abnormalities were profound hypokalemia (1.8 mEq/l) and hyperchloremic metabolic acidosis (pH 7.28, HCO3 – 16.6, Na 141 and Cl 114 mEq/l). Her renal, liver, and thyroid function were all normal (creatinine 0.9 mg/dl). Urinalysis revealed proteinuria (1+), low urine specific gravity (1.010), high K excretion (transtubular K gradient 5, 24-h urine K 38 mEq/day), positive urine anion gap (Na 43, K 16 and Cl 39 mEq/l) and persistent alkaline urine (pH 7–7.5). Electrocardiogram revealed prolonged PR interval with flattened T wave. Abdominal ultrasonography showed bilaterally medullary nephrocalcinosis (Fig. 1b). Questions:

Fatality after Cardiac Arrest in Thyrotoxic Periodic Paralysis due to Profound Hypokalemia Resulting from Intravenous Glucose Administration and Inadequate Potassium Replacement

Fatality after Cardiac Arrest in Thyrotoxic Periodic Paralysis due to Profound Hypokalemia Resulting from Intravenous Glucose Administration and Inadequate Potassium Replacement

Fatality After Cardiac Arrest in Thyrotoxic Periodic Paralysis Due to Profound Hypokalemia Resulting from Intravenous Glucose Administration and Inadequate Potassium Replacement

Thyrotoxic periodic paralysis (TPP) is a variant of periodic paralysis (PP) that occurs in patients with underlying mutations in genes for cation channels, if they develop thyrotoxicosis. It is disabling, and fatalities sometimes occur. Here, we present a patient with TPP who developed hypokalemic paralysis that was probably aggravated by the administration of a carbohydrate, probably contributing to, if not causing, a fatal outcome. A 30-year-old Chinese patient received (131)I treatment for Graves' disease (GD) in our hospital. Three days later in the middle of the night, he developed aggravating paralytic symptoms after a heavy evening meal. The next morning, he was seen in a small clinic and was treated with 1250 mL 5% glucose containing 25 mL 10% potassium chloride (KCl). By early afternoon, he had not improved and was transferred to a city hospital, arriving with grade I muscle strength and severed facial and bulbar paralysis that was shortly followed by cardiac arrest with failure of resuscitation. Shortly before he died, his serum K(+) was 1.15 mEq/L (normal=3.5-5). We postulate that severe hypokalemia developed in our patient in part in response to the high intravenous glucose load that he received. We advocate caution against using intravenous glucose solutions for potassium administration in patients with TPP and recommend a review of guidelines suggesting this form of treatment. In rural settings with limited resources, we favor oral potassium, not to exceed 100 mEq per day, and transfer to a modern medical facility in settings where muscle weakness is developing in patients with TPP.

Effects of K+-deficient diets with and without NaCl supplementation on Na+, K+, and H2O transporters' abundance along the nephron

Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) and H(2)O transporters' pool size regulation in response to removing K(+) from a diet containing 0.74% NaCl, as well as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet electrolytes. Sprague-Dawley rats (n = 5-6) were fed for 6 days with one of these diets: 2% KCl, 0.74% NaCl (2K1Na, control chow) compared with 0.03% KCl, 0.74% NaCl (0K1Na); or 2% KCl, 2%NaCl (2K2Na) compared with 0.03% KCl, 2% NaCl (0K2Na, Na(+) replete). In both 0K1Na and 0K2Na there were significant decreases in: 1) plasma [K(+)] (<2.5 mM); 2) urinary K(+) excretion (<5% of control); 3) urine osmolality and plasma [aldosterone], as well as 4) an increase in urine volume and medullary hypertrophy. The 0K2Na group had the lowest [aldosterone] (172.0 ± 17.4 pg/ml) and lower blood pressure (93.2 ± 4.9 vs. 112.0 ± 3.1 mmHg in 2K2Na). Transporter pool size regulation was determined by quantitative immunoblotting of renal cortex and medulla homogenates. The only differences measured in both 0K1Na and 0K2Na groups were a 20-30% decrease in cortical β-ENaC, 30-40% increases in kidney-specific Ste20/SPS1-related proline/alanine-rich kinase, and a 40% increase in medullary sodium pump abundance. The following proteins were not significantly changed in both the 0 K groups: Na(+)/H(+) exchanger isoform 3; Na(+)-K(+)-Cl(-) cotransporter; Na(+)-Cl(-) cotransporter, oxidative stress response kinase-1; renal outer medullary K(+) channel; autosomal recessive hypercholesterolemia; c-Src, aquaporin 2 isoform; or renin. Thus, despite profound hypokalemia and renal K(+) conservation, we did not confirm many of the changes that were previously reported. We predict that changes in transporter distribution and activity are likely more important for conserving K(+) than changes in total abundance.

Effects of K‐deficient diets ± Na supplementation on Na, K, and H2O transporters’ abundance along the nephron

Previous studies of K deficiency compared chow with 2% KCl, 0.74% NaCl (2K1Na ) to K deficient chow: 0.03% KCl, 0.74% NaCl (0K1Na ). We tested whether previously reported responses to 0K diet are due to low electrolytes, rather than hypokalemia. SD rats were fed 6 d with gelled diet prepared from powdered base adjusted to 2K1Na, 0K1Na, and with added NaCl: 2% KCl, 2% NaCl (2K2Na) and 0.03% KCl, 2% NaCl (0K2Na). Abundance was assessed by immunoblot of homogenates, densities normalized to mean of 2K groups.Results1) In both 0K groups, plasma K fell to 2.5 mM, urine K fell to &lt; 10 μmol/hr and outer medulla hypertrophied. 2) The only differences seen in both 0K groups are: ↓cortex ENaC and ↑medulla Na,K‐ATPase (NKA). 3) The following changed in 0K1Na but not 0K2Na: ↑cortex gastric H,K‐ATPase (HKA), ↑medulla NHE3, NHE3‐P and ↓AQP2. 4) In 0K2Na but not 0K1Na: cortex SPAK and OSR1 ↑ despite lowest plasma aldo in 0K2Na (172 pg/ml) vs. 0K1Na (413 pg/ml) and 2K2Na (417 pg/ml) and with no changes in NCC‐P or NKCC‐P.ConclusionsDespite profound hypokalemia and low urinary K, previously reported changes with 0K diets (↑NHE3, ↓NKCC, ↓NCC, ↓ROMK, ↑c‐Src, ↑HKA, ↓AQP2) were not observed; some may be secondary to low electrolytes. ↓ENaC can decrease driving force for K secretion, and ↑NKA is secondary to hypertrophy. Changes in transporter distribution and activity appear more important for conserving K than changes in abundance. DK0837854

Unilateral paralysis associated with profound hypokalemia

Unilateral paralysis is rarely reported to be primary presentation of severe hypokalemia. We describe a 24-year-old woman who presented to the emergency department with sudden onset of right-sided weakness. Neurologic examination revealed diminished muscle strength and tendon reflexes over the right limbs. Computed tomography of the brain showed no organic brain lesion. However, laboratory data showed hypokalemia (K+ 2.0 mmol/L) with metabolic acidosis (HCO3 − 19 mmol/L). She needed a total of 260 mmol K+ to achieve complete recovery of muscle strength at a serum K+ level of 3.2 mmol/L and was proved to have distal renal tubular acidosis. Severe hypokalemia must be kept in mind as a cause of acute unilateral paralysis without organic lesions to avoid unnecessary examination and potentially life-threatening complications.

Acute barium intoxication following ingestion of soap water solution

We present a rare case in which a young girl ingested a solution of a hair-removing soap. The ingestion resulted in profound hypokalemia and severe acidosis leading to flaccid paralysis, respiratory arrest and ventricular arrhythmias. Ultimately the patient made complete recovery. The soapwas found to contain barium sulfide. The degree of paralysis and acidosis appeared to be directly related to serum potassium levels.

Life‐threatening hypokalaemia associated with ibuprofen‐induced renal tubular acidosis

Renal tubular acidosis is an underreported complication of ibuprofen misuse, and can result in life-threatening hypokalaemia. We describe four patients who presented with profound hypokalaemia and muscle weakness associated with excessive ibuprofen ingestion. Ibuprofen cessation and supportive management resulted in complete biochemical resolution within a few days. These cases remind practitioners about potential complications of unmonitored use of over-the-counter analgesics, including those with potential for misuse due to their codeine content.

Hypokalemic Paralysis as Primary Presentation of Fanconi Syndrome Associated With Sjögren Syndrome

Hypokalemic paralysis is a rare presentation of Fanconi syndrome (FS) caused by Sjögren Syndrome (SS). We describe a 39-year-old man who manifested flaccid paralysis of 4 limbs. Laboratory investigations showed profound hypokalemia (1.6 mmol/L) with renal K wasting, hyperchloremic metabolic acidosis with positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, normoglycemic glycosuria, and abnormal serum creatinine concentration 2.2 mg/dL. A thorough survey for the cause of FS revealed that he had xerophthalmia and xerostomia accompanied by high anti-Ro antibody, positive Schirmer test, and delayed saliva excretion on sialoscintigraphy, confirming the diagnosis of SS. Potassium citrate, active vitamin D3, and high phosphate diet for his FS coupled with mycophenolate mofetil for SS resolved clinical symptoms and ameliorated renal function. Early recognition of HP due to the underlying SS-related FS with prompt therapy not only could terminate potentially life-threatening hypokalemia, but also improve renal outcome.

Intoxication by large amounts of barium nitrate overcome by early massive K supplementation and oral administration of magnesium sulphate

Suicide by ingestion of barium is exceptionally rare. Adverse health effects depend on the solubility of the barium compound. Severe hypokalemia, which generally occurs within 2 hours after ingestion, is the predominating feature of acute barium toxicity, subsequently leading to adverse effects on muscular activity and cardiac automaticity. We report one case of acute poisoning with barium nitrate, a soluble barium compound. A 75-year-old woman was hospitalized after suicidal ingestion of a burrow mole fumigant containing 12.375 g of barium nitrate. About 1 hour post-ingestion, she was only complaining of abdominal pain. The ECG recording demonstrated polymorphic ventricular premature complexes (VPCs). Laboratory data revealed profound hypokalemia (2.1 mmol/L). She made a complete and uneventful recovery after early and massive potassium supplementation combined with oral magnesium sulphate to prevent barium nitrate absorption.