PATHOPHYSIOLOGY OF AKI IN COVID- 19 PATIENTS. AKI appears to involve a complex process driven by virus-mediated injury, cytokine storm, AngII pathway activation, dysregulation of complement, hypercoagulation, and microangiopathy interacting with common and known risk factors for AKI . There is paucity of data regarding clinical and laboratory characteristics of AKI in patients with COVID-19. We urge that further studies describing and analyzing the clinical course of patients with COVID-19 include appropriate indices of kidney function and diagnosis of AKI in their analyses, including kidney injury markers, urine microscopy, quantified urine protein, urine output, and urine electrolytes. Markers of macrophage activation, coagulation, microangiopathy, and complement activation, as well as kidney imaging and need for KRT (with relevant details), are important data needed to further our understanding of AKI pathophysiology associated with COVID-19. Rates of reversibility of, or partial improvement in, kidney function and any kidney biopsy results (including immunofluorescence and electron microscopy) should be reported. In the rush to report medical complications of COVID-19, we are missing valuable clinical information. Speculation about specific interventions would not be appropriate until we obtain appropriate information. We advocate for a complete and standardized appraisal of the clinical and laboratory picture so that preventative and therapeutic strategies for AKI can be appropriately designed and implemented.



Nice post Dr Parveen Yograj. This Covid 19 effects every organ in the body and cause multi organ failure and death. Sars Cov-2 could directly infect the human kidney tubules and induce cytoplasmic tubular inclusions, a feature observed in virus induced nephropathies although Sars Cov-2 RNA is not found in kidney. Direct viral infection and replication in kidney plays a vital role and leads to AKI and hypotension, decreased kidney perfusion secondary to hemodynamic or hemostatic factors or associated with sepsis. The main binding site of Sars Cov-2 is ACE2 protein which is expressed more in kidneys much more than the lungs . Regardless of direct viral infection of kidney , Ang2 is likely increased in acute lung injury. ACE 2 is down regulated in AKI. This may lead to type 1 Angiotensin receptor activation as well as decreased Angiotensin formation and subsequent worsening of AKI. Thus the patients with CKD especially those with DKD who develop Covid 19 may be at higher risk of AkI because of baseline upregulation of ACE and downregulation of ACE2 ,a combination that primes the proinflammatory and profibrotic state in the kidneys. More than 40% of patients with Covid 19 have abnormal proteinuria to AKI. AKI is considered as marker of Covid 19 severity and negative prognostic factor for survival. AKI in COVID 19 patients is reversible or not , don't know because of very limited studies. Most of the cases with AKI in COVID 19 cases require dialysis,and renal replacement therapy and carries poor prognosis. A lot of research is going on this dangerous pandemic COVID 19.

Valuable opinion

Sir there is no theory to stop or put new hypertensive cases on ace or ARB rather new concept has come up to continue Arbs as ace2 inhhlitbion is acceptable As conjugation of covid19 protein with ace 2 protein doesnot affect the Ace or ARB in circulation rathe it holds the conversion of ang1 to -7 I was just on webinar by ipca moderator dr Bhandari cardiologist sms medical college jaipur

Thank you doctor

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Is it advocable to hold ACE inhibitors at least in new HTN cases?

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Tole of ACE Inhabitors is best justified in Coved 19...

But sir as advocated by Dr Sandeep new patients should not be put on ACE inhibitors but patients who are already on ACE,inhibitors it should be continued

When the virus attacks the dynamic vital force tries to limit it to the least important organ of the organism, which may vary from person to person and that's why we see so many different systems getting affected. We even have found covid toes a skin condition in asymptomatic children. And many more can be correlated as the virus gets indigenous.

Thank you doctor @Dr. Parveen Yograj


Thank you doctor

Very informative .


Good information

Very informative and knowledgeable.

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