Atrial Natriuretic Peptide for Management of Acute Kidney Injury

Nigwekar, Sagar U.; Navaneethan, Sankar D.; Parikh, Chirag R.; Hix, John K.

doi:10.2215/cjn.03780808

Cited by 88 publications

(51 citation statements)

References 41 publications

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“…Most of the prospective randomized controlled trials and 3 meta-analyses have not found any benefit associated with these agents [185][186][187][188].…”

Section: Rationalementioning

confidence: 99%

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Ichai

Vinsonneau

Souweine

et al. 2016

Anaesthesia Critical Care & Pain Medicine

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Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called "functional renal insufficiency" or "pre-renal insufficiency". This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, "renal insufficiency" seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.

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“…Most of the prospective randomized controlled trials and 3 meta-analyses have not found any benefit associated with these agents [185][186][187][188].…”

Section: Rationalementioning

confidence: 99%

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Ichai

Vinsonneau

Souweine

et al. 2016

Anaesthesia Critical Care & Pain Medicine

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“…22 A recent meta-analysis reveals that the administration of low-dose ANP may exert beneficial effects in clinical AKI. 23 We previously showed that chronic excess of BNP in mice prevents glomerular injury after subtotal nephrectomy, 24 and ameliorates proteinuria and histologic changes in immune-mediated renal injury 25 as well as in diabetic nephropathy. 26 In addition to exerting direct vasodilating and diuretic actions, natriuretic peptides act to antagonize the RAAS at multiple steps.…”

mentioning

confidence: 96%

Natriuretic Peptide Receptor Guanylyl Cyclase-A Protects Podocytes from Aldosterone-Induced Glomerular Injury

Ogawa

Mukoyama

Yokoi

et al. 2012

Journal of the American Society of Nephrology

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Natriuretic peptides produced by the heart in response to cardiac overload exert cardioprotective and renoprotective effects by eliciting natriuresis, reducing BP, and inhibiting cell proliferation and fibrosis. These peptides also antagonize the renin-angiotensin-aldosterone system, but whether this mechanism contributes to their renoprotective effect is unknown. Here, we examined the kidneys of mice lacking the guanylyl cyclase-A (GC-A) receptor for natriuretic peptides under conditions of high aldosterone and high dietary salt. After 4 weeks of administering aldosterone and a high-salt diet, GC-A knockout mice, but not wild-type mice, exhibited accelerated hypertension with massive proteinuria. Aldosterone-infused GC-A knockout mice had marked mesangial expansion, segmental sclerosis, severe podocyte injury, and increased oxidative stress. Reducing the BP with hydralazine failed to lessen such changes; in contrast, blockade of the renin-angiotensin-aldosterone system markedly reduced albuminuria, ameliorated podocyte injury, and reduced oxidative stress. Furthermore, treatment with the antioxidant tempol significantly reduced albuminuria and abrogated the histologic changes. In cultured podocytes, natriuretic peptides inhibited aldosterone-induced mitogen-activated protein kinase phosphorylation. Taken together, these results suggest that renoprotective properties of the endogenous natriuretic peptide/GC-A system may result from the local inhibition of the renin-angiotensin-aldosterone system and oxidative stress in podocytes.

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“…188 In a meta-analysis published in 2009, high-dose hANP did not significantly decrease mortality or the percentages of patients requiring hemodialysis, and was associated with an increased incidence of hypotension. 189 Alternatively, low-dose hANP did not increase the incidence of hypotension, or decrease the percentages of patients requiring hemodialysis. In summary, we recommend not using hANP for the treatment of CIN because it does not prevent the progression of kidney dysfunction.…”

Section: Rationale Cq X-4mentioning

confidence: 95%

Guidelines on the Use of Iodinated Contrast Media in Patients With Kidney Disease 2012

JSN¹

2013

Circ J

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Atrial Natriuretic Peptide for Management of Acute Kidney Injury

Cited by 88 publications

References 41 publications

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Natriuretic Peptide Receptor Guanylyl Cyclase-A Protects Podocytes from Aldosterone-Induced Glomerular Injury

Guidelines on the Use of Iodinated Contrast Media in Patients With Kidney Disease 2012

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