Monday, August 31, 2015
Friday, August 28, 2015
Topic Discussion: Cocaine and the Kidney
Cocaine and it's effect on the kidney. A quick bullet point list of what cocaine can do to the kidney.
1. Acute renal failure due to Rhabdomyolysis
2. Renal infarction
3. Severe HTN and eventually chronic renal disease---> ESRD
4. TMA
5. Severe arterioscloerosis
6. Levamisol adulterated cocaine leading to ANCA vasculitis
Few nice reviews
http://ndt.oxfordjournals.org/content/15/3/299.full
http://www.ncbi.nlm.nih.gov/pubmed/15335299
http://www.nejm.org/doi/full/10.1056/NEJM200108023450507
1. Acute renal failure due to Rhabdomyolysis
2. Renal infarction
3. Severe HTN and eventually chronic renal disease---> ESRD
4. TMA
5. Severe arterioscloerosis
6. Levamisol adulterated cocaine leading to ANCA vasculitis
Few nice reviews
http://ndt.oxfordjournals.org/content/15/3/299.full
http://www.ncbi.nlm.nih.gov/pubmed/15335299
http://www.nejm.org/doi/full/10.1056/NEJM200108023450507
Labels:
cocaine,
drug toxicities,
topic discussions
Wednesday, August 26, 2015
Thursday, August 20, 2015
Consult Rounds: Scleroderma and the Kidney: Not just Renal Crisis
Scleroderma
and the Kidney: Not just Renal Crisis
Not all renal
failure in scleroderma is HTN related renal crisis. While renal TMA and
endothelial damage is a common cause of AKI in scleroderma, other interesting
cause to keep in mind is vasculitis.
Of all the
vasculitides, small vessel ANCA vasculitis is noted to be seen with
scleroderma.
A
study by Rho
et al. found 31 reports containing 63 cases of ANCA vasculitis with scleroderma up to 1994. Fifty of the 63 cases provided sufficient
clinical and laboratory information and were included in the analysis.
Eighty-four percent were women with a mean age of 57.1 years. Over 70% had ANA positive and 70% with
anti-Scl-70 antibody, and 72% with positive anti-MPO antibody. The most common
end-organ involvement included kidneys (82%) and lungs (70% had pulmonary
fibrosis). Mortality was highest in the first year.
A more recent review has
11 more cases that also were reported.
Most were females, all had anti MPO titers and 9 /11 cases had renal
involvement with crescentic GN.
These findings highlight the importance of considering
crescentic GN related to ANCA vasculitis as a potential cause of renal insufficiency
in scleroderma. Classically, scleroderma renal crisis occurs in up to 20% of
patients with diffuse scleroderma, and renal involvement manifesting as
hypertension, proteinuria, or azotemia can be found in 45–60%. However, causes
other than scleroderma renal crisis should be considered as a differential
diagnosis, especially in settings of normal blood pressure or ANCA positivity.
Labels:
Consult Rounds,
glomerular diseases,
rheumatology
Thursday, August 13, 2015
Onconephrology Textbook
I would like to introduce my first edited textbook on my topic of interest- onconephrology. The book is a question/answer board style material with all topics that relate to cancer and the kidney. The book ends with a list of concept maps that summarize few of the chapters.
Thank you to Springer for giving me this opportunity
Any comments welcomed
The link to the book on Springer's website
The link on amazon.com
Thank you to Springer for giving me this opportunity
Any comments welcomed
The link to the book on Springer's website
The link on amazon.com
Labels:
book,
concept maps,
onco nephrology
Friday, August 7, 2015
Drug induced renal injury:- a consensus classification.
A
recent article in KI 2015 discusses categorizing all drug induced AKI based on
certain types and following few strict guidelines. This ensures that the effect was clearly to a
culprit drug and gives an idea of type of injury.
1.
Phenotype description: Glomerular, tubular dysfunction,
AKI and nephrolithiasis/crystalluria
2.
Tubular dysfunction refers to RTA, Fanconis,
SIADH, DI, phosphate wasting
3.
AKI refers to ATN, AIN or osmotic nephrosis.
While not discussed in article- pre renal insult from pharmacologic agents
might be under this category as well
4.
The mechanism then is divided in two types A and
B. Type A reaction are dose dependent
toxicities and that are predictable based on drug exposure and pharmacology of
agent for example aminoglycoside. Type B
reaction is unpredictable such as AIN from PPI or any agent for the
matter. A Type B reaction in glomerular
category would be hydralazine or PTU induced lupus nephritis.
5.
Same drug can cause Type A or B reaction.
6.
Time course:
Acute ( 1-7 days), sub acute
(8-90 days) and chronic(>90 days).
7.
Setting: Hospitalized vs outpatient
setting. Outpatient setting drug injury
is the most missed type as not easy to recognize as compared to inpatient
setting as more reliable and easily visible data by consultants.
8.
The authors propose that drug induced kidney
injury meet the following criteria:
a.
The drug exposure must be 24 hours before renal
event
b.
Reasonable evidence for biological plausibility
for the casual drug
c.
Complete data( full medication list, biomarker
comparison)
d.
Strength of the relationship between attributable
drug and phenotype should be based on drug exposure and duration, extent of
primary and secondary criteria met and the time course of injury.
9.
Transient factors that affect change is important
to know- BP trends, infections, and medications that can alter hemodynamics
10.
Kidney biopsy should be used to define ATN vs
AIN or Gn to better get the phenotype.
11.
In patients with CKD, reference baseline crt
might be used to use as value to which crt might return back to. In cases of AIN, the crt may take much longer
to return to baseline—making it a sub acute injury.
12.
Tools such as the Naranjo scale can be used to
help guide but sometimes with multi drug exposure and other events, this might
be not that helpful.
13.
This is an interesting start to a common problem
we face. Sometimes biopsies are not that easy in the sick patient and guidance
tools as this paper might be useful.
Labels:
drug toxicities,
topic discussions
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