CMAAO Coronavirus Facts and Myth Buster: Acute Kidney Injury |
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CMAAO Coronavirus Facts and Myth Buster: Acute Kidney Injury
Dr KK Aggarwal,  18 June 2020
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950: Update on COVID-19

IMA-CMAAO Webinar on “Acute kidney injury in COVID-19”

13th June, 2020, 4-5pm

Participants: Dr KK Aggarwal, President CMAAO; Dr RV Asokan, Secretary General IMA; Dr Ramesh K Dutta; Dr Jayakrishnan Alapat; Dr Uday Kakroo; Dr K Kalra; Mr Vivek Kumar; Mr Anil Ahuja; Mr Saurabh Aggarwal; Mr Dheeraj Kumar; Mr Sanjeev Khanna; Ms Ira Gupta; Ms Vandana Rawat; Dr Sanchita Sharma

Faculty: Dr SK Agarwal, Prof & Head, Dept. of Nephrology, AIIMS, New Delhi

This webinar was dedicated to Mr Sanjay Sharma, Asst. Manager - IT & Election Work, Indian Medical Association (IMA) who passed away due to COVID-19.

  • Acute kidney injury (AKI) is a sudden and sustained fall in the glomerular filtration rate (GFR), usually associated with high blood urea and creatinine, and fall in urine output. Most cases of AKI are potentially reversible.
  • AKI is important as it occurs in 3-20% of hospitalized patients and 20-60% of ICU patients; it increases length of stay in hospital as well as morbidity. Mortality is significantly increased. Even transient AKI is as deleterious as sustained AKI and adversely affects outcome.
  • The best accepted definition of AKI includes serum creatinine values and urine output.  Any one is sufficient to define AKI.
  • AKI is divided into three stages depending on the grading of damage. GFR is reasonably preserved in stage 1; the damage goes on increasing in stage 2 and 3.
  • Stage 1 is characterized by increase in serum creatinine of 0.3g/dL or change in urine output >0.5ml/kg/hour for more than 6 hours.In stage 2, the creatinine level increases more than 2-3-fold from baseline, while in stage 3, the rise in creatinine is >3-fold from baseline. When the urine output falls to less than 15 ml/hr in a 60 kg person (<0.3ml/kg/hour) for 24 hours, this is stage 3.
  • AKI is more common in males and advanced age; these points correlated with COVID-19 as we know that COVID is more common in males and prognosis is poor in the elderly.
  • Data from US, China and Europe shows that 20-35% of hospitalized patients have some degree of AKI. The major risk factors for AKI in COVID include pre-existing CKD, diabetes, male, African-American.
  • Patients hospitalized in ICU have more of stage 3 AKI and many of them require dialysis, whereas patients in wards have milder form of AKI and fewer of these patients require dialysis.
  • COVID patients with AKI have about 10 times higher mortality compared to those who do not have any kidney injury.
  • Retrospective data from New York hospitals in more than 5000 COVID-positive patients shows incidence of AKI to be 37%. Of these, 47% had stage 1 kidney injury, 31% had stage 3 kidney injury. Mechanical ventilation is a major risk factor, which correlates with development of AKI.
  • Predisposing factors for AKI per se: Advancing age, volume depletion, excessive use of diuretics, proteinuria, diabetes, pre-existing cardiac/renal failure; in COVID patients, advanced age, diabetes and pre-existing cardiac/renal failure are the risk factors.
  • Factors causing AKI: Combination of vascular injury causing vasoconstriction, tubular injury causing obstruction of passage, release of cytokines and cellular shedding. 
  • COVID causes direct injury to the kidney through direct viral invasion via the ACE2 receptors and the transmembrane serine protease TMPRSS2.  
  • Other mechanisms of pathogenesis of AKI in COVID patients are angiotensin system activation and renal vasoconstriction causing renal ischemia, release of cytokines (cytokine storm), hypercoagulability and microangiopathy (thromboembolism leading to renal infarction), hypoxia, hypotension; secondary sepsis due to secondary bacterial infection also causes kidney injury. COVID antigen has been demonstrated in kidney tubules in biopsy showing direct invasion of the virus in the kidney. 
  • Routine investigation in non-COVID AKI: History and physical examination, urine examination to assess proteinuria, imaging (USG), assess for pre-existing kidney disease (biochemical markers such as anemia, high phosphate, low bicarbonate), renal biopsy. Similar approach is adopted in COVID patients.
  • Biopsy is indicated to diagnose glomerulonephritis, confirm acute interstitial nephritis, evaluate prognosis in clinical acute tubular necrosis (if delay in recovery from ATN, patient may have cortical necrosis), for academic purpose (this holds true for COVID patients, as the mechanism of kidney injury is not yet understood).
  • COVID-19 associated collapsing glomerulonephritis has poor prognosis.
  • The New York-Northwell experience of kidney biopsy has shown ATN to be the most common pathology. But thrombotic microangiopathy, collapsing focal segmental glomerulosclerosis (FSGS), pauci-immune vasculitis and glomerulonephritis have also been demonstrated.
  • Management: Adequate nutrition, enough proteins and calories (CKD patients need protein restriction, but AKI patients do not need to restrict proteins), judicious use of fluids, vitamin C and zinc supplementation. Patients who do not respond to medical management may require intermittent dialysis.
  • Outcome of AKI: varies depending on the extent of kidney injury and other organ damage. Some patients may die in hospital, some recover partially, while some may have continuous need of RRT.
  • Poor prognosis: Advanced age, prolonged oliguria, sepsis, hypercatabolic state, ventilator, multiorgan failure
  • Majority of COVID patients present with asymptomatic urinary abnormalities (proteinuria, hematuria), 20-25% develop AKI, few patients may develop rhabdomyolysis and pigment nephropathy or thrombotic microangiopathy or glomerulonephritis (collapsing and crescent) or renal infarction. 
  • Earlier the use of antiviral drug in COVID patients, chances of response are better.


Dr KK Aggarwal

President CMAAO

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