Acetazolamide and Hydrochlorothiazide Followed by Furosemide Versus Furosemide and Hydrochlorothiazide Followed by Furosemide for the Treatment of Adults With Nephrotic Edema: A Randomized Trial

Fallahzadeh, Mohammad Amin; Dormanesh, Banafshe; Fallahzadeh, Mohammad Kazem; Roozbeh, Jamshid; Sagheb, Mohammad Mahdi

doi:10.1053/j.ajkd.2016.10.022

Cited by 19 publications

(20 citation statements)

References 25 publications

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“…Most patients require high doses of diuretics owing to hypoalbuminaemia, expanded extracellular volume (larger volume of drug distribution) and a slower rate of delivery to the target cells within the kidney 210 . Thiazide diuretics or, alternatively, triamterene 211 or acetazolamide 212 can be combined with loop diuretics in patients with refractory oedema. As proteasuria activates the amiloride-sensitive epithelial sodium channel, amiloride can also be useful 213,214 .…”

Section: Complicationsmentioning

confidence: 99%

Podocytopathies

Kopp

Anders

Suszták

et al. 2020

Nat Rev Dis Primers

307

270

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Podocytopathies are kidney diseases in which direct or indirect podocyte injury drives proteinuria or nephrotic syndrome. In children and young adults, genetic variants in >50 podocyte-expressed genes, syndromal non-podocyte-specific genes and phenocopies with other underlying genetic abnormalities cause podocytopathies associated with steroid-resistant nephrotic syndrome or severe proteinuria. A variety of genetic variants likely contribute to disease development. Among genes with non-Mendelian inheritance, variants in APOL1 have the largest effect size. In addition to genetic variants, environmental triggers such as immune-related, infection-related, toxic and haemodynamic factors and obesity are also important causes of podocyte injury and frequently combine to cause various degrees of proteinuria in children and adults. Typical manifestations on kidney biopsy are minimal change lesions and focal segmental glomerulosclerosis lesions. Standard treatment for primary podocytopathies manifesting with focal segmental glomerulosclerosis lesions includes glucocorticoids and other immunosuppressive drugs; individuals not responding with a resolution of proteinuria have a poor renal prognosis. Renin-angiotensin system antagonists help to control proteinuria and slow the progression of fibrosis. Symptomatic management may include the use of diuretics, statins, infection prophylaxis and anticoagulation. This Primer discusses a shift in paradigm from patient stratification based on kidney biopsy findings towards personalized management based on clinical, morphological and genetic data as well as pathophysiological understanding.

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Section: Complicationsmentioning

confidence: 99%

Podocytopathies

Kopp

Anders

Suszták

et al. 2020

Nat Rev Dis Primers

307

270

View full text Add to dashboard Cite

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“…Combination therapy with metolazone, thiazides, or potassium sparing diuretics including the epithelial sodium channel blocker amiloride and the aldosterone antagonist spironolactone can enhance diuresis as compared with a loop diuretic alone and should be considered in patients with refractory edema [116]. However, patients need to be carefully monitored to avoid severe hypokalemia or hyperkalemia, volume depletion and alkalosis [117][118][119][120].…”

Section: Diureticsmentioning

confidence: 99%

IPNA clinical practice recommendations for the diagnosis and management of children with steroid-resistant nephrotic syndrome

et al. 2020

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Idiopathic nephrotic syndrome newly affects 1-3 per 100,000 children per year. Approximately 85% of cases show complete remission of proteinuria following glucocorticoid treatment. Patients who do not achieve complete remission within 4-6 weeks of glucocorticoid treatment have steroid-resistant nephrotic syndrome (SRNS). In 10-30% of steroid-resistant patients, mutations in podocyte-associated genes can be detected, whereas an undefined circulating factor of immune origin is assumed in the remaining ones. Diagnosis and management of SRNS is a great challenge due to its heterogeneous etiology, frequent lack of remission by further immunosuppressive treatment, and severe complications including the development of end-stage kidney disease and recurrence after renal transplantation. A team of experts including pediatric nephrologists and renal geneticists from the International Pediatric Nephrology Association (IPNA), a renal pathologist, and an adult nephrologist have now developed comprehensive clinical practice recommendations on the diagnosis and management of SRNS in children. The team performed a systematic literature review on 9 clinically relevant PICO (Patient or Population covered, Intervention, Comparator, Outcome) questions, formulated recommendations and formally graded them at a consensus meeting, with input from patient representatives and a dietician acting as external advisors and a voting panel of pediatric nephrologists. Research recommendations are also given.

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“…Anti-aldosterone drugs such as spironolactone and eplerenone should be avoided. Recently, acetazolamide and hydrochlorothiazide followed by furosemide have been reported to be more effective for the treatment of refractory nephrotic edema [ 18 ]. However, the influence of these treatments on acid–base disturbances in nephrotic syndrome should be further studied because acetazolamide induces metabolic acidosis by increasing urinary excretion of Na + and HCO 3 − .…”

Section: Discussionmentioning

confidence: 99%

Acid–base disturbances in nephrotic syndrome: analysis using the CO2/HCO3 method (traditional Boston model) and the physicochemical method (Stewart model)

et al. 2017

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BackgroundThe Stewart model for analyzing acid–base disturbances emphasizes serum albumin levels, which are ignored in the traditional Boston model. We compared data derived using the Stewart model to those using the Boston model in patients with nephrotic syndrome.MethodsTwenty-nine patients with nephrotic syndrome and six patients without urinary protein or acid–base disturbances provided blood and urine samples for analysis that included routine biochemical and arterial blood gas tests, plasma renin activity, and aldosterone. The total concentration of non-volatile weak acids (ATOT), apparent strong ion difference (SIDa), effective strong ion difference (SIDe), and strong ion gap (SIG) were calculated according to the formulas of Agrafiotis in the Stewart model.ResultsAccording to the Boston model, 25 of 29 patients (90%) had alkalemia. Eighteen patients had respiratory alkalosis, 11 had metabolic alkalosis, and 4 had both conditions. Only three patients had hyperreninemic hyperaldosteronism. The Stewart model demonstrated respiratory alkalosis based on decreased PaCO2, metabolic alkalosis based on decreased ATOT, and metabolic acidosis based on decreased SIDa. We could diagnose metabolic alkalosis or acidosis with a normal anion gap after comparing delta ATOT [(14.09 − measured ATOT) or (11.77 − 2.64 × Alb (g/dL))] and delta SIDa [(42.7 − measured SIDa) or (42.7 − (Na + K − Cl)]). We could also identify metabolic acidosis with an increased anion gap using SIG > 7.0 (SIG = 0.9463 × corrected anion gap—8.1956).ConclusionsPatients with nephrotic syndrome had primary respiratory alkalosis, decreased ATOT due to hypoalbuminemia (power to metabolic alkalosis), and decreased levels of SIDa (power to metabolic acidosis). We could detect metabolic acidosis with an increased anion gap by calculating SIG. The Stewart model in combination with the Boston model facilitates the analysis of complex acid–base disturbances in nephrotic syndrome.

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Acetazolamide and Hydrochlorothiazide Followed by Furosemide Versus Furosemide and Hydrochlorothiazide Followed by Furosemide for the Treatment of Adults With Nephrotic Edema: A Randomized Trial

Cited by 19 publications

References 25 publications

Podocytopathies

Podocytopathies

IPNA clinical practice recommendations for the diagnosis and management of children with steroid-resistant nephrotic syndrome

Acid–base disturbances in nephrotic syndrome: analysis using the CO2/HCO3 method (traditional Boston model) and the physicochemical method (Stewart model)

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