Pathophysiology Of Acute Kidney Injury Research Articles

Drug-resistant Salmonella Typhi induced kidney injury with rhabdomyolysis: A case report, and literature review

Salmonella Typhi (ST) is a rod-shaped gram-negative bacterium that infects humans via contaminated food or water. Humans are the only reservoirs for the bacteria. Infection usually manifests as fever, abdominal pain, and diarrhea. However, complications such as intestinal perforation, hepatosplenomegaly, and renal injury can occasionally occur. Acute kidney injury (AKI) is associated more commonly with ST than other bacteria causing gastrointestinal (GI) infections. The exact pathophysiology of AKI in ST infection is unknown. One of the rarely reported mechanisms is rhabdomyolysis. We present a similar case of resistant ST infection leading to AKI with rhabdomyolysis. This article also contains an extensive literature reviews of all reported ST bacteremia cases with AKI secondary to rhabdomyolysis.

COVID-19 and acute kidney injury.

The Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) started in December 2019 and has affected millions of lives worldwide, while many aspects of the illness are still unknown. Current data show that many hospitalized COVID-19 patients suffer from kidney damage, in the form of proteinuria, hematuria or acute kidney injury (AKI). AKI is especially prevalent among severe and critically ill COVID-19 patients and is a predictor of mortality. The pathophysiology of AKI in COVID-19 is unclear. Early reports of histopathologic examination from autopsied kidney tissue show SARS-CoV-2 viral particles in renal tubular cells and podocytes, suggesting direct viral infection, as well as findings of acute tubular necrosis, while rhabdomyolysis-associated AKI and glomerulopathies may also occur. As of today, only remdesivir has been authorized to treat COVID-19. Ongoing research investigates potential of anti-viral and anti-inflammatory agents along with safety and efficacy of commonly prescribed drugs such as renin-angiotensin-aldosterone system blockers. This review discusses the prevalence of AKI and its association with outcome, while highlighting possible mechanisms of AKI and suggesting organ protective measures to prevent the development of kidney damage.

Reversal of renal tissue hypoxia during experimental cardiopulmonary bypass in sheep by increased pump flow and arterial pressure.

Renal tissue hypoxia during cardiopulmonary bypass could contribute to the pathophysiology of acute kidney injury. We tested whether renal tissue hypoxia can be alleviated during cardiopulmonary bypass by the combined increase in target pump flow and mean arterial pressure. Cardiopulmonary bypass was established in eight instrumented sheep under isoflurane anaesthesia, at a target continuous pump flow of 80mL·kg-1min-1 and mean arterial pressure of 65mmHg. We then tested the effects of simultaneously increasing target pump flow to 104mL·kg-1min-1 and mean arterial pressure to 80mmHg with metaraminol (total dose 0.25-3.75mg). We also tested the effects of transitioning from continuous flow to partially pulsatile flow (pulse pressure ~15mmHg). Compared with conscious sheep, at the lower target pump flow and mean arterial pressure, cardiopulmonary bypass was accompanied by reduced renal blood flow (6.8±1.2 to 1.95±0.76mL·min-1kg-1) and renal oxygen delivery (0.91±0.18 to 0.24±0.11mL·O2 min-1kg-1). There were profound reductions in cortical oxygen tension (PO2) (33±13 to 6±6mmHg) and medullary PO2 (31±12 to 8±8mmHg). Increasing target pump flow and mean arterial pressure increased renal blood flow (to 2.6±1.0mL·min-1kg-1) and renal oxygen delivery (to 0.32±0.13mL·O2 min-1kg-1) and returned cortical PO2 to 58±60mmHg and medullary PO2 to 28±16mmHg; levels similar to those of conscious sheep. Partially pulsatile pump flow had no significant effects on renal perfusion or oxygenation. Renal hypoxia during experimental CPB can be corrected by increasing target pump flow and mean arterial pressure within a clinically feasible range.

A review on extracorporeal membrane oxygenation and kidney injury.

Extracorporeal membrane oxygenation (ECMO) is inevitable external life support in case of cardiac and respiratory failure since the 1970s. Acute kidney injury (AKI) and the requirement of renal replacement therapy (RRT) is a potential risk among these patients. This review aimsto give an overview of the risk of AKI, RRT, and associated mortality among the patients who received ECMO for any of its indications. PubMed database was searched to find the relevant literature and the reference list of included studies was also searched for additional studies. The incidence of AKI ranged from 30% to 78% and RRT from 47% to 60% in ECMO patients. The pathophysiology of AKI in ECMO is multifactorial,andincludes ischaemia, RBCs breakdown, comorbidity, conversion of zymogen form of pro-inflammatory mediators, structural alteration of the kidney, coadministration of nephrotoxic drugs, coagulation abnormality, and oxidative stress. ECMO was associated with the higher incidence of renal abnormalities, AKI, requirement of RRT, and associated mortality. Patients who underwentRRT had improved renal function and reduced overall mortality compared to the non-RRT group among the ECMO patients. Currently, there is no consensus evidence to support the superior use of the inline hemofilter system over continuous renal replacement therapy among patients who had AKI during ECMO.

Inhibition of p300 by Garcinol Protects against Cisplatin-Induced Acute Kidney Injury through Suppression of Oxidative Stress, Inflammation, and Tubular Cell Death in Mice.

Emerging evidence suggests that epigenetic mechanisms such as histone modification are crucially involved in the pathophysiology of acute kidney injury (AKI). The histone acetyltransferase p300 regulates several biological processes through the acetylation of histones or transcription factors. However, the role of p300 in cisplatin-induced AKI remains poorly understood. Therefore, we investigated the effects of garcinol, a potent p300 inhibitor, on cisplatin-induced AKI and explored the mechanisms. Administration of garcinol significantly reversed the upregulation of p300 and increased acetylation of histone H3, along with amelioration of renal dysfunction and histopathological injury in the kidneys of cisplatin-injected mice. Garcinol also attenuated oxidative stress and reduced expression of pro-oxidant enzymes. In addition, garcinol reduced the elevated production of cytokines and chemokines and suppressed immune cell accumulation together with downregulation of vascular adhesion molecules. These beneficial effects of garcinol were associated with a reduction in acetylation of the p65 subunit of nuclear factor kappa-B. Further, garcinol significantly inhibited apoptosis and caspase-3 activation, with a decrease in p53 acetylation in cisplatin-injected mice. Taken together, we demonstrated that the inhibition of p300 by garcinol ameliorated cisplatin-induced renal injury, presumably through epigenetic mechanisms. These results suggest that garcinol might be a potential preventive agent for cisplatin-induced AKI.

Acute Kidney Injury is Associated with Lowered Plasma-Free Thiol Levels.

Acute kidney injury (AKI) is associated with the abrupt loss of kidney function. Oxidative stress plays an important role in the pathophysiology of AKI. Free thiols (R-SH) are crucial components of the extracellular antioxidant machinery and reliably reflect systemic oxidative stress. Lower levels of thiols represent higher levels of oxidative stress. In this preliminary study, we hypothesized that plasma-free thiols are associated with AKI upon admission to the intensive care unit (ICU). In this study, 301 critically ill patients were included. Plasma samples were taken upon admission, and albumin-adjusted plasma-free thiols were determined. Albumin-adjusted plasma-free thiols were lower in patients with AKI (n = 43, median (interquartile range) 7.28 µmol/g (3.52, 8.95)) compared to patients without AKI (8.50 μmol/g (5.82, 11.28); p < 0.05) upon admission to the ICU. Higher age (B = −0.72), higher levels of neutrophil gelatinase-associated lipocalin (B = −0.002), creatinine (B = −0.01) and lower serum albumin (B = 0.47) were associated with lower free thiol levels. Further, albumin-adjusted free thiol levels were significantly reduced in patients with sepsis (8.30 (5.52–10.64) µmol/g) compared to patients without sepsis (6.95 (3.72–8.92) µmol/g; p < 0.05). Together, albumin-adjusted plasma-free thiols were significantly reduced in patients with AKI and patients with sepsis compared with patients without AKI and sepsis.

The endoplasmic reticulum stress and the unfolded protein response in kidney disease: Implications for vascular growth factors.

Acute kidney injury (AKI) and chronic kidney disease (CKD) represent an important challenge for healthcare providers. The identification of new biomarkers/pharmacological targets for kidney disease is required for the development of more effective therapies. Several studies have shown the importance of the endoplasmic reticulum (ER) stress in the pathophysiology of AKI and CKD. ER is a cellular organelle devolved to protein biosynthesis and maturation, and cellular detoxification processes which are activated in response to an insult. This review aimed to dissect the cellular response to ER stress which manifests with activation of the unfolded protein response (UPR) with its major branches, namely PERK, IRE1α, ATF6 and the interplay between ER and mitochondria in the pathophysiology of kidney disease. Further, we will discuss the relationship between mediators of renal injury (with specific focus on vascular growth factors) and ER stress and UPR in the pathophysiology of both AKI and CKD with the aim to propose potential new targets for treatment for kidney disease.

New imaging techniques in AKI.

Acute kidney injury (AKI) is a common complication in critically ill patients. Understanding the pathophysiology of AKI is essential to guide patient management. Imaging techniques that inform the pathogenesis of AKI in critically ill patients are urgently needed, in both research and ultimately clinical settings. Renal contrast-enhanced ultrasonography (CEUS) and multiparametric MRI appear to be the most promising imaging techniques for exploring the pathophysiological mechanisms involved in AKI. CEUS and MRI can be used to noninvasively and safely evaluate renal macrocirculation and microcirculation and oxygenation in critical ill patients. These techniques show that a decrease in renal blood flow, particularly cortical blood flow, may be observed in septic AKI and may contribute to its development. MRI may be a valuable method to quantify long-term renal damage after AKI that cannot currently be detected using standard clinical approaches. CEUS and multiparametric renal MRI are promising imaging techniques but more evidence is needed to show how they can first be more widely used in a research setting to test key hypotheses about the pathophysiology and recovery of AKI, and then ultimately be adopted in clinical practice to guide patient management.

New drugs for acute kidney injury.

To describe recent advances in the development of therapeutic agents for acute kidney injury (AKI). Traditional care for AKI is mostly supportive. At present, no specific therapy has been developed to prevent or treat AKI. However, based on a better understanding of the pathophysiology of AKI, various potential compounds have been recently identified and tested. A variety of pathways has been targeted, including oxidative and mitochondrial stress, cellular metabolism and repair, inflammation, apoptosis and hemodynamics. Many of these potential agents are currently ongoing early-phase clinical trials, and the purpose of this review is to provide a summary of those with the most potential. Despite the lack of therapies specifically approved for AKI, many interesting potential agents are entering clinical trials, with the potential to transform the care of patients with AKI.

Molecular pathophysiology of acute kidney injury: The role of sirtuins and their interactions with other macromolecular players.

Acute kidney injury (AKI), a rapid drop in kidney function, displays high mortality and morbidity, and its repeated or severe status can shift into chronic kidney disease or even end-stage renal disease. How and which events cause AKI still is controversial. In addition, no specific therapies have emerged that can attenuate AKI or expedite recovery. Some central mechanisms including tubular epithelial cells injury, endothelial injury, renal cell apoptosis, and necrosis signaling cascades, and inflammation have been reported in the pathophysiology of AKI. However, the timing of the activation of each pathway, their interactions, and the hierarchy of these pathways remain unknown. The main molecular mechanisms that might be complicated in this process are the mitochondrial impairment and alteration/shifting of cellular metabolites (e.g., acetyl-CoA and NAD+ /NADH) acting as cofactors to alter the activities of many enzymes, for instance, sirtuins. Moreover, alteration of mitochondrial structure over the fusion and fission mechanisms can regulate cellular signaling pathways by modifying the rate of reactive oxygen species generation and metabolic activities. The aim of this review is to better understand the underlying pathophysiological and molecular mechanisms of AKI. In addition, we predicted the main other molecular players in interaction with sirtuins as energy/stresses monitoring proteins for the development of future approaches in the treatment or prevention of ischemic AKI.

Pathophysiology and Pathology of Acute Kidney Injury in Patients With COVID-19.

Acute kidney injury (AKI) is common among hospitalized patients with Coronavirus Infectious Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. The variability in the occurrence of AKI has been attributed to the difference in geographic locations, race/ethnicity, and severity of illness. AKI among hospitalized patients is associated with increased length of stay and in-hospital deaths. Even patients with AKI who survive to hospital discharge are at risk of developing chronic kidney disease or end-stage kidney disease. An improved knowledge of the pathophysiology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who developed AKI during COVID-19. The goal of this article is to provide our current understanding of the etiology and the pathophysiology of AKI in the setting of COVID-19.

Acute kidney injury in cardiogenic shock: A comprehensive review.

Acute kidney injury (AKI) is an ominous predictor of mortality in cardiogenic shock. The present review examines the pathophysiology of AKI in cardiogenic shock (CS), summarizes the pertinent literature including the diagnostic criteria/definitions for AKI and possible role of biomarkers, and identifies risk factors and possible therapeutic interventions for AKI in CS. Our review finds that AKI is common in patients with CS and is associated with increased morbidity and mortality. Urinary biomarkers of renal tubular injury appear more sensitive for detection of AKI but have yet to be incorporated into daily practice. Emerging data would suggest vasopressor choices, mechanical circulatory support, and renal replacement therapy may have important therapeutic roles in the management of CS.

Knockdown of LncRNA DLX6-AS1 inhibits HK-2 cell pyroptosis via regulating miR-223-3p/NLRP3 pathway in lipopolysaccharide-induced acute kidney injury

Sepsis-induced acute kidney injury (AKI) represents a severe medical complication. Recently, there is growing evidence indicating the regulatory role of long non-coding RNAs (lncRNAs) in AKI pathophysiology. The present study investigated lncRNA DLX6 antisense RNA 1 (DLX6-AS1) expression in septic AKI patients and to decipher the relevant mechanisms underlying DLX6-AS1-mediated HK-2 cell pyroptosis in lipopolysaccharide (LPS)-induced AKI. The results revealed that DLX6-AS1 was up-regulated in the serum from septic AKI patients. DLX6-AS1 expression were positively associated with the creatinine levels in the serum from the septic AKI patients. In vitro studies showed that LPS induced cytotoxicity and enhanced DLX6-AS1 expression of HK-2 cells; increased NLR family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β and IL-18 expression. DLX6-AS1 overexpression promoted cytotoxicity and pyroptosis of HK-2 cells; while DLX6-AS1 knockdown counteracted the LPS-induced cytotoxicity and pyroptosis of HK-2 cells. More importantly, DLX6-AS1 sponged miR-223-3p resulting in repression of miR-223-3p expression in HK-2 cells. MiR-223-3p could bind to the 3' untranslated region of NLRP3, which results in the suppressed NLRP3 expression of HK-2 cells. Further rescue experiments showed that enhanced miR-223-3p expression partially reversed the cytotoxicity and pyroptosis of HK-2 cells upon LPS stimulation or with DLX6-AS1 overexpression. Conclusively, this study identified enhanced DLX6-AS1 expression in the serum from AKI patients. Further mechanistic findings deciphered that DLX6-AS1 mediated LPS-mediated cytotoxicity and pyroptosis in HK-2 via miR-223-3p/NLRP3 axis.

AKI: an increasingly recognized risk factor for CKD development and progression.

Acute kidney injury (AKI) is an increasing health burden with high morbidity and mortality rates worldwide. AKI is a risk factor for chronic kidney disease (CKD) development and progression to end stage renal disease (ESRD). Rapid action is required to find treatment options for AKI, plus to anticipate the development of CKD and other complications. Therefore, it is essential to understand the pathophysiology of AKI to CKD transition. Over the last several years, research has revealed maladaptive repair to be an interplay of cell death, endothelial dysfunction, tubular epithelial cell senescence, inflammatory processes and more-terminating in fibrosis. Various pathological mechanisms have been discovered and reveal targets for potential interventions. Furthermore, there have been clinical efforts measures for AKI prevention and progression including the development of novel biomarkers and prediction models. In this review, we provide an overview of pathophysiological mechanisms involved in kidney fibrosis. Furthermore, we discuss research gaps and promising therapeutic approaches for AKI to CKD progression.

Curcumin and LOXblock-1 ameliorate ischemia-reperfusion induced inflammation and acute kidney injury by suppressing the semaphorin-plexin pathway.

AimsIschemia/reperfusion (I/R) is one of the most important causes of acute kidney injury (AKI), a clinical syndrome with kidney dysfunction and high mortality rates. New diagnostic biomarkers need to be defined to better illuminate the pathophysiology of AKI. For the first time, we aim to investigate the protective effects of Curcumin which is known for its antioxidant and anti-inflammatory properties and 12/15 lipoxygenase inhibitor LOXblock-1 on I/R induced AKI by modulating inflammatory processes, oxidative stress, apoptosis and semaphorin-plexin pathway. Main methodsThe rats were divided into five groups, with eight animals per group: Sham, I/R, I/R + DMSO (1%, i.p.), I/R + Curcumin (100 mg/kg, i.p.), I/R + LOXblock-1 (2 μg/kg, i.p.). Key findingsThe renal function biomarkers (BUN, CREA and UA) in serum were significantly increased in the I/R group. The inflammatory (TNF-α, IL-6 and MCP-1), apoptotic (CYCS and CASP3) and oxidative stress parameters (MDA, MPO, TAS and TOS) measured by ELISA were significantly increased in the I/R group. In histopathological analysis, it was observed that I/R caused serious damage to kidney tissue. SEMA3A was found to increase both serum level and mRNA expression in I/R group. It was observed that curcumin and LOXblock-1 reduce inflammatory processes, oxidative stress and apoptosis via the semaphorin-plexin pathway by both measurements and histopathological analysis. Curcumin was proved more effective than LOXblock-1 with its antioxidant feature in I/R injury. SignificanceThe current study reveals the protective effects of Curcumin and LOXblock-1 on acute kidney injury by suppressing SEMA3A as a new biomarker.

Mortality and pathophysiology of acute kidney injury according to time of occurrence in acute heart failure.

AimsAcute kidney injury (AKI) during acute heart failure (AHF) is common and associated with increased morbidity and mortality. The underlying pathophysiological mechanism appears to have prognostic relevance; however, the differentiation of true, structural AKI from hemodynamic pseudo‐AKI remains a clinical challenge.Methods and resultsThe Basics in Acute Shortness of Breath Evaluation Study (NCT01831115) prospectively enrolled adult patients presenting with AHF to the emergency department. Mortality of patients was prospectively assessed. Haemoconcentration, transglomerular pressure gradient (n = 231) and tubular injury patterns (n = 253) were evaluated to investigate pathophysiological mechanisms underlying AKI timing (existing at presentation vs. developing during in‐hospital period). Of 1643 AHF patients, 755 patients (46%) experienced an episode of AKI; 310 patients (19%; 41% of AKI patients) presented with community‐acquired AKI (CA‐AKI), 445 patients (27%; 59% of AKI patients) developed in‐hospital AKI. CA‐AKI but not in‐hospital AKI was associated with higher mortality compared with no‐AKI (adjusted hazard ratio 1.32 [95%‐CI 1.01–1.74]; P = 0.04). Independent of AKI timing, haemoconcentration was associated with a lower two‐year mortality. Transglomerular pressure gradient at presentation was significantly lower in CA‐AKI compared to in‐hospital AKI and no‐AKI (P < 0.01). Urinary NGAL ratio concentrations were significantly higher in CA‐AKI compared to in‐hospital AKI (P < 0.01) or no‐AKI (P < 0.01).ConclusionsCA‐AKI but not in‐hospital AKI is associated with increased long‐term mortality and marked by decreased transglomerular pressure gradient and tubular injury, probably reflecting prolonged tubular ischemia due to reno‐venous congestion. Adequate decongestion, as assessed by haemoconcentration, is associated with lower long‐term mortality independent of AKI timing.

Activation of the renin-angiotensin-aldosterone system is associated with Acute Kidney Injury in COVID-19

The pathophysiology of acute kidney injury (AKI) in COVID-19 patients is still poorly understood. SARS-CoV-2 has been suggested to modulate the renin-angiotensin-aldosterone system (RAAS). In this series of COVID-19 critically ill patients, we report evidence of activation of the RAAS in COVID-19 patients with AKI.

P0023RNA-BINDING PROTEIN HUR REGULATES HYPOXIA-INDUCED PARKIN/BNIP3L EXPRESSIONS AND MITOPHAGY IN RENAL TUBULAR CELLS

Abstract Background and Aims Mitochondrial dysfunction contributes to the pathophysiology of acute kidney injury (AKI). Mitophagy selectively degrades damaged mitochondria and thereby regulates cellular function and homeostasis. RNA-binding proteins (RBPs) regulate RNA processing at multiple levels and thereby control cellular function. In this study, we report that RBP, human antigen R (HuR) regulates mitophagy in renal tubular cells (HK-2) under hypoxia condition. Method Human kidney proximal tubular 2 (HK-2) were cultured in Rosewell Park Memorial Institute (RPMI) 1640 medium (Gibco, Invitrogen, GmbH, Germany) supplemented with 10% fetal bovine serum (FBS) (Gibco, Invitrogen, GmbH, Germany), 1% penicillin/streptomycin (Gibco, Invitrogen, GmbH, Germany) at 37°C and 5% CO2. The cells were exposed to normoxia (37°C; 5% CO2) or hypoxia (serum and glucose deprived RPMI medium, 37°C, 1% O2) conditions. Mitophagy marker expressions (Parkin, p-Parkin, PINK1, BNIP3L, BNIP3, LC3) were determined by western blot analysis. ROS and mitochondrial membrane potential were determined using DCF-DA and JC-1 dye. Parkin and LC3 localization to mitochondria were performed by confocal laser scanning microscopy. HuR bound Parkin/BNIP3L mRNA expressions were determined by RNA-immunoprecipitation analysis. Results In this study, up-regulated mitophagy markers such as Parkin, PINK1, BNIP3 and BNIP3L protein expressions and mitophagosome formation were found in HK-2 cells under hypoxia condition. Stable HuR knockdown studies revealed that, HuR regulates mitophagy by mitophagosome (LC3 co-localization with mitochondria) and mitolysosome (mitochondria co-localization with lysosome) formation under hypoxia. Further, we show that HuR significantly regulated hypoxia-induced mitophagy by regulating Parkin/BNIP3L protein expressions and their mitochondrial localization. Bioinformatics studies showed that, HuR specifically binds to the AU-rich region in 3’UTR and CDS of Parkin and BNIP3L mRNA sequence. HuR was significantly bound to Parkin and BNIP3L mRNA and thereby regulated their mRNA stability under hypoxic conditions. Conclusion Altogether our data highlight on the functional importance of HuR in regulating mitophagy under hypoxic conditions in renal tubular cells through Parkin/BNIP3L expressions.

Novel biomarkers of acute kidney injury in children: an update on recent findings.

The clinical diagnosis of acute kidney injury (AKI) relies largely on changes in serum creatinine; a delayed biomarker. Research in children has been focused on developing novel AKI biomarkers, which can improve the prediction, early detection and diagnosis of kidney injury, as well as our understanding of AKI pathophysiology. In this review, we describe recently published studies on urine or blood biomarkers of AKI. The mechanistic relevance of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1, interleukin (IL)-18, liver-type fatty acid binding protein, tissue inhibitor of metalloproteinase (TIMP)-2/insulin-like growth factor-binding protein (IGFBP)-7, uromodulin, as well as other inflammatory biomarkers are discussed in the context of AKI pathophysiology, as well as their performance predicting or diagnosing AKI. Biomarkers of tubular injury, cell cycle arrest and inflammation are presented in this review. NGAL continues to be the most frequently studied biomarker and continues to have good performance in a variety of clinical settings, most notably after cardiopulmonary bypass. We also found promising results with less studied biomarkers for the prediction of AKI in children, including TIMP2, IGFBP7, uromodulin, tumor necrosis factor-α and IL-8. Identifying new AKI biomarkers is a priority in pediatric nephrology research because of the morbidity associated with AKI, as well as the lack of therapies for AKI. Recent research suggests that novel AKI biomarkers have the potential to predict the development of AKI and diagnose AKI earlier than changes in serum creatinine. The diverse causes of AKI, the different settings where patients develop AKI and the changing biomarker reference ranges throughout childhood remain challenges in biomarker development.

Covid-19 and kidney; a mini-review on current concepts and new data

In late December 2019, some cases of acute respiratory illness occurred in Wuhan, Hubei province, China that caused by a virus named "severe acute respiratory syndrome 2" (SARS-Cov2). More susceptible patients to this disease are elderly male patients since these patients with comorbid diseases are disposed to severe infection and more death. The most important comorbid diseases with COVID-19 pneumonia are hypertension, diabetes mellitus, cerebrovascular disease, chronic obstructive pulmonary disease, coronary heart disease. The most common symptoms of SARS-Cov2 infection are dyspnea, cough, fatigue, diarrhea and vomiting. High number of kidney disease in hospitalized patients with COVID-19 has been reported. Furthermore, a large group of patients with COVID-19 pneumonia had signs of kidney disease, with a high level of serum creatinine and blood urea nitrogen that could be justified with different pathophysiologies happened in COVID-19 pneumonia. However, massive differences were found in the prevalence of acute kidney injury (AKI) in patients with acute respiratory distress syndrome (ARDS) secondary to COVID-19 pneumonia, since various studies have shown that AKI correlates with higher mortality rate, upper morbidity and more severe cases of illness. Therefore, we should be informed about the pathophysiology of AKI in COVID-19 pneumonia to find the modalities to decrease the incidence of AKI and subsequent decrease mortality and morbidity of this disease.