Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease

Sasongko, Teguh Haryo; Nagalla, Srikanth; Ballas, Samir K.

doi:10.1002/14651858.cd009191.pub2

Cited by 19 publications

(16 citation statements)

References 38 publications

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“…Thus earlier treatment, as assessed by treatment of 1-month- versus 3-month-old animals, had no benefit. This lack of benefit might be explained by existent kidney damage possibly being irreversible (Miller, et al 2010, Sasongko, et al 2015), with our 1-month-old mice at baseline having similar defective urine concentrating ability as our 3-month-old mice (see Materials and Methods , Sickle mice ). We regard this as unlikely considering that the normal mouse age span is about 2 years and so 1-month-old mice are about 3 years old in human years, assuming a normal human age span of about 80 years.…”

Section: Discussionmentioning

confidence: 92%

Sustained treatment of sickle cell mice with haptoglobin increases HO‐1 and H‐ferritin expression and decreases iron deposition in the kidney without improvement in kidney function

et al. 2016

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There is growing evidence that extracellular haemoglobin and haem mediate inflammatory and oxidative damage in sickle cell disease. Haptoglobin (Hp), the scavenger for free haemoglobin, is depleted in most patients with sickle cell disease due to chronic haemolysis. Although single infusions of Hp can ameliorate vaso-occlusion in mouse models of sickle cell disease, prior studies have not examined the therapeutic benefits of more chronic Hp dosing on sickle cell disease manifestations. In the present study, we explored the effect of Hp treatment over a three-month period in sickle mice at two dosing regimens: the first at a moderate dose of 200 mg/kg thrice weekly and the second at a higher dose of 400 mg /kg thrice weekly. We found that only the higher dosing regimen resulted in increased haem-oxygenase-1 and heavy chain ferritin (H-ferritin) expression and decreased iron deposition in the kidney. Despite the decreased kidney iron deposition following Hp treatment, there was no significant improvement in kidney function. However, there was a nearly significant trend towards decreased liver infarction.

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Section: Discussionmentioning

confidence: 92%

Sustained treatment of sickle cell mice with haptoglobin increases HO‐1 and H‐ferritin expression and decreases iron deposition in the kidney without improvement in kidney function

et al. 2016

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“…ACE inhibitors (ACEi) and Ang II receptor blockers (ARB) are routinely used for the control of nephropathy in diseases such as diabetes and chronic kidney disease (CKD) (Lambers Heerspink and de Zeeuw, 2013;Lewis and Maxwell, 2014) and a number of reports relate the use of these classes of drugs in SCD patients presenting albuminuria and proteinuria with a view to preventing evolution to CKD Fitzhugh et al, 2005;Foucan et al, 1998;Lima et al, 2008;Sasongko et al, 2013;Sharpe and Thein, 2011). Higher relative systemic blood pressure in SCD has been associated with an increased risk for pulmonary hypertension and renal dysfunction (Gordeuk et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Renal disease is frequently experienced by SCD patients, especially in older individuals Sasongko et al, 2013;Sharpe and Thein, 2014). Repeated cycles of ischemic injury in the kidney may cause chronic microvascular disease, causing hyperfiltration and proteinuria and potentially contributing to the onset of chronic kidney disease in some individuals (Sharpe and Thein, 2014).…”

Section: Introductionmentioning

confidence: 99%

Reduced plasma angiotensin II levels are reversed by hydroxyurea treatment in mice with sickle cell disease

et al. 2014

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“…55 Although this approach has not been vigorously tested in patients with SCD, 81 it is recommended on the basis of the general efficacy of these agents in CKD. Recommendations made by an expert panel in 2014 include the initiation of treatment with these agents in patients with microalbuminuria and macroalbuminuria, even when blood pressure is normal.…”

Section: Pathogenesis Of Scnmentioning

confidence: 99%

Sickle cell disease: renal manifestations and mechanisms

2015

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Sickle cell disease (SCD) substantially alters renal structure and function, and causes various renal syndromes and diseases. Such diverse renal outcomes reflect the uniquely complex vascular pathobiology of SCD and the propensity of red blood cells to sickle in the renal medulla because of its hypoxic, acidotic, and hyperosmolar conditions. Renal complications and involvement in sickle cell nephropathy (SCN) include altered haemodynamics, hypertrophy, assorted glomerulopathies, chronic kidney disease, acute kidney injury, impaired urinary concentrating ability, distal nephron dysfunction, haematuria, and increased risks of urinary tract infections and renal medullary carcinoma. SCN largely reflects an underlying vasculopathy characterized by cortical hyperperfusion, medullary hypoperfusion, and an increased, stress-induced vasoconstrictive response. Renal involvement is usually more severe in homozygous disease (sickle cell anaemia, HbSS) than in compound heterozygous types of SCD (for example HbSC and HbSβ+-thalassaemia), and is typically mild, albeit prevalent, in the heterozygous state (sickle cell trait, HbAS). Renal involvement contributes substantially to the diminished life expectancy of patients with SCD, accounting for 16–18% of mortality. As improved clinical care promotes survival into adulthood, SCN imposes a growing burden on both individual health and health system costs. This Review addresses the renal manifestations of SCD and focuses on their underlying mechanisms.

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Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease

Cited by 19 publications

References 38 publications

Sustained treatment of sickle cell mice with haptoglobin increases HO‐1 and H‐ferritin expression and decreases iron deposition in the kidney without improvement in kidney function

Sustained treatment of sickle cell mice with haptoglobin increases HO‐1 and H‐ferritin expression and decreases iron deposition in the kidney without improvement in kidney function

Reduced plasma angiotensin II levels are reversed by hydroxyurea treatment in mice with sickle cell disease

Sickle cell disease: renal manifestations and mechanisms

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