Increase In Potassium Excretion Research Articles

Polymyxin-B induced bartter-like syndrome: an unusual adverse effect

Introduction and Importance: Bartter syndrome is a rare autosomal recessive disorder affecting renal tubular function, leading to electrolyte and volume homeostasis disturbances. It can also manifest as Bartter-like syndrome, a rare side effect of certain medications. Polymyxin-B, used to treat multidrug-resistant infections, is infrequently associated with BLS, making early recognition crucial to prevent severe electrolyte imbalances. Case Presentation: A 73-year-old female with coronary artery disease, COPD, hyperlipidemia, and other comorbidities presented with fever, respiratory distress, and hypoxia on mechanical ventilation. Initial labs showed leukocytosis, anemia, and normal potassium. Despite broad-spectrum antibiotics, sputum cultures revealed pandrug-resistant Acinetobacter baumannii, sensitive only to Polymyxin-B. After six days of Polymyxin-B, the patient developed fever, hypotension, hypokalemia, hypomagnesemia, and polyuria. Urine studies indicated increased potassium excretion. A diagnosis of Bartter like syndrome was made. Polymyxin-B was discontinued, and the patient’s electrolytes normalized, resolving the polyuria. She was discharged with daily potassium and magnesium supplements. Clinical Discussion: Bartter-like syndrome can result from Polymyxin-B-induced tubular dysfunction, characterized by hypokalemia and hypomagnesemia. Close electrolyte monitoring is essential for patients receiving this antibiotic, particularly in those with complex medical conditions. Early recognition allowed for timely discontinuation of Polymyxin-B, which rapidly reversed the electrolyte disturbances. Conclusion: This case underscores the importance of recognizing Polymyxin-B-induced Bartter-like syndrome. Clinicians should be vigilant for electrolyte disturbances in patients undergoing treatment with Polymyxin-B, ensuring timely interventions to mitigate adverse outcomes.

6568 A Novel Case of Liddle Syndrome in Siblings: Insights into a Rare Genetic Mutation

Abstract Disclosure: A.B. Humrickhouse: None. M. Peltsverger: None. Introduction: Liddle syndrome (LS) is an inherited form of hypertension caused by a mutation in the epithelialsodium channel (ENaC). This condition is characterized by hypertension (HTN), hypokalemia,hyporeninemia, and metabolic alkalosis, although clinical presentation can vary. Asymptomaticearly-onset HTN is common, and if left undiagnosed, it can lead to advanced renal disease,cardiovascular complications, stroke, and even sudden death. Treatment typically involves theadministration of ENaC blockers such as amiloride and triamterene. We present a novel case ofLS in two siblings resulting from a missense mutation in the SCNN1B gene. Case Presentation: The patient is a 24-year-old Hispanic female who presented for evaluation of poorly controlledHTN and severe hypokalemia of 2.9 mmol/L during the first trimester of pregnancy. She wasdiagnosed with HTN at age eighteen. The family history was notable for resistant HTN in herfather and younger brother. Biochemical evaluation revealed normal plasma-free metanephrinesand 24-hour urine-free cortisol. Low plasma renin activity (0.530 ng/mL/hr) and aldosterone(<1.0 ng/dL) were detected on multiple tests. The urine-free cortisol-to-cortisone ratio was <0.5,excluding the diagnosis of apparent mineralocorticoid excess syndrome. The diagnosis of LS wasconfirmed by genetic analysis, which identified a novel heterozygous mutation, c.1859 A>G(Tyr620Cys), in the SCNN1B gene, which had not been reported in the literature to date. Thesame mutation was identified in her brother. The patient was treated with a high dose ofamiloride (15 mg daily), which controlled her HTN and hypokalemia throughout her pregnancy. Discussion: LS is an autosomal dominant disorder with genetic heterogeneity. It is characterized by HTN,low plasma aldosterone and renin activity, and increased potassium excretion. This leads tohypokalemia and metabolic alkalosis. LS is caused by germline mutations found in theSCNN1A, SCNN1B, and SCNN1G genes, which encode the alpha, beta, and gamma subunits ofthe ENaC channel. These mutations lead to enhanced sodium reabsorption in the kidneys,independent of aldosterone. Our patient was diagnosed with hypertension at the age of 18.However, the diagnosis of LS was not made until six years later when she presented during herfirst trimester of pregnancy. Treatment with amiloride effectively controlled her hypertension andhypokalemia, which allowed her to deliver a healthy child. Amiloride was also prescribed for thepatient's brother. A combination of biochemical analysis and genetic testing enables a betterunderstanding of the various clinical presentations, ensuring appropriate treatment andprevention of end-organ damage. Genetic counseling is essential for families affected by LS. Presentation: 6/1/2024

O81 EFFECT OF ANTIHYPERTENSIVE MEDICATIONS ON URINARY SODIUM TO POTASSIUM (Na/K) RATIO

Background: The urinary sodium to potassium ratio (Na/K) greater than 2 indicating either excess sodium or insufficient potassium intake. However, the effect of antihypertensive medications on the urinary Na/K ratio has not been evaluated. We hypothesized that antihypertensive medication would acutely affect the urinary Na/K ratio. Methods: Male and female C57BL/6J mice, 14 weeks old, and a separate cohort of 24-month-old mice were subjected to a regular chow diet (NaCl 0.4%) and a high salt diet (4%). Urinary Na/K ratios in spot urine samples were measured three times a week. After baseline measurements, all animals were treated with one antihypertensive medication for 2 weeks, followed by a one-week washout period. The effects of enalapril (25 mg/kg/day), hydrochlorothiazide (25 mg/kg/day), and amlodipine (10 mg/kg/day)—were compared under a high salt diet mimicking human salt consumption. Urinary Na/K ratios collected on day 1 (acute) and day 8 (subacute) after initiating medication were compared to the vehicle period using a two-way ANOVA. Medication was administered with food using gel food pellets. Results: Under regular chow, the urinary Na/K ratio was 0.65±0.58 (n=15) with no interaction between sex or age (all p>0.05). Under a high salt diet, the urinary Na/K ratio increased to 4.5±2.2 (p<0.01 vs. regular chow) with no differences between sex and age. After the washout period, enalapril, both acutely and subacutely, did not affect the Na/K ratio. Similarly, hydrochlorothiazide did not affect the Na/K ratio in either period. However, amlodipine reduced the Na/K ratio in both acute and subacute periods (p<0.001). No interaction was observed with sex or age. The effect of amlodipine was related to higher potassium excretion (43.9±23 vs. 81.6±33 meq/L; p<0.001) with no changes in sodium excretion (152.2±75 vs. 173.3±43.5 meq/L; p=0.8). Conclusion: The Na/K ratio reflects salt and potassium consumption. The Na/K ratio is not affected by enalapril or hydrochlorothiazide. Amlodipine decreases the Na/K ratio acutely and subacutely due to increased potassium excretion.

Impact of a nudge-based food environment intervention in a hospital convenience store on staff’s food intake and Na/K

BackgroundA food environment intervention using nudge tactics was implemented at a hospital convenience store (CVS) in Tokyo to improve employees’ eating habits. The objective of this study was to evaluate its effects on the urinary sodium-to-potassium ratio (Na/K), food intake, eating attitude, and behavior.MethodsUsing a pre–post design; the intervention incorporated nudge tactics, healthier options, easy-to-pick food placement, and eye-catching information. We also used price incentives. The primary outcomes included changes in Na/K and sodium and potassium excretion assessed using spot urine samples at health checkups. Secondary outcomes were changes in staff food intake, eating attitude, and behavior which were assessed using questionnaire surveys. All outcomes were evaluated statistically. Furthermore, we investigated how the intervention led to outcomes using path analysis.ResultsA total of 140 participant (52men and 88women) were analyzed. Significant changes were observed in Na/K (3.16 to 2.98 in median, p = 0.02) and potassium excretion (43.4 to 45.2 mmol/day in mean, p = 0.03). However, sodium excretion did not change significantly. The intake of fruits and dairy products increased with improved self-efficacy. The most influential factor for lowering Na/K and increasing potassium excretion was information from the CVS; purchasing “balanced meals” to lower Na/K and salads to increase potassium excretion were second.ConclusionsFood environment intervention using nudge tactics can improve staff’s food intake and lower Na/K.Trial registrationRegistration number: UMIN000049444 (UMIN-CTR).Date of registration: November. 7. 2022.

#1704 GLP-1RA versus DPP-4 inhibitors and rates of hyperkalemia and discontinuation of renin-angiotensin system (RAS) blockade in Swedish routine care

Abstract Background and Aims Emerging evidence suggest that glucagon-like peptide-1 receptor agonists (GLP-1RA) influence tubular handling of electrolytes and increase potassium excretion, which may translate into reduced risk of hyperkalemia. Hyperkalemia is a common complication that limits persistence on guideline-recommended RAS inhibitors (RASi). Here, we quantified and compared rates of hyperkalemia and RASi discontinuation among users of GLP-1RA versus dipeptidyl peptidase-4 inhibitors (DPP-4i) in a large healthcare system. Method We used data from the SCREAM project (Jan 2008-Dec 2021) to conduct a population-based active-comparator, new-user cohort study of adults with type-2 diabetes who started GLP-1RA or DPP-4i. The primary outcome was hyperkalemia occurrence, overall (plasma potassium>5.0 mmol/L) and by severity (mild -potassium >5-≤5.5 mmol/L- and moderate-severe -potassium >5.5 mmol/L- hyperkalemia). Among ongoing RASi users, we assessed time to RASi discontinuation through evaluation of subsequent RASi dispensations. Cox regression with inverse probability of treatment weighting (IPTW) was used to estimate pooled hazard ratios (HRs) and rate differences. Major cardiovascular events (MACEs) served as positive control outcome to evaluate unmeasured confounding bias. Results During a median follow-up of 3.0 (Interquartile range [IQR] 1.2-5.6) years, we identified 33 280 eligible participants, of which 13 633 started GLP-1RA and 19 647 DPP-4i. Mean age was 64 years and 40% were women. Compared with DPP-4i, starting GLP-1RA was associated with a lower rate of hyperkalemia (Hazard ratio [HR] 0.91; 95% CI: 0.84-0.99, Fig. 1), with no suggestion of effect modification by baseline eGFR strata (HR 0.91 (0.78-1.07) for eGFR ≥60 and HR 0.92 (0.83-1.01) for eGFR <60 ml/min/1.73 m2, P for interaction >0.05). Similar findings were observed for mild (HR 0.90; 0.83-0.98) and moderate-severe (HR 0.92; 0.80-1.06) hyperkalemia. Out of 21 751 participants that were using RASi, 8 463 discontinued this therapy during median 2.0 (0.7, 4.1) years of follow-up. Initiation of GLP-1RA vs. DPP-4i was associated with lower rate of RASi discontinuation (HR: 0.93; 0.87-0.98), with no interaction across strata of baseline eGFR (HR 0.97 (0.83-1.12) for eGFR ≥60 and HR 0.93 (0.87-0.99) for <60 ml/min/1.73 m2, P for interaction >0.05). Consistent with trial evidence, we observed a lower rate of MACE for GLP-1RA vs DPP-4i (HR 0.87; 0.78-0.98). Conclusion In patients with diabetes managed in routine care, the use of GLP-1RA was associated with lower rates of hyperkalemia and discontinuation of RASi compared with DPP-4i, providing further observational evidence in support of the use of these medications.

Kir7.1 knockdown and inhibition alter renal electrolyte handling but not the development of hypertension in Dahl salt-sensitive rats.

High K+ supplementation is correlated with a lower risk of the composite of death, major cardiovascular events, and ameliorated blood pressure, but the exact mechanisms have not been established. Inwardly rectifying K+ (Kir) channels expressed in the basolateral membrane of the distal nephron play an essential role in maintaining electrolyte homeostasis. Mutations in this channel family have been shown to result in strong disturbances in electrolyte homeostasis, among other symptoms. Kir7.1 is a member of the ATP-regulated subfamily of Kir channels. However, its role in renal ion transport and its effect on blood pressure have yet to be established. Our results indicate the localization of Kir7.1 to the basolateral membrane of aldosterone-sensitive distal nephron cells. To examine the physiological implications of Kir7.1, we generated a knockout of Kir7.1 (Kcnj13) in Dahl salt-sensitive (SS) rats and deployed chronic infusion of a specific Kir7.1 inhibitor, ML418, in the wild-type Dahl SS strain. Knockout of Kcnj13 (Kcnj13-/-) resulted in embryonic lethality. Heterozygous Kcnj13+/- rats revealed an increase in K+ excretion on a normal-salt diet but did not exhibit a difference in blood pressure development or plasma electrolytes after 3 wk of a high-salt diet. Wild-type Dahl SS rats exhibited increased renal Kir7.1 expression when dietary K+ was increased. K+ supplementation also demonstrated that Kcnj13+/- rats excreted more K+ on normal salt. The development of hypertension was not different when rats were challenged with high salt for 3 wk, although Kcnj13+/- rats excrete less Na+. Interestingly, chronic infusion of ML418 significantly increased Na+ and Cl- excretion after 14 days of high salt but did not alter salt-induced hypertension development. Here, we found that reduction of Kir7.1 function, either through genetic ablation or pharmacological inhibition, can influence renal electrolyte excretion but not to a sufficient degree to impact the development of SS hypertension.NEW & NOTEWORTHY To investigate the role of the Kir7.1 channel in salt-sensitive hypertension, its function was examined using complementary genetic and pharmacological approaches. The results revealed that although reducing Kir7.1 expression had some impact on maintaining K+ and Na+ balance, it did not lead to a significant change in the development or magnitude of salt-induced hypertension. Hence, it is probable that Kir7.1 works in conjunction with other basolateral K+ channels to fine-tune membrane potential.

Acute hyperkalemia in adults.

Hyperkalemia is a common, life-threatening medical situation in chronic renal disease patients in the emergency department (ED). Since hyperkalemia does not present with any specific symptom, it is difficult to diagnose clinically. Hyperkalemia causes broad and dramatic medical presentations including cardiac arrhythmia and sudden death. Hyperkalemia is generally determined through serum measurement in the laboratory. Treatment includes precautions to stabilize cardiac membranes, shift potassium from the extracellular to the intracellular, and increase potassium excretion. The present article discusses the management of hyperkalemia in the ED in the light of current evidence.

Review on Kalemic Conditions in Pregnancy

Hypokalemia and hyperkalemia, are common electrolyte electrolyte diseases related to changes in potassium intake, excretion, or transcellular shifts. Hypokalemia is commonly induced by diuretics and gastrointestinal losses, whereas hyperkalemia is typically caused by kidney disease, hyperglycemia, and pharmaceutical use. The aetiology of kalemia can range from minor to severe, and it can be caused by diet, drugs, or another disease. Symptoms of hypokalemia include sinus bradycardia, ventricular tachycardia or fibrillation and acute muscle weakness, gestational hypertension, adrenal insufficiency, and renal failure are the symptoms associated with hyperkalemia. Chronic kidney disease and intrauterine fetal death are life-threatening complications associated kalemia in child bearing mother. The medical profile remitted promptly on potassium intake for hypokalemia or increase potassium excretion for hyperkalemia. This review gives an insight into the causes, symptoms, complications as well as pharmacological and non-pharmacological treatments of Kalemic conditions in pregnancy. This review also reported some cases of hypo and hyperkalemia in pregnancy in both human and animals.
 Keywords: Hypokalemia, Hyperkalemia, Pregnancy, Potassium.

24 hours urinary sodium and potassium excretion and association with blood pressure among people aged 18-75 years old in six Chinese provinces

Objective: To analyze the level of sodium and potassium intake and their association with blood pressure among people aged 18 to 75 years old in six provinces. Methods: From October to December 2018, participants aged 18 to 75 years were selected from Hebei, Hunan, Sichuan, Jiangxi, Qinghai and Heilongjiang provinces by using cluster random sampling method. Demographic characteristics and lifestyle information were collected by using questionnaire survey. Physical measurement and 24-hour urine collection were also conducted. Results: A total of 2 636 subjects were finally included in the analysis. The average urine sodium, potassium and sodium-to-potassium molar ratio were(4 438.4±1 822.8)mg/d, (1 566.2±646.3)mg/d, and 5.2±2.2, respectively. According to World Health Organization standards, 94.5% and 98.7% of the respondents had excessive sodium intake and insufficient potassium intake. After adjusting for related factors, each 1 000 mg increase in sodium excretion was associated with increased systolic blood pressure (1.65 mmHg, 95%CI: 1.07, 2.22) and diastolic blood pressure (0.53 mmHg, 95%CI: 0.21, 0.84), and each 1 000 mg increase in potassium excretion was associated with decreased systolic blood pressure (3.02 mmHg, 95%CI:-4.25, -1.80) and diastolic blood pressure (1.27 mmHg, 95%CI:-2.05, -0.48). Conclusion: The sodium intake in Chinese population remains excessive and potassium intake is insufficient. Sodium and potassium could be associated with blood pressure and the intervention of reducing sodium and supplementing potassium should be conducted in the corresponding population.

Overview of Monogenic Forms of Hypertension Combined With Hypokalemia.

Hypertension is an important risk factor in many conditions and creates a heavy burden of disease and mortality globally. Polygenic hypertension is the most common form; however, it is increasingly recognized that monogenic hypertension is not rare, especially in patients with electrolyte disorders. Single genetic alterations are associated with plasma volume expansion and catecholamines/sympathetic excess with simultaneously increased potassium excretion in the urine and potassium intracellular shift. Early-onset refractory hypertension and profound hypokalemia are characteristics of monogenic hypertension. However, accumulated evidence shows the existence of phenotypic heterogeneity in monogenic hypertension meaning that, even for mild symptoms, clinicians cannot easily exclude the possibility of monogenic hypertension. Genetic, epigenetic and non-genetic factors are all possible mechanisms influencing phenotypic diversity. Genetic sequencing is a precise and efficient method that can broaden the mutant gene spectrum of the disease and is very helpful for understanding the pathophysiology of monogenic hypertension. Genetic sequencing, along with biochemical tests and imaging modalities, is essential for the early diagnosis and targeted management of monogenic hypertension to avoid long-term catastrophic complications.

Hypokalemia in peritoneal dialysis patients in Thailand: the pivotal role of low potassium intake.

Hypokalemia is highly prevalent in chronic peritoneal dialysis (PD) patients worldwide, particularly in Thailand. This study aims to investigate the major determinants of hypokalemia in Thai PD patients. A cross-sectional study was performed in chronic PD patients at 4 PD centers in Bangkok, Thailand. Hypokalemia was defined if the average serum potassium level during the last 3 consecutive visits was < 3.5mEq/L. Patients and/or their caregivers were asked to perform a 3-day dietary food record and take pre- and post-meal pictures following the instructed protocol. Daily dietary nutrients, including potassium, were estimated by a single dietician using INMUCAL-N software. Total potassium excretion was determined by 24-h PD effluents and urine collection. Intracellular and extracellular water values (ICW and ECW, respectively) were measured by electrical bioimpedance assay (BIA) to indirectly explore the role of intracellular potassium shift in hypokalemia. Among 60 eligible PD patients, 19 (31%) had hypokalemia. Hypokalemic patients had significantly lower dietary potassium intake (24.4 ± 11.1 vs. 30.5 ± 9.4mEq/day, p = 0.031) and lower total potassium excretion (28.5 ± 8.4 vs. 36.7 ± 11.2mEq/day, p = 0.006) compared to normokalemic patients. Both groups had comparable values of ICW and ECW. On logistic regression, there was no significant correlation between hypokalemia and daily PD exchange volume, total Kt/Vurea, residual renal function, concurrent medications (insulin, diuretics, renin-angiotensin-aldosterone inhibitor, and beta-blockers) or ICW. Low dietary potassium was an independent risk factor for hypokalemia. Low dietary potassium intake, rather than increased potassium excretion or intracellular shift, is the major contributing factor of hypokalemia in Thai chronic PD patients. Dietary intervention or potassium supplement protocol should be implemented.

Twenty-Four–Hour Urinary Sodium and Potassium Excretion and Their Associations With Blood Pressure Among Adults in China

This study aimed to assess current level of sodium and potassium intake and their associations with blood pressure (BP) using the 24-hour urinary data in a large sample of China. Data from participants aged 18 to 75 years were collected as the baseline survey of Action on Salt China in 2018. Of 5454 adults, 5353 completed 24-hour urine collection. The average sodium, potassium excretion, and sodium-to-potassium molar ratio were 4318.1±1814.1 mg/d (equivalent to 11.0±4.6 g/d of salt), 1573.7±627.1 mg/d, and 5.0±2.1, respectively. After adjusting for potential confounding factors and correcting for regression dilution, each 1000-mg increase in sodium excretion was associated with increased systolic BP (1.32 mm Hg [95% CI, 0.92-1.81]) and diastolic BP (0.34 mm Hg [95% CI, 0.09-0.60]). Each 1000-mg increase in potassium excretion was inversely associated with systolic BP (-3.19 mm Hg [95% CI, -4.38 to -2.20]) and diastolic BP (-1.56 mm Hg [95% CI, -2.29 to -0.90]). Each unit increase in sodium-to-potassium molar ratio was associated with an increase of systolic BP by 1.21 mm Hg (95% CI, 0.91-1.60) and diastolic BP by 0.44 mm Hg (95% CI, 0.24-0.64). The relationships between sodium and BP mostly increase with the rise of BP quantiles. Potassium shows the opposite trend. The current sodium intake in Chinese adults remains high and potassium intake is low. Sodium and sodium-to-potassium ratio were positively associated with BP, whereas potassium was inversely associated with BP. Registration- URL: https://tinyurl.com/vdr8rpr; Unique identifier: ChiCTR1800017553. URL: https://tinyurl.com/w8c7x3w; Unique identifier: ChiCTR1800016804. URL: https://tinyurl.com/s3ajldw; Unique identifier: ChiCTR1800018119.

Increased potassium excretion in children with monosymptomatic nocturnal enuresis: could it be related to Kir 4.1- KCNJ10 gene polymorphism?

There are controversial results in the literature regarding urinary electrolytes, especially potassium, in enuretic children. KCNJ10 channel protein, a member of the Kir 4.1 family is expressed in renal distal tubules and has an important function in renal ion transport. We investigated whether KCNJ10 gene polymorphisms are associated with clinical and laboratory findings of a group of Turkish children with monosymptomatic primary nocturnal enuresis (MNE). Ninety-seven MNE children and 100 healthy controls were tested for three single nucleotide polymorphisms (SNPs) in the KCNJ10 gene. The transversions in SNPs were G to A for intron 1(SNP1), G to A for exon 2 (SNP2), and T to C transition for promoter (SNP3). All SNPs were genotyped by PCR-restriction fragment length polymorphism. SNP3 in promoter of KCNJ10 gene showed strong association with MNE children for distribution of genotype and allele frequency, while SNP1 in intron 1 and SNP2 in exon 2 were noninformative. The distribution of TT, TC, and CC genotypes for SNP3 was 66%, 26.8% and 7.2% respectively in MNE compared with 38%, 59% and 3% respectively in controls (p < 0.0001). In enuretic children, TT genotype was higher and there was an increased potassium excretion in children with TT genotype (P < 0.05). We conclude that KCNJ10 gene promoter polymorphism may have a role on potassium excretion in Turkish MNE children. This is the first study in literature evaluating KCNJ10 gene polymorphism in this patient population. Future studies investigating the other SNPs, mutations or altered regulation of Kir4.1 in larger samples would help clarify the role (s) of KCNJ10 gene in enuresis.

IN VITRO ANTIOXIDANT ACTIVITY, DIURETIC AND HYPOGLYCEMIC ACTIVITIES OF ETHANOL EXTRACT FROM LEAF OF CHRYSOPHYLLUM ALBIDUM G. IN WISTAR ABINO RATS

Chrysophyllum albidum G. is generally regarded as a plant with many ethno-medicinal uses. The study was aimed at evaluating the in vitro antioxidant, diuretic, and hypoglycemic properties of the ethanol extract of leaves of C. albidum Male Wistar albino rats weighing between 150g and 200g were used for the experiment. The DPPH scavenging activity was determined using DPPH assay, inhibition of lipid peroxidation was carried out using the reactions of peroxides with thiobarbituric acid, while nitric oxide was conducted based on the Greiss reaction. Diuretic activity was carried out using the method of Lipschitz with slight modifications. Alloxan (140 mg/kg) was used to induce diabetes in the rats. The extract showed a concentration-dependent increase in DPPH radical scavenging activity, anti-lipid peroxidation activity, and nitric oxide inhibition activity maximal at 200 mg/ml (84.99±7.97, 79.82±6.10, 69.99±2.22 respectively) and this was significant (p&lt;0.05) when compared with that of 100 mg/ml of vitamin C (97.68±0.84, 99.05±0.24 and 98.15±0.29 respectively) which served as the control. The extract also significantly (p&lt;0.05) increased; urine volume, urinary sodium, and urinary chloride particularly at 2000 mg/kg (1.55±0.07, 109.60±0.57, and 106.00±1.41 respectively) when compared with the standard drug (1.85±0.07, 115.20±0.57, and 112.85±0.49 respectively). The increase in potassium excretion was also significant (p&lt;0.05) particularly at 2000 mg/kg (13.70±0.28) but less than those of sodium (109.60±0.57) and chloride (106.00±1.41) at the same concentration. There was no significant (p&lt;0.05) increase in urinary bicarbonate the maximum being at 250 mg/kg (22.55±0.78). The extract caused a non-significant (p&lt;0.05) decrease in the fasting blood glucose level of the rats. It was concluded that the leaves of C. albidum could be used as a source of natural antioxidant boosters and also a diuretic.

Diagnosis and management of primary aldosteronism.

Primary aldosteronism (PA) is the most common form of secondary hypertension (HTN), with an estimated prevalence of 4% of hypertensive patients in primary care and around 10% of referred patients. Patients with PA have higher cardiovascular morbidity and mortality than age- and sex-matched patients with essential HTN and the same degree of blood pressure elevation. PA is characterized by an autonomous aldosterone production causing sodium retention, plasma renin supression, HTN, cardiovascular damage, and increased potassium excretion, leading to variable degrees of hypokalemia. Aldosterone-producing adenomas (APAs) account for around 40% and idiopathic hyperaldosteronism for around 60% of PA cases. The aldosterone-to-renin ratio is the most sensitive screening test for PA. There are several confirmatory tests and the current literature does not identify a "gold standard" confirmatory test for PA. In our institution, we recommend starting case confirmation with the furosemide test. After case confirmation, all patients with PA should undergo adrenal CT as the initial study in subtype testing to exclude adrenocortical carcinoma. Bilateral adrenal vein sampling (AVS) is the gold standard method to define the PA subtype, but it is not indicated in all cases. An experienced radiologist must perform AVS. Unilateral laparoscopic adrenalectomy is the preferential treatment for patients with APAs, and bilateral hyperplasia should be treated with mineralocorticoid antagonist (spironolactone or eplerenone). Cardiovascular morbidity caused by aldosterone excess can be decreased by either unilateral adrenalectomy or mineralocorticoid antagonist. In this review, we address the most relevant issues regarding PA screening, case confirmation, subtype classification, and treatment.

Effect of Sesbania grandiflora Linn leaf extracts on diuresis in wistar rats

Background: This study was designed to evaluate the effect of sesbania grandiflora linn leaf extracts on diuretic activity in wistar rats.Methods: Healthy male wistar albino rats divided into 9 groups and weighing 150-200gm.diuretic activity was expressed by Natriuretic activity, saluretic activity, carbonic anhydrase inhibition, Diuretic index or Diuretic action, saluretic index, Natriuretic index. Animalgroups are divided into: group1 treated as control, 2and 3 treated as standards, group 4, 5 and 6 treated with aqueous leaf extract of Sesbania grandiflora Linn. in different doses of 150,300,450mg/kg. Group 7,8and 9 treated with methanolic leaf extract of Sesbania grandiflora Linn. Doses of 150,300,450mg/kg.Results: No change in body weight group treated with AE-150 (p&gt;0.05) with AE-150 (0.1%), increase in urine volume with increasing doses both with aqueous and methanolic extracts, sodium excretion with methanolic extract was high compared with the aqueous extract, significant increase in potassium excretion in both aqueous and methanolic extract treated groups.All the statistical tests were done by using SPSS version 6. The level of significance was 5% (p≤0.05).Conclusions: All the electrolytes concentration was increased in the urine, hence excluding osmotic diuretic action. Diuretic index, saluretic activity, saluretic index and natriuretic index of ME-450 were more than the value of hydrochlorothiazide hence excludes thiazide diuretic action. But these values were less than furosemide.

Renal effects of a novel endogenous natriuretic agent xanthurenic acid 8-o-β-d-glucoside in rats

Xanthurenic acid 8-o-β-d-glucoside is an endogenous derivative of tryptophan metabolism, isolated from urine of patients with chronic renal disease. This compound was suggested previously to act as a natriuretic hormone based on its ability to block short circuit currents in a frog skin assay and to induce a sustained natriuresis when injected into rats (C. D. Cain et al., Proc. Natl. Acad. Sci. USA 2007: 17873–17878). The present communication describes the effects of the compound on renal clearance and hemodynamic parameters in male Sprague–Dawley rats maintained on a normal salt (0.4–0.5%) diet. Intravenous administration of synthetic xanthurenic acid 8-o-β-d-glucoside in two consecutive incremental doses (6.3 and 31.5 nmol) resulted in a significant increase (P < 0.05), in urine flow (43.91 ± 6.31 μL/min vs. 10.54 ± 2.21 μL/min), absolute rate of sodium excretion (3.99 ± 0.95 μEq/min vs. 1.15 ± μEq/min), and percentage sodium excretion (1.63 ± 0.46% vs. 0.37 ± 0.12%, peak response vs. baseline, respectively). The natriuretic/diuretic effect was associated also with a significant increase in potassium excretion. These effects were not related to changes in renal hemodynamics or in arterial blood pressure. Pretreatment with the sodium channel blocker, amiloride, completely abolished the natriuretic and kaluretic actions of the compound. Administration of the xanthurenic acid derivative caused a dose-related increase in urinary nitrite/nitrate excretion. Moreover, under chronic nitric oxide blockade by l-NG-Nitro-Arginine-Methyl-Esther (l-NAME) sodium excretion was similar in rats treated or untreated with the compound. Our data demonstrate that xanthurenic acid 8-o-β-d-glucoside has significant diuretic/natriuretic and kaluretic properties. An intact amiloride-sensitive sodium channel is required for the renal effects of the compound. The data further suggest that the natriuretic effect is mediated in part by a nitric oxide-dependent mechanism.

Effect of chronic treatment with angiotensin receptor ligands on water-salt balance in wistar and spontaneously hypertensive rats

The renin-angiotensin system plays a crucial role in the regulation of cardiovascular function and maintenance of water-electrolyte balance. The two major receptor types of the system, AT1 and AT2, have different, often opposite effects on these functions. To elucidate the impact of long-term treatment with selective angiotensin receptor antagonists and an agonist on water-salt balance in normotensive Wistar and spontaneously hypertensive rats (SHRs). 12-week-old male Wistar rats and SHRs were individually housed in metabolic cages and 24-h food and water intake and urine and electrolyte excretion were measured. Urinary sodium (UNa), potassium (UK) and chlorine (UCl) were determined by a flame photometer. Losartan, a selective AT1 receptor antagonist, was administered in the Wistar rats and SHRs at a dose of 10 mg/kg/day subcutaneously (sc). Wistar rats were also given the AT2 receptor antagonist, PD123319, subcutaneously at a dose of 10 mg/kg/ day. CGP 42112A, an AT2 receptor agonist, was administered intracerebroventricularly in Wistar rats at a dose of 12 microg/rat/day. The drugs were infused continuously for 14 days through osmotic minipumps. Losartan selectively increased sodium excretion in both rat strains and decreased weight gain in SHRs. PD123319 increased potassium excretion and decreased weight gain in Wistar rats. CGP 42112A increased food and water intake, urine output and UNa+ and UK+ excretion and decreased weight gain in normotensive Wistar rats. Chronic treatment with selective angiotensin receptor ligands modifies water-salt balance in rats through changes both in renal excretory function and ingestive behaviors.

Evaluation of diuretic activity of &lt;i&gt;Paspalidium flavidum&lt;/i&gt; in rats

This study was conducted to investigate the diuretic potential of aqueous methanolic extract of Paspalidium flavidum in rats. The extract at doses of 10, 30 50 and 100 mg/kg was administered intraperitoneally in acute diuretic model. Furosemide (10 mg/kg i.p) was used as standard drug. Total urine volume and urinary excretion of electrolytes were measured. Preliminary phytochemical tests were also performed using standard procedures. The extract exhibiteda significant dose dependent diuretic effect at all the doses when compared to control group. Urinary excretion of sodium was significantly increased by the extract while a significant increase in potassium excretion was only observed at higher doses. Phytochemical analysis illustrated that the extract contained compounds such as alkaloids, saponins, tannins, flavonoids, cardiac glycosides and reducing sugars. It is conceivable therefore that the aqueous methanolic extract of P. flavidum contain certain biologically active compounds that might be responsible for the diuretic activity.

The Effect of Sodium Bicarbonate Upon Urinary Citrate Excretion in Calcium Stone Formers

To evaluate the effects of oral sodium bicarbonate (NaBic) supplementation upon urinary citrate excretion in calcium stone formers (CSFs). Sixteen adult calcium stone formers with hypocitraturia were enrolled in a randomized, double-blind, crossover protocol using 60 mEq/day of NaBic during 3 days compared to the same period and doses of potassium citrate (KCit) supplementation. Blood and 24-hour urine samples were collected at baseline and during the third day of each alkali salt. NaBic, similarly to KCit supplementation, led to an equivalent and significant increase in urinary citrate and pH. Compared to baseline, NaBic led to a significant increase in sodium excretion without concomitant increases in urinary calcium excretion, whereas KCit induced a significant increase in potassium excretion coupled with a significant reduction in urinary calcium. Although NaBic and KCit both reduced calcium oxalate supersaturation (CaOxSS) significantly vs baseline, KCit reduced calcium oxalate supersaturation significantly further vs NaBic. Both KCit and NaBic significantly reduced urinary phosphate and increased calcium phosphate supersaturation (CaPSS) compared to baseline. Finally, a significantly higher sodium urate supersaturation (NaUrSS) was observed after the use of the 2 drugs. This short-term study suggests that NaBic represents an effective alternative for the treatment of hypocitraturic calcium oxalate stone formers who cannot tolerate or afford the cost of KCit. In view of the increased sodium urate supersaturation, patients with pure uric acid stones and high urate excretion may be less suited for treatment with NaBic.