Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of furosemide syrup in China. Welcome to wholesale bulk high quality furosemide syrup for sale here from our factory. Good service and reasonable price are available.
Furosemide Syrup is an oral solution formulation mainly composed of Furosemide. Its chemical name is 2- [(2-furanmethyl) amino] -5- (sulfamoyl) -4-chlorobenzoic acid, and its molecular formula is C₁₂H₁₁ClN₂O₅S, with a molecular weight of 330.75. This drug belongs to Loop Diuretics, which exerts a potent diuretic effect by inhibiting the reabsorption of sodium and chloride ions by the thick segment of the ascending branch of the renal tubular medullary loop, while also having a vasodilatory effect. It inhibits the active reabsorption of Na ⁺ and Cl ⁻ by the thick segment of the ascending branch of the renal tubular medullary loop, reduces the osmotic pressure of the renal medullary interstitium, lowers the renal tubular concentration function, and thus increases the excretion of electrolytes such as water, sodium, chloride, potassium, calcium, and magnesium. Its diuretic effect is potent and rapid, taking effect 30 minutes after oral administration and within 5 minutes after intravenous injection, with a duration of 4-6 hours. As an oral solution formulation, this substance has the flexibility to adjust the dosage according to the patient's age, weight, and condition, especially suitable for children, elderly people, or patients with swallowing difficulties. At the same time, the oral absorption rate is 60% -70%. Eating may slow down absorption but does not affect the efficacy, taking effect within 30-60 minutes. Compared to tablets, syrup formulations can reduce gastrointestinal irritation and improve patient compliance.
Our products
Furosemide COA
Bartter syndrome (BS) is a rare genetic renal tubular disease characterized by hypokalemia, metabolic alkalosis, and hyperrenin hyperaldosteronism. Its core pathological mechanism is electrolyte transport disorders caused by mutations in the ion channel genes of the renal tubules. According to the type of genetic mutation, BS can be divided into five subtypes, among which type II (classical type) is caused by the loss of ROMK potassium channel function encoded by KCNJ1 gene, manifested as neonatal polyuria, polyhydramnios, and severe electrolyte imbalance. Furosemide Syrup, as a representative drug of loop diuretics, exerts potent diuretic effects by inhibiting the Na ⁺ - K ⁺ -2Cl ⁻ cotransporter (NKCC2). Its therapeutic mechanism is intricately related to the pathophysiological processes of BS II.
Molecular pathological mechanism of Bartter syndrome type II
Gene mutations and ion channel dysfunction
BS type II is caused by a mutation in the KCNJ1 gene (located at 11q24), which encodes ROMK (Renal Outer Medullary Potassium Channel), a potassium ion channel located in the thick segment of the ascending branch of the medullary loop and the apical membrane of the cortical collecting duct. The functions of ROMK include:
Maintain the electrical neutrality of Na ⁺ - K ⁺ -2Cl ⁻ coordinated transport in the ascending branch of the medullary loop: by recovering K ⁺ into the lumen, provide an ion gradient for NKCC2 and drive the reabsorption of Na ⁺ and Cl ⁻.
Regulating the secretion of K ⁺ in the collecting duct: involved in the fine regulation of urinary potassium excretion.
KCNJ1 gene mutation (such as homozygous or compound heterozygous inactivation mutation) leads to loss of ROMK function, triggering the following chain reaction:
Partial inhibition of NKCC2 function: Due to impaired K ⁺ recovery, NKCC2 transport efficiency decreases, Na ⁺ and Cl ⁻ reabsorption decreases, and urinary electrolyte loss increases.
Renin angiotensin aldosterone system (RAAS) activation: Decreased blood volume stimulates the secretion of renin by the periglomerular apparatus, which in turn activates angiotensin II and aldosterone, attempting to compensate for electrolyte loss by preserving sodium and excreting potassium.
Increased synthesis of prostaglandins: Low blood volume and low blood potassium stimulate renal medullary stromal cells to synthesize prostaglandin E2 (PGE2), further dilating blood vessels, inhibiting RAAS sensitivity, and forming a "decompensated compensatory" cycle.
Pathological and physiological characteristics
Electrolyte disorders: hypokalemia (blood potassium<2.5mmol/L), hypochloremia, hyperkalemia (urine potassium>20mmol/24h).
Acid base imbalance: metabolic alkalosis (blood HCO ∝⁻>30mmol/L, pH>7.45).
Renin aldosterone system activation: Plasma renin activity (PRA) and aldosterone levels are significantly elevated, but blood pressure is normal (a key difference from primary aldosteronism).
Periglomerular apparatus proliferation: Renal biopsy shows the proliferation of granulosa cells and medullary stromal cells in the periglomerular apparatus.
Clinical manifestations and diagnosis of Bartter syndrome type II
Clinical Manifestations
BS type II often occurs in the neonatal or infant period, and typical manifestations include:
Polyuria and thirst: osmotic diuresis caused by impaired reabsorption of Na ⁺ and Cl ⁻ in the ascending branch of the spinal cord.
Delayed growth: Long term electrolyte imbalance and nutrient absorption disorders affect growth and development.
Muscle weakness and convulsions: Hypokalemia and metabolic alkalosis lead to abnormal excitability of the neuromuscular system.
Hyperhydramnios: Excessive amniotic fluid caused by polyuria during fetal development may lead to premature birth.
Special facial features: Some patients may have features such as a large head, protruding forehead, triangular face, and prominent earlobes.
Diagnostic criteria
The diagnosis of BS type II requires a combination of clinical manifestations, laboratory tests, and genetic testing
Laboratory test: Blood potassium<2.5mmol/L, urine potassium>20mmol/24h. Blood chlorine<95mmol/L, blood HCO ∝⁻>30mmol/L. Plasma PRA and aldosterone levels are elevated, but blood pressure is normal. Elevated levels of urinary prostaglandin E2 (PGE2) and prostaglandin metabolites (such as PGF2 α).
Genetic testing: Detecting KCNJ1 gene mutations through high-throughput sequencing (NGS) to confirm homozygous or compound heterozygous inactivating mutations.
Renal biopsy (optional): shows proliferation of granulosa cells and medullary stromal cells in the glomerulus, and rough endoplasmic reticulum and Golgi apparatus dilation can be observed under electron microscopy.
Differential Diagnosis
It needs to be differentiated from the following diseases:
Primary aldosteronism: hypertension, low renin, high aldosterone, sensitive to spironolactone treatment.
Pseudo Bartter syndrome: caused by long-term use of diuretics, vomiting, or a low potassium diet, without genetic mutations.
Gitelman syndrome: A mutation in the SLC12A3 gene leads to dysfunction of the thiazide sensitive Na ⁺ - Cl ⁻ cotransporter (NCC), manifested as hypokalemia and metabolic alkalosis, but with reduced urinary calcium excretion.
The role and controversy of furosemide in the treatment of Bartter syndrome type II
Furosemide Syrup is a representative drug of loop diuretics, exerting potent diuretic effects through the following mechanisms:
Inhibition of NKCC2: Competitive binding to the Cl ⁻ binding site of NKCC2 blocks the reabsorption of Na ⁺, K ⁺, and 2Cl ⁻, leading to the disappearance of osmotic pressure gradient in the thick segment of the ascending branch of the medullary loop and a decrease in water reabsorption.
Vasodilation: Inhibits prostaglandin degrading enzyme, increases PGE2 levels, and reduces peripheral vascular resistance.
Reduce blood volume: Reduce circulating blood volume and alleviate cardiac preload through diuretic action.
Theoretical basis for the treatment of BS type II with furosemide
The pathological core of BS II is electrolyte loss caused by partial inhibition of NKCC2 function, and furosemide may have the following effects by further inhibiting NKCC2:
Short term effect: Increasing urine output may temporarily alleviate high-capacity conditions (such as pulmonary edema), but BS II patients usually do not have edema, and the significance of this effect is limited. Aggravating electrolyte loss (Na ⁺, K ⁺, Cl ⁻) may induce severe hypokalemia and metabolic alkalosis.
Long term effects: Continuous inhibition of NKCC2 may activate RAAS and prostaglandin systems, forming a vicious cycle and exacerbating electrolyte imbalances.
Controversial point:
Treatment contradiction: BS type II already has NKCC2 functional inhibition, and furosemide may worsen the condition.
Indications limitations: Furosemide Syrup is mainly used in scenarios that require rapid diuresis, such as acute pulmonary edema and hypertensive crisis, while BS II patients do not have such indications.
Practical application:
Rare use: Currently, there is no evidence to support the use of furosemide as a routine treatment for BS type II.
Special scenario: When combined with acute heart failure or severe high-capacity load, it can be used cautiously in the short term, but electrolyte and acid-base balance need to be closely monitored.
Standard treatment plan for BS II type
The treatment of BS II mainly focuses on correcting electrolyte imbalance, inhibiting RAAS and prostaglandin system, including:
Potassium supplementation therapy: Oral potassium chloride (1-3mmol/kg/d), taken in divided doses to avoid gastrointestinal irritation. Intravenous potassium supplementation requires strict control of concentration and rate (<0.3% KCl,<0.5mmol/kg per hour).
Potassium sparing diuretic: Spironolactone (1-2mg/kg/d) reduces urinary potassium excretion by antagonizing aldosterone. Aminopheniramine (2-5mg/kg/d) directly blocks Na ⁺ channels in the distal tubules and collecting ducts, reducing K ⁺ secretion.
Prostaglandin synthesis inhibitors: Indomethacin (1-3mg/kg/d) or Ibuprofen (10-30mg/kg/d) reduce PGE2 synthesis and RAAS activity by inhibiting COX enzyme.
Angiotensin converting enzyme inhibitors (ACEIs): Enalapril (0.1-0.5mg/kg/d) or Captopril (0.5-2mg/kg/d) reduce aldosterone secretion by inhibiting the production of angiotensin II.
Future research directions and treatment prospects
Gene therapy and targeted drugs
ROMK channel agonist: Develop drugs that enhance residual ROMK function and partially restore K recovery ability.
NKCC2 activator: Upregulates NKCC2 expression through small molecule compounds or gene editing techniques to compensate for functional decline caused by ROMK deficiency.
Individualized treatment strategies
Genotyping phenotype association study: Clarify the association between KCNJ1 gene mutation types and clinical severity, and guide precision medication.
Biomarker monitoring: dynamically adjust treatment plans through indicators such as urinary PGE2 and blood renin levels.
Development of new diuretics
Selective NKCC2 inhibitors: Develop drugs with higher selectivity for NKCC2 and reduce their impact on other ion channels.
K ⁺ channel regulator: compensates for ROMK dysfunction by regulating other K ⁺ channels (such as BK channels).
Frequently Asked Questions
Why is sodium benzoate often added as a preservative in syrup formulations, but this may have subtle interactions with furosemide?
+
-
Both sodium benzoate and furosemide are excreted in the body after binding with glycine. In theory, the two may compete for limited glycine resources, especially in infants and young children with liver and kidney dysfunction, which may slightly affect the metabolism and clearance of either drug, but the clinical significance is usually not significant.
What potential impact does the high osmotic pressure environment of syrup have on the stability of the drug itself?
+
-
The high osmotic pressure environment created by high concentration syrup may accelerate the migration of water molecules into the syrup. If the packaging is not tightly sealed, it may cause changes in local water activity, which theoretically may promote the hydrolysis or physical properties of furosemide (such as crystallization), affecting the uniformity of the content.
Hot Tags: furosemide syrup, suppliers, manufacturers, factory, wholesale, buy, price, bulk, for sale