Just a month ago, I was on call at North Shore University Hospital in Manhasset and covering a census of >50 patients. It was a great mix of cases from AL amyloidosis, Anca vasculitis, Anti GBM, cardio renal syndromes, check pt inhibitor induced AIN, and several onconephrology electrolyte disorders. In addition, our center had also just done their first heart-kidney transplant recently and it was an amazing feeling.
Fast forward, a month later, I am on call again and I sense a census >60 and over 80% of those cases are COVID-19+ with either AKI or ESRD. What just happened here????
As the pandemic knocked the doors of NY, the hospital I have worked for 10 years now had turned into a different place. In the last 3 weeks, all surgeries were cancelled, all non elective admissions postponed... outpatient clinics slowing down.. and what do I see now..
I walk in and I can't recognize people. The make up and gel that people used to have is replaced by N95s and surgical masks. Nice suits,dresses all gone and replaced by scrubs and surgical gowns.
CT ICU, NS ICU, SICU, CCU and transplant ICU - are now all medical ICU beds.
ER is overflowing with COVID-19 patients.
ICU has vented patients from ages 31-83y of age, both males and females.
CRRT machines being deployed at almost every floor.
Surgical floors converted to medical COVID-19 floors. Only 4-5 floors remain as non COVID floors in the hospital...
Hallways are empty, cafe empty since no family is allowed....
This transformation -- just in 3 weeks. What a change.. Shock is an understatement.
What is more clear was the fear and anxiety in the eyes of the providers. People I used to see always joking around, making Trump Jokes, and laughing and smiling -- you could now sense fear in their voice.
Fatigue was evident in the nurses and ICU docs... but they were not giving up.
Renal consultations came every hour and it was all COVID-19 intubated patient in AKI, needing CRRT. It was pre renal, ATN, AIN, who knows-- we were just trying to save whoever we could...
The fellow and I scared to enter rooms, no time to even take a bathroom break and not sure how to even eat at the cafeteria.
Sadness, fear and anxiety was evident everywhere....1/3 of admitted COVID-19 patients end up in ICU, staying longer and longer stays ( 2 weeks) on a ventilator.. and what happens after that.. renal failure, cardiac failure.
But....what also was evident and most inspiring to me was...
Never before seen- working together of teams of residents and attendings ever imagined.
One of the covid-19 ICUS was headed by a surgical intensivists, vascular surgery attending, medicine residents, and pulmonary team helping out-- what amazing team work..
Then comes the NSICU, another converted COVID-19 unit- intensivists out of their comfort zone providing amazing medical ICU care to these COVID patients.
Finally, pediatric ICU docs coming to help the adult ICU patients- working hand in hand with pulmonary fellows, medical residents, neurology residents... amazing amazing!!
Kudos to the hospital management, CEO, CMOs, and department chairs to get this together in 2 weeks and creating this team work environment.
While the hospital is now a COVID-19 hospital and increasing number of ICU beds, everyone has stepped up outside their comfort zone and created history at our institution.
There are some wins-some patients coming extubated and many getting discharged.. While we may loose many, we are also saving many lives.. Kudos to our ER, hospital medicine and ICU staff and amazing nurses and health care providers...
Consults have become real, people are not calling "non needed' consults
Note writing has been minimized... and communication has improved.
While there is fear in everyone's eyes, we also sensed and felt a sense of pride to battle this war with our invisible enemy...
One of my Nephrology friends said it perfectly "This is literally a battle zone which we are dealing with. Quite honestly, for the most part could exhilarating. You are living history. Nothing has prepared us for this. Soak it in.... Hopefully, 40 years from now, you will be telling your grandkids how you served on the front lines of the great 2020 pandemic. You may never again have the opportunity to be involved in something more meaningful again."
Sunday, March 29, 2020
Wednesday, March 11, 2020
Topic Discussion: COVID-19 and hemodialysis patients
As we all learn more and more about COVID-19, the burning question in many nephrologists is the risk to patients on dialysis mainly in-center HD? While we all are developing guidelines of how to triage and place patients on in-center HD who have symptoms of COVID-19, what is their risk of severe infection vs. death from this virus compared to the general population?
So far, while we are still learning about the Italian, South Korean, Japanese experience, the only pre published data is from Wuhan, China dialysis units. Ma et al describe their experience and it is quite interesting what they found.
Brief summary of the study
1. It is a single HD unit epidemic course of infected patients compared to non infected and staff that were effected.
2. Of 230 HD patients, 37 were infected( 37%) and 2 medical staff of 33 staff members. During that time frame, the HD center had 7 deaths, 6 were COVID-19 positive patients. This made the mortality of 3%( higher than usual for that dialysis unit)
3. Presumed cause of death was hyperkalemia and cardiac events and not pulmonary cause
4. 62% were men, mean age 66 years.
5. 59% patients had bilateral CT scan involvement, 41% had unilateral findings
6. Serum levels of all cytokines measured( Il-4,6,10, TNF .etc) were lower levels compared to non HD patients with COVID-19
7. In their discussion, they do mention that the deaths were due to under-dialysis and hyperkalemia given the fear of contracting the virus-- interesting analysis.
8. Interestingly, none of the 37 patients in their center were admitted to the ICU due to severe PNA
9. The authors think that the HD patients don't mount a severe immune response and don't have that cytokine storm as seen in healthy adults leading to the "itis" leading to less organ damage.
This study is a start. More data from S.Korea, USA, Japan and Italy might help us in better information to decide on the care of the HD patient with COVID-19
Recently also, there is a case report published on HD patient treated successfully with anti virals in China in Kidney Medicine
So far, while we are still learning about the Italian, South Korean, Japanese experience, the only pre published data is from Wuhan, China dialysis units. Ma et al describe their experience and it is quite interesting what they found.
Brief summary of the study
1. It is a single HD unit epidemic course of infected patients compared to non infected and staff that were effected.
2. Of 230 HD patients, 37 were infected( 37%) and 2 medical staff of 33 staff members. During that time frame, the HD center had 7 deaths, 6 were COVID-19 positive patients. This made the mortality of 3%( higher than usual for that dialysis unit)
3. Presumed cause of death was hyperkalemia and cardiac events and not pulmonary cause
4. 62% were men, mean age 66 years.
5. 59% patients had bilateral CT scan involvement, 41% had unilateral findings
6. Serum levels of all cytokines measured( Il-4,6,10, TNF .etc) were lower levels compared to non HD patients with COVID-19
7. In their discussion, they do mention that the deaths were due to under-dialysis and hyperkalemia given the fear of contracting the virus-- interesting analysis.
8. Interestingly, none of the 37 patients in their center were admitted to the ICU due to severe PNA
9. The authors think that the HD patients don't mount a severe immune response and don't have that cytokine storm as seen in healthy adults leading to the "itis" leading to less organ damage.
This study is a start. More data from S.Korea, USA, Japan and Italy might help us in better information to decide on the care of the HD patient with COVID-19
Recently also, there is a case report published on HD patient treated successfully with anti virals in China in Kidney Medicine
Wednesday, March 4, 2020
Topic Discussion: COVID-19 and the Kidney
Coronavirus disease 2019 (COVID-19) causes a severe acute respiratory syndrome. Similar to SARS outbreak, this virus has caused the 2019-2020 outbreak. It presents with a dry cough, fever, running nose, fatigue and shortness of breath. The elderly, hx of pulmonary disease, immunocompromised are at risk. Mortality rate is around 2-3% from ongoing outbreaks.
How does this virus affect the Kidney. First and foremost, what is the data on transmission via dialysis units and infection in dialysis patients. Wuhan, China was where the outbreak occurred and started. In a single center study under open access review, 37 cases ( 16%) of HD patients were infected. 7 HD patients died and 6 had COVID-19 during this epidemic. The precaution measures taken by HD units prevented further cases. For some unclear reason, while HD patients were more likely to get this infection, the cases were milder than non HD counterparts.
Here is the ASN suggestions for HD units for COVID-19 screening and precautions.
What about AKI? Is it common? Again from Wuhan, in the month of the major outbreak in China, < 20 patients showed mild elevations in BUN and crt and trace albuminuria. 5 patients required CRRT.
All patients that had CKD after this survived. Moreover, SARS-CoV-2 RNA in urine sediments was positive only in 3 patients from 48 cases without renal illness before, and one patient had a positive for SARS-CoV-2 from 5 cases with CKD. Interpretation Acute renal impairment was uncommon in COVID-19. SARS-CoV-2 infection does not significantly cause obvious acute renal injury, or aggravate CKD in the COVID-19 patients.
Interestingly, another center reported a different finding. A large tertiary center in China studied 710 consecutive COVID19 patients, 89 (12.3%) of whom died in hospital. On admission, 44% of patients have proteinuria hematuria and 26.9% have hematuria, and the prevalence of elevated serum creatinine and blood urea nitrogen were 15.5% and 14.1% respectively. During the study period, AKI occurred in 3.2% patients. Kaplan-Meier analysis demonstrated that patients with kidney impairment have higher risk for in-hospital death. Cox proportional hazard regression confirmed that elevated serum creatinine, elevated urea nitrogen, AKI, proteinuria and hematuria was an independent risk factor for in-hospital death after adjusting for age, sex, disease severity, leukocyte count and lymphocyte count. Conclusion: The prevalence of kidney impairment (hematuria, proteinuria and kidney dysfunction) in hospitalized COVID-19 patients was high. After adjustment for confounders, kidney impairment indicators were associated with higher risk of in-hospital death. This was in strike contrast to the prior study.
Finally, hypokalemia was a common electrolyte finding in these patients. One would think GI cause as the cause, but GI symptoms were not associated with hypokalemia among 108 hypokalemia patients. Body temperature, CK, CK-MB, LDH, and CRP were significantly associated with the severity of hypokalemia. 93% of severe and critically ill patients had hypokalemia which was most common among elevated CK, CK-MB, LDH, and CRP. Urine K+ loss was the primary cause of hypokalemia.
How does this virus affect the Kidney. First and foremost, what is the data on transmission via dialysis units and infection in dialysis patients. Wuhan, China was where the outbreak occurred and started. In a single center study under open access review, 37 cases ( 16%) of HD patients were infected. 7 HD patients died and 6 had COVID-19 during this epidemic. The precaution measures taken by HD units prevented further cases. For some unclear reason, while HD patients were more likely to get this infection, the cases were milder than non HD counterparts.
Here is the ASN suggestions for HD units for COVID-19 screening and precautions.
What about AKI? Is it common? Again from Wuhan, in the month of the major outbreak in China, < 20 patients showed mild elevations in BUN and crt and trace albuminuria. 5 patients required CRRT.
All patients that had CKD after this survived. Moreover, SARS-CoV-2 RNA in urine sediments was positive only in 3 patients from 48 cases without renal illness before, and one patient had a positive for SARS-CoV-2 from 5 cases with CKD. Interpretation Acute renal impairment was uncommon in COVID-19. SARS-CoV-2 infection does not significantly cause obvious acute renal injury, or aggravate CKD in the COVID-19 patients.
Interestingly, another center reported a different finding. A large tertiary center in China studied 710 consecutive COVID19 patients, 89 (12.3%) of whom died in hospital. On admission, 44% of patients have proteinuria hematuria and 26.9% have hematuria, and the prevalence of elevated serum creatinine and blood urea nitrogen were 15.5% and 14.1% respectively. During the study period, AKI occurred in 3.2% patients. Kaplan-Meier analysis demonstrated that patients with kidney impairment have higher risk for in-hospital death. Cox proportional hazard regression confirmed that elevated serum creatinine, elevated urea nitrogen, AKI, proteinuria and hematuria was an independent risk factor for in-hospital death after adjusting for age, sex, disease severity, leukocyte count and lymphocyte count. Conclusion: The prevalence of kidney impairment (hematuria, proteinuria and kidney dysfunction) in hospitalized COVID-19 patients was high. After adjustment for confounders, kidney impairment indicators were associated with higher risk of in-hospital death. This was in strike contrast to the prior study.
Finally, hypokalemia was a common electrolyte finding in these patients. One would think GI cause as the cause, but GI symptoms were not associated with hypokalemia among 108 hypokalemia patients. Body temperature, CK, CK-MB, LDH, and CRP were significantly associated with the severity of hypokalemia. 93% of severe and critically ill patients had hypokalemia which was most common among elevated CK, CK-MB, LDH, and CRP. Urine K+ loss was the primary cause of hypokalemia.
Saturday, February 29, 2020
Nephrology Learning Bytes
A pathology report says in the IF section: LINEAR IgG stainingUsually the classic disease that is associated with that is
1) Anti GBM disease
But 2 other disorders can also have such staining
2) Fibrillary GN
3) Diabetic Nephropathy
Path image courtesy: Utah webpath
Sunday, February 2, 2020
Gender equality for invited speakers in Nephrology, comparing to other fields in medicine.
How does Nephrology do compared to other fields in Medicine in terms of female representation at academic conferences?
Here is a breakdown from articles all published in the last 2 years in medicine/surgery
In general medicine vs surgery, in one study 181 conferences with 701 individual meetings were analyzed, including 100 medical and 81 surgical specialty conferences. The proportion of women ranged from 0% to 82.6% of all speakers. The mean (SD) proportion of female conference speakers for all meetings analyzed significantly increased from 24.6% (14.6%) for 40 meetings in 2007 to 34.1% (15.1%) for 181 meetings in 2017 (P < .001). The mean proportion of female speakers at medical specialty conferences was 9.8% higher (SE, 1.9%; P < .001) than the mean proportion of female speakers at surgical specialty conferences for all years analyzed.
In dermatology, women spoke less than men at their main conferences.
In Anesthesiology, when studied in Canada, the representation of women speakers at the their annual meeting was similar to the representation of women in the anesthesiology workforce in Canada over the study period. Gender representation varied widely by subspecialty symposia, subject area, and women were absent from nearly half of all symposia at the annual meetings.
In General Surgery, women remain in the minority of panelists and moderators at their main meetings, and approximately 1 in 5 panels are composed entirely of men.
In Neurology, at Stroke conferences, women are less likely to be invited speakers.
In colo-rectal conferences, program representation of women was similar to meeting demographics, although with low numbers in some topics. An imbalance in the formality of speaker introductions between genders was observed. This introduction concern was also raised recently at ASCO(Oncology meetings)
Interestingly, at the Critical care conferences, Over the 7 years, Society of Critical Care Medicine had the highest representation of female (27% overall) and nursing/allied health professional (16-25%) speakers; notably, male physicians substantially outnumbered female physicians in all years (62-70% vs 10-19%, respectively)
In our analysis recently published in CJASN, time series analyses showed that the proportion of women moderators increased significantly by 3.5% per year (p=0.009, CI 1.2% - 5.9 %), and women speakers increased by 2.3% per year (p=0.001, CI 1.3% - 3.3%). This is impressive and kudos to nephrology leadership and association. Comparing to other specialities outside of internal medicine and within internal medicine( nephrology clearly is leading the way in terms of gender equality in invited speakers are conferences).
Here is a breakdown from articles all published in the last 2 years in medicine/surgery
In general medicine vs surgery, in one study 181 conferences with 701 individual meetings were analyzed, including 100 medical and 81 surgical specialty conferences. The proportion of women ranged from 0% to 82.6% of all speakers. The mean (SD) proportion of female conference speakers for all meetings analyzed significantly increased from 24.6% (14.6%) for 40 meetings in 2007 to 34.1% (15.1%) for 181 meetings in 2017 (P < .001). The mean proportion of female speakers at medical specialty conferences was 9.8% higher (SE, 1.9%; P < .001) than the mean proportion of female speakers at surgical specialty conferences for all years analyzed.
In dermatology, women spoke less than men at their main conferences.
In Anesthesiology, when studied in Canada, the representation of women speakers at the their annual meeting was similar to the representation of women in the anesthesiology workforce in Canada over the study period. Gender representation varied widely by subspecialty symposia, subject area, and women were absent from nearly half of all symposia at the annual meetings.
In General Surgery, women remain in the minority of panelists and moderators at their main meetings, and approximately 1 in 5 panels are composed entirely of men.
In Neurology, at Stroke conferences, women are less likely to be invited speakers.
In colo-rectal conferences, program representation of women was similar to meeting demographics, although with low numbers in some topics. An imbalance in the formality of speaker introductions between genders was observed. This introduction concern was also raised recently at ASCO(Oncology meetings)
Interestingly, at the Critical care conferences, Over the 7 years, Society of Critical Care Medicine had the highest representation of female (27% overall) and nursing/allied health professional (16-25%) speakers; notably, male physicians substantially outnumbered female physicians in all years (62-70% vs 10-19%, respectively)
In our analysis recently published in CJASN, time series analyses showed that the proportion of women moderators increased significantly by 3.5% per year (p=0.009, CI 1.2% - 5.9 %), and women speakers increased by 2.3% per year (p=0.001, CI 1.3% - 3.3%). This is impressive and kudos to nephrology leadership and association. Comparing to other specialities outside of internal medicine and within internal medicine( nephrology clearly is leading the way in terms of gender equality in invited speakers are conferences).
Tuesday, January 28, 2020
Concept map: Copeptin in Natremias
The above figure summarizes the best data on use of serum copeptin level for diagnosis of diabetes inspidus and primary polydipsia. Copeptin derives from the precursor protein of AVP and has been correlated well with AVP production
What about in cases of increased ADH- such as SIADH? Data on that is poor and only one large study of >200+ patients showed that in hypovolemic hyponatremia ( appropriate ADH), the copeptin levels were >84pmol/L ( spec 90%, sens 23%) and SIADH fell in the 10-30pmol/L categories( not helping much) and hypervolemic and diuretic induced fell in 30-65pmol/L category. Use of this test is currently not recommended in diagnosis of increased AVP production disorders.
Finally in patients with nephrogenic syndrome of inappropriate anti diuresis, copeptin levels were are low or suppressed.
This article is an excellent summary of the use of copeptin in Na related disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850413/
Monday, January 20, 2020
Topic Discussion: Hypertension and TMA- chicken or the egg?
A recent discussion on twitter and ASN Communities has sparked this age old battle if HTN related TMA exists? Some believe that TMA is the initial insult and that leads to endothelial damage and HTN is a symptom and not the disease. Some believe that HTN is the start - leading to sheer stress and endothelial damage and in severe cases-- TMA
Check out the amazing twitter discussion by TMA experts on this topic.
What i found was this amazing image
As one can see in this image- with some data existing on this - that malignant HTN can lead to endothelial dysfunction and some complement activation but not as severe as aHUS.
So if HTN does cause TMA, how does one distinguish that from a complement mediated TMA or aHUS? What if we are missing a mutation or an antibody that we haven't discovered.
1) Kidney biopsy cannot distinguish HTN induced TMA from complement mediated TMA 2) C3 being low is more valuable for an over active complement cascade compared to C5b-9 as even HTN can cause that to be elevated
3)) Doing a fundus exam can help significantly- there is no value in genetic testing in grade 3/4 retinopathy and especially with DBP>130mm Hg 4) No value in genetic testing in those that have a good response to bp control and eventually stabilized kidney function.
5) Ongoing TMA despite bp control and recovering of renal function- likely is then not HTN mediated and additional complement testing should be done.
Does having chronic or acute hypertension cause endothelial damage and TMA or does TMA cause endothelial damage and HTN as a result? @purvasharma821 @KidneyKhanin @VBijol @renalmyeloma @NephRodby @GlassockJ— Kenar Jhaveri (@kdjhaveri) January 15, 2020
Check out the amazing twitter discussion by TMA experts on this topic.
What i found was this amazing image
As one can see in this image- with some data existing on this - that malignant HTN can lead to endothelial dysfunction and some complement activation but not as severe as aHUS.
So if HTN does cause TMA, how does one distinguish that from a complement mediated TMA or aHUS? What if we are missing a mutation or an antibody that we haven't discovered.
1) Kidney biopsy cannot distinguish HTN induced TMA from complement mediated TMA 2) C3 being low is more valuable for an over active complement cascade compared to C5b-9 as even HTN can cause that to be elevated
3)) Doing a fundus exam can help significantly- there is no value in genetic testing in grade 3/4 retinopathy and especially with DBP>130mm Hg 4) No value in genetic testing in those that have a good response to bp control and eventually stabilized kidney function.
5) Ongoing TMA despite bp control and recovering of renal function- likely is then not HTN mediated and additional complement testing should be done.
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