BACKGROUND

Observational studies have increasingly reported transthyretin amyloid cardiomyopathy (ATTR-CM) as an under-recognized cause of heart failure. We report the first ATTR-CM diagnosed via multi-modality imaging in the Philippines signifying an important milestone in recognition and management of this formerly believed rare disease, locally. Utilization of non-invasive imaging such as echocardiography, cardiac MRI and technetium-99m pyrophosphate scintigraphy (PYP) demonstrates the potential for accurate diagnosis as well as timely and appropriate treatment strategies.

DISCUSSION

An 81/M Filipino with a history of carpal tunnel surgery, post-percutaneous coronary intervention (PCI), had three months’ history of refractory heart failure symptoms despite optimized medical treatment. His 2D-echo showed an ejection fraction (EF): 45%-50%, increased left ventricular (LV) posterior wall thickness with mild basal inferior wall hypokinesia and ECG: atrial fibrillation with low voltage. Speckle tracking imaging showed average global longitudinal strain: - 6.5% with cherry-on-top pattern on polar strain map. Cardiac MRI demonstrated diffuse late gadolinium enhancement from endocardial to transmural layers of biventricular and biatrial walls, highly suggestive of cardiac amyloidosis (CA). Light-chain amyloidosis was excluded by negative serum/urine protein electrophoresis/immunofixation. Tc-99m PYP scan revealed greater myocardial-than-bone uptake with a Perugini score 3 and calculated heart-to-contralateral ratio of 1.7. Congestion was controlled with intravenous loop diuretics and he was discharged stable with metoprolol succinate, dapagliflozin and apixaban. At the time of paper submission, he is currently being evaluated for tafamidis treatment.

CONCLUSION

The case highlighted the advantage of multi-modality imaging for noninvasive yet accurate identification of the disease. A tailored approach is required in slowing the disease progression and improving outcomes.

Human ; Male ; Amyloidosis ; Cardiomyopathies ; Percutaneous Coronary Intervention ; Sodium Potassium Chloride Symporter Inhibitors

Hyponatremia is a commonly observed complication that is related to hypoalbuminemia and portal hypertension in patients with advanced liver cirrhosis. Hyponatremia in patients with liver cirrhosis is mostly dilutional hyponatremia and is defined when the serum sodium concentration is below 130 meq/L. The risk of complications increases significantly in cirrhotic patients with hyponatremia, which includes spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic encephalopathy. In addition, hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis, and is an important prognostic factor before and after liver transplantation. The conventional therapies of hyponatremia are albumin infusion, fluid restriction and loop diuretics, but these are frequently ineffective. This review investigates the pathophysiology and various therapeutic modalities, including selective vasopressin receptor antagonists, for the management of hyponatremia in patients with liver cirrhosis.
Antidiuretic Hormone Receptor Antagonists ; Fibrosis ; Hepatic Encephalopathy ; Hepatorenal Syndrome ; Humans ; Hypertension, Portal ; Hypoalbuminemia ; Hyponatremia* ; Liver Cirrhosis* ; Liver Transplantation ; Liver* ; Mortality ; Peritonitis ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors

Diuretic therapy for the treatment of edema in patients with end-stage renal disease (ESRD) is unsatisfactory, and a combination of thiazide and loop diuretics may produce better clinical effects. To evaluate the influence of thiazide on loop diuretic therapy for ESRD, we performed a crossover study of furosemide versus hydrochlorothiazide plus furosemide treatment. The diuretic effects of furosemide (160 mg i.v.) alone versus a combination of hydrochlorothiazide (100 mg p.o.) and furosemide were studied in ten ESRD patients with proteinuria greater than 1 g/day. The diuretic effects were compared for 24 h urine volume and electrolyte excretion. To detect the influence of thiazide that may have been obscured in the widely dispersed data, pharmacodynamic analysis of urine furosemide excretion rate versus fractional excretion of sodium (FeNa) was also performed using mixed-effect modeling. Combination therapy was not significantly different from furosemide monotherapy in terms of 24 h urine volume, chloride, or sodium excretion. Hydrochlorothiazide was not a significant covariate in the furosemide effect for the pharmacodynamic model. In patients with ESRD and severe proteinuria (>1,000 mg/day), the combination of hydrochlorothiazide with furosemide therapy did not increase the diuretic effect of furosemide.
Cross-Over Studies ; Diuretics ; Edema ; Furosemide ; Humans ; Hydrochlorothiazide* ; Kidney Failure, Chronic* ; Proteinuria ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors

Heart Failure ; Humans ; Sodium Potassium Chloride Symporter Inhibitors

Diuretics are commonly used to control edema across various clinical fields. Diuretics inhibit sodium reabsorption in specific renal tubules, resulting in increased urinary sodium and water excretion. Loop diuretics are the most potent diuretics. In this article, we review five important aspects of loop diuretics, in particular furosemide, which must be considered when prescribing this medicine: (1) oral versus intravenous treatment, (2) dosage, (3) continuous versus bolus infusion, (4) application in chronic kidney disease patients, and (5) side effects. The bioavailability of furosemide differs between oral and intravenous therapy. Additionally, the threshold and ceiling doses of furosemide differ according to the particular clinical condition of the patient, for example in patients with severe edema or chronic kidney disease. To maximize the efficiency of furosemide, a clear understanding of how the mode of delivery will impact bioavailability and the required dosage is necessary.
Biological Availability ; Diuretics ; Edema ; Furosemide ; Humans ; Renal Insufficiency, Chronic ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors*

Acute decompensated heart failure syndrome is the most common cause of cardiovascular hospitalization with a high rate of in-hospital mortality. The clinical presentation is characterized by different clinical profiles due to various underlying causes, precipitating factors, volume status, and tissue perfusion status. Therefore, clinicians should carefully examine the hemodynamic status of acute decompensated heart failure patients in the initial management. Risk stratification might provide guidance to clinicians who care for patients with acute decompensated heart failure syndromes, and might improve decision-making in emergent care when decisions must be made quickly and accurately. Intravenous loop diuretics are the main treatment option for the relief of congestive symptoms. This article reviews how to assess hemodynamic status of acute decompensated heart failure patients and how to perform risk stratification of patients. Additionally, the initial treatment approach with a variety of pharmacological therapies including inotropic agents, diuretics, beta-blockers, angiotensinogen converting enzyme-inhibitors, angiotensin receptor blockers, digoxin, and other medications that are routinely prescribed in the management of acute decompensated heart failure patients are also discussed.
Angiotensin Receptor Antagonists ; Angiotensinogen ; Digoxin ; Diuretics ; Estrogens, Conjugated (USP) ; Heart Failure* ; Hemodynamics ; Hospital Mortality ; Hospitalization ; Humans ; Perfusion ; Precipitating Factors ; Sodium Potassium Chloride Symporter Inhibitors

The prevalence of kidney stone disease is increasing, and newer research is finding that stones are associated with several serious morbidities. These facts suggest that emphasis needs to be placed not only on stone treatment but also stone prevention. However, there is a relative dearth of information on dietary and medical therapies to treat and avoid nephrolithiasis. In addition, studies have shown that there are many misconceptions among both the general community and physicians about how stones should be managed. This article is meant to serve as a review of the current literature on dietary and drug therapies for stone prevention.
Allopurinol/therapeutic use ; Calcium Oxalate/analysis ; Cystine/analysis ; *Diet ; Humans ; Kidney Calculi/chemistry/*prevention & control ; Potassium Citrate/therapeutic use ; Sodium Chloride Symporter Inhibitors/therapeutic use ; Uric Acid/analysis ; Urological Agents/*therapeutic use

OBJECTIVETo observe the level of blood sodium in patients hospitalized for heart failure with water-sodium retention treated with loop diuretics and risk factors of low blood sodium.

METHODSWe selected 1 378 acute decompensated heart failure patients who visited Anzhen Hospital, and they are treated with loop diuretics, 259 patients with weight loses more than 1 kg in one week was enrolled in the final analysis, and divided into 3 groups: Group A (weight reduction between 1-3 kg), Group B (weight reduction between 3-5 kg) and Group C (weight reduction over 5 kg). Blood sodium, creatinine and uric acid were compared among groups and risk factors of low blood sodium were analyzed.

RESULTSBlood sodium was similar before and post loop diuretics treatment in Group A, and reduced in group B ((138.28 ± 3.73) mmol/L vs. (139.34 ± 3.66) mmol/L, P < 0.05) and in Group C((137.60 ± 4.07) mmol/L vs. (139.44 ± 4.12) mmol/L, P < 0.05). Forty-six (17.8%) patients developed hyponatremia post loop diuretics treatment. Duration of loop diuretics use was the independent risk infector for hyponatremia (OR = 1.191, 95%CI 1.010-1.385).

CONCLUSIONSLoop diuretics use is safe for treating hospitalized patients for heart failure with water-sodium retention and the risk of developing hyponatremia is low. Duration of loop diuretics use is the independent risk factor of hyponatremia.

Acute Disease ; Creatinine ; Heart Failure ; complications ; drug therapy ; Humans ; Hyponatremia ; Risk Factors ; Sodium ; blood ; Sodium Potassium Chloride Symporter Inhibitors ; adverse effects ; therapeutic use ; Sodium, Dietary

During treatment of acute heart failure (AHF), worsening renal function is often complicated and results in a complex clinical course. Furthermore, renal dysfunction is a strong independent predictor of long-term adverse outcomes in patients with AHF. Traditionally, the predominant cause of renal dysfunction has been attributed to impairment of cardiac output and relative underfilling of arterial perfusion. Recently, emerging data have led to the importance of venous congestion and elevated intra-abdominal pressure rather than confining it to impaired forward cardiac output as the primary driver of renal impairment. Relief of congestion is a major objective of AHF treatment but therapy is still based on the administration of loop diuretics. The results of the recently performed controlled studies for the assessment of new treatments to overcome resistance to diuretic treatment to protect kidneys from untoward effects have been mostly neutral. Better treatment of congestion in heart failure remains a major problem.
Cardiac Output ; Cardio-Renal Syndrome ; Estrogens, Conjugated (USP) ; Heart ; Heart Failure ; Humans ; Hyperemia ; Kidney ; Perfusion ; Sodium Potassium Chloride Symporter Inhibitors

Thiazide is known to decrease urinary calcium excretion. We hypothesized that thiazide shows different hypocalciuric effects depending on the stimuli causing hypercalciuria. The hypocalciuric effect of hydrochlorothiazide (HCTZ) and the expression of transient receptor potential vanilloid 5 (TRPV5), calbindin-D(28K), and several sodium transporters were assessed in hypercalciuric rats induced by high calcium diet and vitamin D3. Urine calcium excretion and the expression of transporters were measured from 4 groups of Sprague-Dawley rats; control, HCTZ, high calcium-vitamin D, and high calcium-vitamin D with HCTZ groups. HCTZ decreased urinary calcium excretion by 51.4% in the HCTZ group and only 15% in the high calcium-vitamin D with HCTZ group. TRPV5 protein abundance was not changed by HCTZ in the high calcium-vitamin D with HCTZ group compared to the high calcium-vitamin D group. Protein abundance of NHE3, SGLT1, and NKCC2 decreased in the hypercalciuric rats, and only SGLT1 protein abundance was increased by HCTZ in the hypercalciuric rats. The hypocalciuric effect of HCTZ is attenuated in high calcium and vitamin D-induced hypercalciuric rats. This attenuation seems to have resulted from the lack of HCTZ's effect on protein abundance of TRPV5 in severe hypercalciuric condition induced by high calcium and vitamin D.
Animals ; Calcium/therapeutic use/urine ; Calcium Channels/genetics/metabolism ; Cholecalciferol/*toxicity ; Hydrochlorothiazide/*therapeutic use ; Hypercalciuria/chemically induced/*drug therapy ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride Symporter Inhibitors/*therapeutic use ; Sodium-Glucose Transporter 1/genetics/metabolism ; Sodium-Hydrogen Antiporter/genetics/metabolism ; Sodium-Potassium-Chloride Symporters/genetics/metabolism ; TRPV Cation Channels/genetics/metabolism