Wednesday, April 21, 2021
Here is a schematic of what we know for now in 2021 in relation to anti cancer agents leading to low phosphorus. This was made using biorender.com and inspired by the article Adhikari et al.
Wednesday, April 14, 2021
Hydralazine- you can love or hate as a nephrologist. Hydralazine is used a lot for both inpatient and outpatient setting my several internists, cardiologists and nephrologists for management of blood pressure. In clinical practice, many times we have noticed vasculitis from hydralazine : both of the lupus or the ANCA kind. Drug induced kidney diseases are important to keep in mind when the clinical picture doesn't make any sense.
See this exhaustive table from Izzedine and Ng in the recent Kidney News issue on drug induced glomerular diseases.
A recent study in KI just focused on hydralazine induced ANCA vasculitis and looked at 80 patients.
As suspected, the clinical clues are: many have low complements, +ANCA( both p and c in some cases- 40%), ANA and anti histone positive and even dsDNA positive. When you see several auto antibodies come back positive- think drug induced. Treatment is cessation of the agent and treat like regular vasculitis.
Check out an old detective nephron from 2013 on this topic.
Saturday, March 20, 2021
Sunday, March 14, 2021
At recent ASN Kidney Week 2020, Dr. Amir Kazory really gave a great lecture highlighting the importance of an important ion that often is ignored in CHF and Cardio-renal syndrome.
We should perhaps move away from the Na centric view of CHF.
Some interesting points made in his talk and overall what we know.
1. Hyponatremia is a predictor of CHF outcomes. But when we correct the Na, mortality doesn't improve. - classic V2R antagonist EVEREST trial showed no benefit
2. When we give 3% saline as shown by the Yale group recently in JACC, there is significant weight loss in diuretic resistant patients.
3. The Na restriction in diet has limited evidence that it works
Some interesting data on Cl in CHF.
Contemporary advanced CHF cohort suggest that serum chloride levels at admission are independently and inversely associated with mortality in this one study. The prognostic value of serum sodium in CHF was diminished compared with chloride.
Why does this matter?
Two physiological reasons:
1. Low Chloride can stimulate renin release in macula densa
2. Low intracellular chloride can increase TAL NKCC activity and DCT NCC activity
Interestingly, low chloride patients are also diuretic resistant.
It would be fascinating to see if increasing Cl, without Na really has a good effect on diuresis. Azetazolamide trials are ongoing as a potential way to do this. Could SLGT2i be potentially working via this mechanism? It is very possible that Cl is a more important player than Na in CHF and Cardio-renal syndrome. Fascinating!!
Check out this excellent review. ( also for figure source)
Saturday, March 6, 2021
A recent study published in Kidney International looked at a single health system 4 hospital admissions of AKI with COVID19 and MISC in children in NY. It was during the first wave in 2020.
Over 150 patients met inclusion criteria; 97 (63.8%) with acute-COVID-19 and 55 (36.2%) with MIS-C, AKI occurred in 11.8% of the cohort; 8 with acute-COVID-19 and 10 with MIS-C. All but one patient with AKI were admitted to a pediatric intensive care unit (PICU). There was no significant difference in age, or ethnicity in those with and without AKI. Those who identified as black had 2.86 times higher odds of AKI (p=0.042; 95%CI 1.04-7.93).
Majority of AKI occurred early in
the course of hospitalization, 72% (N=13) within 24 hours of admission. MIS-C patients with AKI had greater
rates of systolic dysfunction, compared to those without AKI (80% vs 49%, p=
Strengths of this study: One of the largest, detailed cohorts of pediatric patients at the epicenter of the COVID-19 outbreak and represents a diverse racial, ethnic and socioeconomic population.
AKI, in unadjusted models, was associated with a lower serum albumin level (OR 0.17)and higher white blood cell counts (OR 1.11). In addition, patients with AKI had 8.4 day greater length of stay. Major Limitations: 1. Small sample size precluded adjustment for confounders 2. As this was an observational study, we are unable to determine causal associations. 3. Single health system/region of the country
Similar to reports in other PICU patients, pediatric COVID-19-related AKI was associated with longer lengths of stay published in Kidney360 also from NY area. In that study, 57 children who met inclusion criteria, 46% (26/57) were found to have AKI. All patients had resolution of AKI at discharge, with 61% achieving recovery by day 2. One patient required dialysis. When compared to those without renal injury, the AKI cohort was older (p < 0.001) and with higher median peak values of CRP (p <0.001), IL-6 (p <0.05), ferritin (p < 0.001), and procalcitonin (p <0.05). More patients with AKI had left ventricular systolic dysfunction (p < 0.001) and lymphopenia (p <0.01), when compared to those without AKI. No differences in Body Mass Index or sex were found.
These findings may reflect the inflammatory cascade’s complex role in development and perpetuation of COVID-19 related AKI. In addition, decreased intravascular volume and distributive/cardiogenic shock may have contributed to AKI in the MIS-C cohort.
Check out the tweetorial by Abby Baselely
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