Systematic review: The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence

Kellum, John A.

doi:10.1186/cc103

Cited by 85 publications

(4 citation statements)

References 52 publications

(90 reference statements)

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“…In terms of potential nephroprotective effects, researchers have previously attempted to use low dose dopamine (0.5–3 µg/kg/min) to increase renal blood flow and potentially protect the kidneys from cisplatin ( Kellum, 1997 ). The results of multiple studies were conflicting, and do not currently support the use of dopamine as a nephroprotectant ( Crona et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

The identification of dual protective agents against cisplatin-induced oto- and nephrotoxicity using the zebrafish model

Wertman

Melong

Stoyek

et al. 2020

eLife

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Dose-limiting toxicities for cisplatin administration, including ototoxicity and nephrotoxicity, impact the clinical utility of this effective chemotherapy agent and lead to lifelong complications, particularly in pediatric cancer survivors. Using a two-pronged drug screen employing the zebrafish lateral line as an in vivo readout for ototoxicity and kidney cell-based nephrotoxicity assay, we screened 1280 compounds and identified 22 that were both oto- and nephroprotective. Of these, dopamine and L-mimosine, a plant-based amino acid active in the dopamine pathway, were further investigated. Dopamine and L-mimosine protected the hair cells in the zebrafish otic vesicle from cisplatin-induced damage and preserved zebrafish larval glomerular filtration. Importantly, these compounds did not abrogate the cytotoxic effects of cisplatin on human cancer cells. This study provides insights into the mechanisms underlying cisplatin-induced oto- and nephrotoxicity and compelling preclinical evidence for the potential utility of dopamine and L-mimosine in the safer administration of cisplatin.

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Section: Discussionmentioning

confidence: 99%

The identification of dual protective agents against cisplatin-induced oto- and nephrotoxicity using the zebrafish model

Wertman

Melong

Stoyek

et al. 2020

eLife

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“…At low doses (i.e., 3 µg/kg/min) dopamine is vasodilatory and promotes diuresis primarily through the D-1 receptor and has beneficial effects in multiple models of AKI (121). Despite this, multiple studies have consistently demonstrated that renal-dose dopamine or the dopamine agonist fenoldapam, do not influence outcome of AKI in patients despite producing diuresis (45, 254, 255, 288, 560). Similarly, atrial natriuretic peptide can produce diuresis in AKI patients but does not provide any improvement in renal function or recovery (305).…”

Section: Pathophysiology Hemodynamics and Inflammationmentioning

confidence: 99%

Pathophysiology of Acute Kidney Injury

Basile

Anderson

Sutton

2012

Comprehensive Physiology

936

906

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Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.

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“…Diuretics have also been used in patients with oliguric AKI to improve urine output, which may decrease the concentration of toxins and improve clearance of solute and medications. It should be noted, however, that the increase in urine flow provided by diuretic therapy does not reflect an improvement in GFR, nor has it been demonstrated to prevent or facilitate recovery from acute tubular necrosis [177]. In addition, children with AKI may deteriorate further with diuresis, particularly patients with prerenal or radiocontrast-induced AKI [178].…”

Section: Diagnosis Treatment and Outcomementioning

confidence: 99%

Nephrotoxicity as a cause of acute kidney injury in children

2008

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Many different drugs and agents may cause nephrotoxic acute kidney injury (AKI) in children. Predisposing factors such as age, pharmacogenetics, underlying disease, the dosage of the toxin, and concomitant medication determine and influence the severity of nephrotoxic insult. In childhood AKI, incidence, prevalence, and etiology are not well defined. Pediatric retrospective studies have reported incidences of AKI in pediatric intensive care units (PICU) of between 8% and 30%. It is widely recognized that neonates have higher rates of AKI, especially following cardiac surgery, severe asphyxia, or premature birth. The only two prospective studies in children found incidence rates of 4.5% and 2.5% of AKI in children admitted to PICU, respectively. Nephrotoxic drugs account for about 16% of all AKIs most commonly associated with AKI in older children and adolescents. Nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, amphotericin B, antiviral agents, angiotensin-converting enzyme (ACE) inhibitors, calcineurin inhibitors, radiocontrast media, and cytostatics are the most important drugs to indicate AKI as significant risk factor in children. Direct pathophysiological mechanisms of nephrotoxicity include constriction of intrarenal vessels, acute tubular necrosis, acute interstitial nephritis, and-more infrequently-tubular obstruction. Furthermore, AKI may also be caused indirectly by rhabdomyolysis. Frequent therapeutic measures consist of avoiding dehydration and concomitant nephrotoxic medication, especially in children with preexisting impaired renal function.

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Systematic review: The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence

Cited by 85 publications

References 52 publications

The identification of dual protective agents against cisplatin-induced oto- and nephrotoxicity using the zebrafish model

The identification of dual protective agents against cisplatin-induced oto- and nephrotoxicity using the zebrafish model

Pathophysiology of Acute Kidney Injury

Nephrotoxicity as a cause of acute kidney injury in children

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