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Tropical Medicine and Infectious Disease (TropicalMed). The nephrotoxicity of some antimicrobial
drugs is a common problem. The mechanism of the subsequent damage to renal tissue is not
understood fully but probably results from a combination of factors including hypoperfusion, haem-
catalysed free radical tubular cytotoxicity and haem cast formation and precipitation leading to
tubular injury. The natriuretic peptides have utility in AKI patients. We use cookies on our website to
ensure you get the best experience. The involvement of miR-155-5p in the pathophysiological
pathway to the development of diabetic kidney disease is probably explained by the signaling axis of
p53 and sirt1 genes with regulation of autophagic and fibrotic processes in renal tubular injury. Type
4 is applicable to a patient undergoing hemodialysis who also manifests congestive heart failure.
Monitoring fluid balance in acute kidney disease Maintaining appropriate fluid balance in AKI is a
critical component of the clinical management of the patient. The concentration of biomarkers and
the risk of death or need for dialysis treatment within 9 months, were the highest in the combination
group. Gout, Urate, and Crystal Deposition Disease (GUCDD). Journal of Experimental and
Theoretical Analyses (JETA). This highlights the importance of promoting effective decongestion in
patients with CRS1 and vascular congestion, regardless of AKI status. Rapid increases in serum
creatinine in the first few hours of surgery can help predict the development of AKI in the following
days. A comprehensive review describing pathophysiology and potential biomarkers of septic and
toxic acute kidney injury in septic patients was conducted. Previous Article in Journal Urinary Tract
Infection and Microbiome. All authors have read and agreed to the published version of the
manuscript. Note that from the first issue of 2016, this journal uses article numbers instead of page
numbers. Editors select a small number of articles recently published in the journal that they believe
will be particularly. The basic explanation of the pathophysiological pathway in septic AKI
development via activation of TLR-4 receptors in proximal tubular cells very likely lies in
dysregulation of tubular integrity, with induction of tight junction disruption. A number of factors
can contribute to AKI and progression to renal failure, including cardiovascular and hepatic
disorders, malignancies, hypovolemia, intoxication, drug nephrotoxicity, anemia and surgical and
vascular interventions. Drugs that inhibit the RAAS, such as angiotension converting enzyme
inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs), or block the production of
prostaglandins, such as non-steroidal anti-inflammatory drugs (NSAIDs), can pre-dispose to the
development of pre-renal AKI. Predicting who will develop this syndrome before surgery can
improve clinical management and prognosis. Many kidney and cardiac biomarkers have been
explored in this setting because the moment of renal insult is known during cardiac surgery. Various
other parameters should be monitored through the course of AKI. Acute Kidney Injury in Septic
Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A
Review. Int. J. Mol. Sci. 2020, 21, 7115. The vascular bed and development of acute tubular necrosis
Regional blood flow within the kidney varies, resulting in relatively hypoxic regions such as the
outer medulla. A wide variety of definitions for AKI are still used in the cancer literature, despite
existing guidelines on definitions and staging of AKI. Drugs that need monitoring or dose
adjustment owing to accumulation or other effects on the kidneys Analgesics Benzodiazepines,
opioids, tramadol. Conflicts of Interest The authors declare no conflict of interest. The
lipopolysaccharide inhibited the growth of animal podocytes besides the upregulation of XIST and
CUL3 and downregulated miR-15a-5p.
Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic
Agents—Pathophysiology and Biomarkers—A Review. European Journal of Investigation in Health,
Psychology and Education (EJIHPE). Several biomarkers have been identified, validated, and
incorporated into clinical practice, and their usefulness in predicting clinical outcomes is increasingly
being realized. Note that from the first issue of 2016, this journal uses article numbers instead of
page numbers. A meta-analysis evaluated the predictive capacity of different biomarkers (Kidney
injury molecule 1 (KIM1), NGAL, liver-type fatty acid-binding protein (L-FABP), and Cystatin C)
in the development of AKI after cardiac surgery. Common causes of each type of AKI are outlined
in Table 17.1. The kidneys are pre-disposed to haemodynamic injury owing to hypovolaemia or
hypoperfusion. International Journal of Environmental Research and Public Health (IJERPH). The
mechanism is unclear but enhanced by hypovolaemia and other nephrotoxic drugs NSAIDs
Vasodilator prostaglandins, mainly E 2, D 2 and I 2 (prostacyclin), produce an increase in blood flow
to the glomerulus and medulla. Acute Kidney Injury in Septic Patients Treated by Selected
Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review. However, severe
AKI, as defined by the requirement for dialysis treatment, is often associated with failure of one or
more non-renal organs (this is called multi-organ failure); in this setting there is a mortality rate of
70% in patients with sepsis and AKI and 45% in patients without sepsis. Biomarkers in CRS can be
grouped into biomarkers of function, which reflect glomerular filtration and integrity, biomarkers of
damage, and biomarkers of cell-cycle arrest ( Table 2 ). These include the drug targets and
mechanism of action of available agents; clinical goals and criteria for timing of intervention;
adaptation of therapy for specific clinical settings and measures required for monitoring
effectiveness and patient safety. This review covers the pathophysiology of vancomycin and
gentamicin nephrotoxicity in particular, septic AKI and the microRNAs involved in the
pathophysiology of both syndromes. Although overt fluid overload is often seen in AKI and may
prompt attention for the use of diuretics, often these agents are used in the absence of fluid
retention. Type 4 is applicable to a patient undergoing hemodialysis who also manifests congestive
heart failure. This article is an open access article distributed under the terms and conditions of the
Creative Commons Attribution (CC BY) license ( ). Journal of Low Power Electronics and
Applications (JLPEA). B-Type natriuretic peptide (BNP) and N-terminal-proBNP have become
essential diagnostic tools for evaluating patients who present with acute dyspnea. You can download
the paper by clicking the button above. Post-renal AKI is caused by obstruction of urinary flow
within the renal tract (e.g. owing to enlarged prostate, medicines that precipitate insoluble crystals or
kidney stones). Paper should be a substantial original Article that involves several techniques or
approaches, provides an outlook for. It has a highly negative impact on patient morbidity, mortality
and clinical outcome. We reviewed the literature on this topic and addressed four key questions for
the appropriate utilization of these agents. Two clinical trials have evaluated a diuretic strategy
guided by plasma concentrations of CA125 versus standard of care, resulting in significant
reductions in composite endpoints and improved kidney function. Most cases of FSNGN are caused
by anti-neutrophil cytoplasmic antibody-associated small-vessel vasculitis (SVV). Subscribe to
receive issue release notifications and newsletters from MDPI journals. However, the use of
biomarkers in CRS is still in its infancy, and further research is needed to establish their utility in
routine clinical practice. Petejova, N.; Martinek, A.; Zadrazil, J.; Kanova, M.; Klementa, V.; Sigutova,
R.; Kacirova, I.; Hrabovsky, V.; Svagera, Z.; Stejskal, D. Tropical Medicine and Infectious Disease
(TropicalMed).
Funding This research received no external funding. These include the drug targets and mechanism
of action of available agents; clinical goals and criteria for timing of intervention; adaptation of
therapy for specific clinical settings and measures required for monitoring effectiveness and patient
safety. It is extremely unusual for drugs to be responsible for post-renal AKI. Common causes of
acute tubular necrosis Table 17.2 shows a summary of some of the common factors encountered
clinically that may cause ATN. These precautions also apply to newer liposomal formulations
Immunosuppressants Ciclosporin and tacrolimus cause intra-renal vasoconstriction that may result in
ischaemic ATN. The most important receptor in septic AKI pathophysiology appears to be TLR-4,
that can bind the endotoxin lipopolysaccharide (LPS), leading to activation of a number of
intracellular signaling pathways via the nuclear-?B (NF-?B) transcription factor. Thus, it is plausible
that they play a crucial role in predicting declining kidney function among those with AHF. Acute
Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic
Agents—Pathophysiology and Biomarkers—A Review. Int. J. Mol. Sci. 2020, 21, 7115. However,
when the systolic blood pressure (BP) drops below 80 mmHg, AKI may develop. A meta-analysis
evaluated the predictive capacity of different biomarkers (Kidney injury molecule 1 (KIM1), NGAL,
liver-type fatty acid-binding protein (L-FABP), and Cystatin C) in the development of AKI after
cardiac surgery. AKI—acute kidney injury, GSTM1 —glutathione-S-transferase Mu 1 gene, IL-
6—interleukin 6, IL-1?—interleukin 1?, NF-?B—nuclear factor—kappa B, TNF?—tumor necrosis
factor alpha, TNIP2 —tumor necrosis factor alpha induced protein 3-interacting protein 2,
TLR4—Toll-like receptor 4. Other important causes of RPGN include Goodpasture’s disease, which
is caused by antibodies against glomerular basement membrane (anti-GBM antibodies), Systemic
lupus erythematosis (SLE) which usually affects young women and is more common with black
ethnicity, and secondary vasculitis are triggered by drugs, infection and tumours. Another
explanation of gentamicin nephrotoxicity is experimental evaluation of toxicity biomarkers through
specific gene expression associated with apoptosis or cell necrosis. Therefore, the serum
concentration of those substances normally excreted by the kidney will rise and differentially applies
to all molecules up to a molecular weight of around 50 kDa. The nephrotoxicity of gentamicin is a
very complex pathophysiological process with both tubular and glomerular involvement ( Figure 1 ).
We reviewed the literature on this topic and addressed four key questions for the appropriate
utilization of these agents. Of potential acute kidney injury (AKI) biomarkers, non-protein-coding
RNAs are a subject of ongoing research. Maintenance of renal blood flow then becomes more reliant
on the release of vasodilatory prostaglandins. Petejova, N.; Martinek, A.; Zadrazil, J.; Kanova, M.;
Klementa, V.; Sigutova, R.; Kacirova, I.; Hrabovsky, V.; Svagera, Z.; Stejskal, D. Biomarkers in CRS
can be grouped into biomarkers of function, which reflect glomerular filtration and integrity,
biomarkers of damage, and biomarkers of cell-cycle arrest ( Table 2 ). Hypovolaemia This results
from any condition that causes intravascular fluid depletion, either directly by haemorrhage or
indirectly to compensate for extravascular loss. All authors have read and agreed to the published
version of the manuscript. By definition, the worse the baseline kidney function, the smaller the
trigger required for the development of AKI. Journal of Functional Morphology and Kinesiology
(JFMK). Exosomal miR-155 promoted endotoxin-induced (LPS) inflammation in one study
(Alexander et al., 2015) by an increase in TNF. The development of AKI in this setting is more likely
to occur in people with pre-existing CKD. Experimental modulation of gene expression in salt-
sensitive hypertensive animals showed the important role of circular RNAs in the development of
hypertensive kidney injury. In the following section, we discuss the different biomarkers used to
predict AKI in cardiac surgery, ranging from the most affordable and available to the most novel and
experimental. Of 10 analyzed genes associated with apoptosis, in four, TP53, CASP3, CASP8 and
CASP9, an increase in expression was found. Immune and inflammatory renal disease The kidney is
vulnerable to a range of immunological processes that can cause AKI.