China
Africa
Explore chapters and articles related to this topic
Medicines in neonates
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Indomethacin reduces bloodflow in different organ systems. A decreased renal perfusion leads to the clinically frequently observed renal impairment: a transient decrease in glomerular filtration rate, urine production, fractional excretion of sodium and chloride [35,36]. A careful fluid balance can partly prevent this side effect. Many centres consider a serum creatinine above 1.2 to 1.6 mg/dL, a rising serum creatinine concentration or a urine production of less than 1 mL/kg per hour as a contraindication for starting indomethacin treatment. Furosemide has been tried to prevent the renal side effects but may increase circulating pros-taglandin levels and promote ductal patency [37]. Sufficient data are lacking to recommend its use during treatment of PDA [38,39]. Irrespective of this, diuretics seem to have little value for the treatment of PDA in preterms, unless there is congestive heart failure.
Nephrology, including fluid and electrolytes
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
10.14. A 2-year-old boy presents with generalized swelling which has developed over the preceding week. His urine output has diminished considerably during this period. Physical examination reveals generalized pitting oedema. Blood pressure is 100/75 mmHg. Urine contains protein +++, hyaline casts +, no RBC or WBC. He is likely to haveraised blood urea,increased susceptibility to pneumococcal infection.low fractional excretion of sodium.selective proteinuria.low levels of serum complement.
Role Of Kidney Dopamine In Sodium Excretion
Published in M.D. Francesco Amenta, Peripheral Dopamine Pathophysiology, 2019
In studies performed in humans, procedures of lower body positive pressure and water immersion is employed to produce central hypervolemia. In a group of subjects, a lower body positive pressure application caused natriuresis, diuresis, and increased fractional excretion of sodium.28 DA receptor blockade with domperidone abolished the natriuretic response and attenuated the diuresis seen during lower body positive pressure.28 However, in the absence of lower body positive pressure, domperidone had no effect on basal sodium excretion.28 In another study, domperidone was reported to attenuate the natriuretic response to water immersion in normotensive humans.29 In a separate study in normotensive subjects and essential hypertensive patients, it was reported that water immersion caused an exaggerated natriuresis in hypertensive compared to normotensive individuals.30 This response was accompanied by suppression of plasma renin activity, plasma aldosterone, and plasma prolactin. DA receptor blockade with metoclopramide significantly attenuated the natriuretic response to water immersion in normotensives and completely abolished the exaggerated natriuresis observed in hypertensive patients.30 Metoclopramide also prevented the suppression of aldosterone during water immersion. Therefore, these studies suggest than endogenous DA may play an important role in mediating the natriuretic response to hypervolemia caused by lower body positive pressure as well as water immersion in humans.28-30
Ameliorative role of inducible nitric oxide synthase inhibitors against sodium arsenite-induced renal and hepatic dysfunction in rats
Published in Drug and Chemical Toxicology, 2022
Ashwani Kumar Sharma, Anmoldeep Kaur, Tajpreet Kaur, Sarabjit Kaur, Devendra Pathak, Amrit Pal Singh
Creatinine level in rat urine was determined using colorimetric kit (Tulip Diagnostics, Mumbai, India). Creatinine clearance (CrCl) was calculated as: (CrCl = urine volume × urine creatinine/serum creatinine × 24 × 60 × rat wt) and presented as mL/min/kg (Sharma et al. 2021). Sodium level in urine sample was assayed using kit (Tulip Diagnostics, Mumbai, India). Fractional excretion of sodium (FeNa) was calculated as: [(FeNa=urine creatinine × serum sodium/serum creatinine × urine sodium)×100]. The FeNa was presented as percentage change in values (Arora et al. 2014, Brar et al. 2014). Microproteins in urine samples were determined using kit (Tulip Diagnostics, Bambolim, India) and microproteinuria was calculated as: (microproteinuria = microproteins × urine collected in 24-h). Microproteinuria was presented as mg/day (Brar et al. 2014, Sharma et al. 2021).
Nrf2 inhibition induces oxidative stress, renal inflammation and hypertension in mice
Published in Clinical and Experimental Hypertension, 2021
Zeba Farooqui, Razia Sultana Mohammad, Mustafa F. Lokhandwala, Anees Ahmad Banday
The effect of SKF38393 on sodium excretion was determined by following a previously detailed protocol (23). Briefly, mice were anesthetized as aforementioned and the right jugular vein was catheterized with PE-10 tubing for infusing saline or SKF38393. A midline abdominal incision was performed, and the urinary bladder was catheterized with PE-50 tubing to collect urine samples. The blood was collected simultaneously through the tail vein. Blood plasma was obtained by centrifuging blood samples at 2000 rpm for 15 minutes at 4°C. Urine and plasma samples were stored at −80°C for further analysis. Urine and plasma sodium concentrations were measured by atomic absorption spectroscopy (AAnalyst 400, PerkinElmer, Waltham, MA) to determine urinary sodium excretion (UNaV) and fractional excretion of sodium (FENa).
Flecainide toxicity in renal failure
Published in Baylor University Medical Center Proceedings, 2018
Rogin Subedi, Ryan K. Dean, Arbind Chaudhary, Tamas Szombathy
A 44-year-old woman with a body mass index of 47 kg/m2 was admitted for progressive dyspnea and lower-extremity edema. She had obstructive sleep apnea, heart failure with preserved ejection fraction, paroxysmal atrial fibrillation treated with a maze procedure, and a history of mitral and tricuspid valve repair. For sinus rhythm maintenance, she was taking flecainide 150 mg twice daily and metoprolol. Vital signs revealed a blood pressure of 102/62 mm Hg, heart rate of 62 beats per minute, and respiratory rate of 26 breaths per minute. Physical examination showed elevated jugular venous pulse, bilateral pitting pedal edema, and bilateral pulmonary crackles. Laboratory analysis showed a blood urea nitrogen of 23 mg/dL, creatinine of 2.53 mg/dL (baseline 0.8 mg/dL), aspartate transaminase of 13 U/L, and alanine transaminase of 18 U/L. Fractional excretion of sodium was 0.1%, suggesting a renal hypoperfusion state. The electrocardiogram on admission showed sinus rhythm with a PR interval of 212 milliseconds and a QRS duration of 112 milliseconds. An echocardiogram showed an ejection fraction of 55% with grade II left ventricular diastolic dysfunction. The patient was treated with intravenous furosemide at 2.5 mg an hour. She subsequently became hypotensive and was transferred to the intensive care unit. At this time, medication included flecainide, which was continued at a dosage of 150 mg twice daily.