Short-Term Supplemental Dietary Potassium from Potato and Potassium Gluconate: Effect on Calcium Retention and Urinary pH in Pre-Hypertensive-to-Hypertensive Adults

Potassium supplementation has been associated with reduced urinary calcium (Ca) excretion and increased Ca balance. Dietary interventions assessing the impact of potassium on bone are lacking. In this secondary analysis of a study designed primarily to determine blood pressure effects, we assessed the effects of potassium intake from potato sources and a potassium supplement on urinary Ca, urine pH, and Ca balance. Thirty men (n = 15) and women (n = 15) with a mean ± SD age and BMI of 48.2 ± 15 years and 31.4 ± 6.1 kg/m2, respectively, were enrolled in a cross-over, randomized control feeding trial. Participants were assigned to a random order of four 16-day dietary potassium interventions including a basal diet (control) of 2300 mg/day (~60 mmol/day) of potassium, and three phases of an additional 1000 mg/day (3300 mg/day(~85 mmol/day) total) of potassium in the form of potatoes (baked, boiled, or pan-heated), French fries (FF), or a potassium (K)-gluconate supplement. Calcium intake for all diets was approximately 700–800 mg/day. Using a mixed model ANOVA there was a significantly lower urinary Ca excretion in the K-gluconate phase (96 ± 10 mg/day) compared to the control (115 ± 10 mg/day; p = 0.027) and potato (114 ± 10 mg/day; p = 0.033). In addition, there was a significant difference in urinary pH between the supplement and control phases (6.54 ± 0.16 vs. 6.08 ± 0.18; p = 0.0036). There were no significant differences in Ca retention. An increased potassium intake via K-gluconate supplementation may favorably influence urinary Ca excretion and urine pH. This trial was registered at ClinicalTrials.gov as NCT02697708.

Eyelid ptosis and muscle weakness in a child with Kawasaki disease: a case report

Background Kawasaki disease (KD) is an acute febrile vasculitis that often occurs in children under 5 years. Ptosis and muscle weakness associated with KD are rarely documented. Case presentation We present a case of KD with eyelid ptosis and muscle weakness in a 3-year-old boy. At admission, grade IV and grade III muscle strength were recorded for upper and lower limbs, respectively. Diminished patellar tendon reflex was noted. Laboratory evaluation showed hypokalemia with the serum potassium concentration of 2.62 mmol/L. Intravenous immunoglobulin (IVIG) and aspirin were initiated immediately accompanied with methylprednisolone for adjunctive therapy. Potassium supplement was administered at the same time, which resulted in the correction of hypokalemia on the 2nd day of admission but no improvement in ptosis and muscle weakness. Neostigmine testing, lumber puncture, electromyography, and cerebral and full spine MRI were performed, which, however, did not find evidence for neural and muscle diseases. On the 5th day, the fever was resolved. On the 6th day, eyelid ptosis disappeared. And on the 14th day, the muscle strength and muscle tension returned to normal, patellar tendon reflex could be drawn out normally, and the boy regained full ambulatory ability. Conclusions KD might affect the neural and muscular systems, and KD complicated with eyelid ptosis and muscle weakness is responsive to the standard anti-inflammatory treatment plus adjunctive corticosteroid therapy.

Diet or Additional Supplement to Increase Potassium Intake: Protocol For An Adaptive Clinical Trial

Background High blood pressure is the leading cause of cardiovascular disease worldwide. The prevalence of high blood pressure is steadily rising, with the growing and ageing population. Many medicines are available to decrease blood pressures successfully, as well as many non-medical options, such as dietary changes and exercise. There is a marked preference amongst patients, reiterated in a Hypertension Canada report, for more research into methods for controlling blood pressure without medicines or to reduce the burden of taking many pills to control high blood pressure. Indeed, effective options do exist, especially with diet, specifically decreasing sodium and increasing potassium in diet. Current public health outreach mostly focusses on sodium intake, even as the potassium intake in diet remains low especially in the Western world. Excellent data exist in the published research reporting that increasing potassium intake, either as diet or even as supplements, reduces blood pressure and reduces risk of cardiovascular outcomes such as stroke. However, the advice most often provided is to ‘eat more fruits and vegetables’ which does not get translated into concrete change. Methods We propose to do a clinical trial in two stages, with an adaptive trial design. In the first stage, participants with high blood pressure and proven low potassium intake (measured on the basis of a 24 hour urine collection) will get individually tailored dietary advice, reinforced by weekly supportive phone/email support. If at 4 weeks, there has not been a desired increase in potassium intake, they will be prescribed an additional potassium supplement. Testing will be conducted again at 4 weeks post initiating the potassium supplement, to confirm the efficacy of the potassium supplement. Final measurements will be planned at 52 weeks to observe and measure the persistence of the effect of diet or additional supplement. Concurrent measurements of sodium intake, blood pressure, participant satisfaction, and safety measures will also be done. Discussion The results of the study would help determine the most effective method of increasing potassium intake, thus reducing blood pressure, need for blood pressure lowering medicines, at the same time potentially increasing participant satisfaction. The current guidelines recommend changes in diet, not supplement, to increase potassium intake, hence the two stage design will only add supplements if the most rigorous dietary advice does not work. Trial registration: This study has been registered on ClinicalTrials.gov identifier NCT03809884, registered on January 18, 2019. URL: https://clinicaltrials.gov/ct2/show/NCT03809884

Levetiracetam Treatment Causing False Negative Screening Test in a Woman With Aldosterone Producing Adenoma

Background: Endocrine hypertension accounts for 5–10% of hypertensive population, with primary hyperaldosteronism being the most frequently encountered diagnosis. Biochemical tests are subject to interference with many drugs that may lead to false positive or negative results. We present a case of aldosterone producing adenoma associated with false negative screening test due to Levetiracetam use. Clinical Case: A 30 year-old Middle Eastern woman was referred to endocrinology clinic for evaluation of secondary hypertension and persistent hypokalemia. Six years ago, she presented to emergency room during the 3rd trimester of her second pregnancy with severe preeclampsia and seizure. Postpartum, she was discharged on Levetiracetam (Keppra) 500 mg orally BID. Upon follow up visits, she continued to have persistent elevation of blood pressure readings with spontaneous hypokalemia ranging 2.5–3.2 mEq/L. She was started on Perindopril 10 mg daily and potassium supplement. Amlodipine 5 mg daily was added shortly later on. Clinically, she had regular menstrual cycle. She did not have plethora, central obesity, easy bruising, or proximal muscle weakness. Her review of systems including thyroid-related symptoms were normal. There was no family history of hypertension or adrenal tumors. On examination, BP 180/110, pulse rate 78, weight 58 kg and BMI 25. Her physical examination was otherwise unremarkable. After holding Perindopril for 4 weeks, biochemical tests showed creatinine 0.52 mg/dL (0.49–1.1), urea 16.8 mg/dL, potassium 2.9 mEq/L (3.5–5.2), direct renin concentration (DRC) 100.6 pg/mL, aldosterone 54.25 ng/dL. Plasma fractionated metanephrines were normal and morning cortisol level after 1 mg overnight dexamethasone suppression test was 0.72 mcg/dL. Renal arterial doppler showed normal renal blood flow without any significant stenosis. Despite increasing potassium supplement she continued to have hypokalemia. As levetiracetam was reported by literature review to cause severe hypokalemia, it was stopped after discussion with neurology. Four weeks later, repeated DRC was suppressed 4.0 pg/mL with elevated aldosterone 62.73 ng/dL. Furthermore, primary hyperaldosternism was confirmed after normal saline suppression test revealed unsuppressed aldosterone 15 ng/dL. An Adrenal CT scan showed a small hypodense right adrenal lesion measuring 11x9 mm with a pre-contrast density of 7 HU and post contrast absolute washout more than 60%. Patient elected to undergo right adrenalectomy. 24 hours post surgery, aldosterone level dropped to 4.0 ng/dL and potassium increased to 5 mEq/L. Fortunately, hypertension and hypokalemia have both resolved after surgery. Conclusion: We are first to report that Levetiracetam can cause unsuppressed direct plasma rennin concentration (DRC) and potentially could result in a false negative screening test for primary hyperaldosteronism.

Effect of Increased Potassium Intake on Adrenal Cortical and Cardiovascular Responses to Angiotensin II: A Randomized Crossover Study

Background Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure‐raising hormone aldosterone. Besides its well‐described renal effects, aldosterone is also believed to have vascular effects, acting through mineralocorticoid receptors present in endothelial and vascular smooth muscle cells, although mineralocorticoid receptors‐independent actions are also thought to be involved. Methods and Results To gain further insight into the effect of increased potassium intake and potassium‐stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo‐controlled double‐blind crossover study in 25 healthy normotensive men, where 4 weeks treatment with a potassium supplement (90 mmol/day) was compared with 4 weeks on placebo. At the end of each treatment period, we measured potassium and aldosterone in plasma and performed an angiotensin II (AngII) infusion experiment, during which we assessed the aldosterone response in plasma. Hemodynamics were also monitored during the AngII infusion using ECG, impedance cardiography, finger plethysmography (blood pressure‐monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean±SD, 4.3±0.2 versus 4.0±0.2 mmol/L; P =0.0002) and aldosterone (median [interquartile range], 440 [336–521] versus 237 [173–386] pmol/L; P <0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII‐stimulated aldosterone secretion ( P =0.0020). In contrast, the hemodynamic responses (blood pressure, total peripheral resistance, cardiac output, and renal artery blood flow) to AngII were similar after potassium and placebo. Conclusions Increased potassium intake potentiates AngII‐stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. Registration EudraCT Number: 2013‐004460‐66; URL: https://www.ClinicalTrials.gov ; Unique identifier: NCT02380157.

Effect of increased potassium intake on the renin–angiotensin–aldosterone system and subcutaneous resistance arteries: a randomized crossover study

Background Increased potassium intake lowers blood pressure (BP) in hypertensive patients. The underlying mechanism is not fully understood but must be complex because increased potassium intake elevates circulating concentrations of the BP-raising hormone aldosterone. Methods In a randomized placebo-controlled crossover study in 25 normotensive men, we investigated the effect of 4 weeks of potassium supplement (90 mmol/day) compared with 4 weeks of placebo on the renin–angiotensin–aldosterone system (RAAS), urine composition and 24-h ambulatory BP. Vascular function was also assessed through wire myograph experiments on subcutaneous resistance arteries from gluteal fat biopsies. Results Higher potassium intake increased urinary potassium excretion (144.7 ± 28.7 versus 67.5 ± 25.5 mmol/24-h; P &lt; 0.0001) and plasma concentrations of potassium (4.3 ± 0.2 versus 4.0 ± 0.2 mmol/L; P = 0.0002), renin {mean 16 [95% confidence interval (CI) 12–23] versus 11 [5–16] mIU/L; P = 0.0047}, angiotensin II [mean 10.0 (95% CI 6.2–13.0) versus 6.1 (4.0–10.0) pmol/L; P = 0.0025] and aldosterone [mean 440 (95% CI 336–521) versus 237 (173–386) pmol/L; P &lt; 0.0001]. Despite RAAS activation, systolic BP (117.6 ± 5.8 versus 118.2 ± 5.2 mmHg; P = 0.48) and diastolic BP (70.8 ± 6.2 versus 70.8 ± 6.3 mmHg; P = 0.97) were unchanged. In the wire myograph experiments, higher potassium intake did not affect endothelial function as assessed by acetylcholine [logarithmically transformed half maximal effective concentration (pEC50): 7.66 ± 0.95 versus 7.59 ± 0.85; P = 0.86] and substance P (pEC50: 8.42 ± 0.77 versus 8.41 ± 0.89; P = 0.97) or vascular smooth muscle cell reactivity as assessed by angiotensin II (pEC50: 9.01 ± 0.86 versus 9.02 ± 0.59; P = 0.93) and sodium nitroprusside (pEC50: 7.85 ± 1.07 versus 8.25 ± 1.32; P = 0.25) but attenuated the vasodilatory response of retigabine (pEC50: 7.47 ± 1.16 versus 8.14 ± 0.90; P = 0.0084), an activator of Kv7 channels. Conclusions Four weeks of increased potassium intake activates the RAAS in normotensive men without changing BP and this is not explained by improved vasodilatory responses ex vivo.

Effect of potassium and sowing time on potato yield and quality

The current study was conducted the effect of sowing time and different doses of a potassium supplement on yield attributes of potato at Gollen valley Chitral, the Northern Pakistan during summer 2018. Sowing Potato (cv. Roko) commenced from 5thMay and continued till 5thJune keeping an interval of 15 days among sowing times. Potassium (K) was applied at the rate of 100, 150, 200 and 250 kg ha-1 as potassium chloride. Basal doses of nitrogen (N) and phosphorus (P) were applied at the rate 120 and 100 kg ha-1 respectively, as urea and DAP. All yield attributes like number of leaves per plant, plant height, the number of tubers per plant, tuber volume and yield of potato were higher for May 5th (early sowing date) with potassium dose of 200 kg ha-1. Interaction of sowing dates and Potassium (SD×K) for yield, tuber volume and soil potassium content was statistically significant (P≤0.05). The study showed that by delaying the sowing season, yield traits and yield of potato decreased significantly; hence early cultivation and K fertilization of 200 kg ha-1 resulted in maximum production of potato as well as improved soil properties under agroclimatic conditions of the region which is a dry temperate zone of Pakistan

Thyrotoxic Hypokalemic Periodic Paralysis Triggered by Dexamethasone Administration

Thyrotoxic hypokalemic periodic paralysis (THPP) is a disease characterized by recurrent episodes of muscle weakness due to intracellular potassium shifting in the presence of high levels of thyroid hormone. It occurs more commonly amongst young Asian men with underlying Graves’ disease. Attacks are commonly precipitated by ingestion of carbohydrate-rich meals or alcohols, stress or strenuous exercise. Herein, we describe an adult Thai man suffering from a hypokalemic periodic paralysis attack after receiving a dexamethasone injection. The diagnosis of Graves’ disease was confirmed by his thyroid function test and a presence of thyrotropin-receptor antibody. His weakness and hypokalemia responded well to potassium supplement and a non-selective beta blocker, while his thyrotoxicosis was initially controlled by an anti-thyroid medication and subsequently with a subtotal thyroidectomy. Clinicians should beware of this manifestation when administering steroids in the thyrotoxic patients, especially of Asian male descent.