Monday, August 31, 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.

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 

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.    

Friday, July 31, 2015

Journal Club: CAPTAIN TRIAL: ACEI /ARB pre cardiac cath: Hold or not to hold


There is unclear evidence on holding ACEi/ ARB prior to coronary angiography reduces contrast induced nephropathy (CIN). The CAPTAIN trail just published in the American Heart Journal was a randomized trial to investigate whether holding ACEi/ ARB prior to cardiac catheterization reduces the incidence of contrast-induced AKI in patients with chronic kidney disease (CKD).


Some key points:
Total of 208 patients underwent randomization over 6 years with CKD as defined - creatinine >1.7mg/dl w/in 3 months before  cardiac catheterization and/or serum creatinine > 1.5 mg/dl w/in 1 week before cardiac catheterization
Primary outcome: incidence of AKI defined as an absolute rise in Scr of >0.5 mg/dl from baseline and/or a relative rise in Scr of > 25% compared with baseline at any time between 48 and 96 hrs post-cardiac catheterization.
Secondary outcome: absolute difference in post-procedure creatinine compared with baseline creatinine
Safety outcome was a composite of CHF or hypertension after the procedure
Results of the study demonstrate that in patients with CKD, holding compared w/ continuing ACEi/ARB prior to cardiac catheterization, with-holding ACEi/ARB resulted in a:
1.       Non-significant reduction in contrast-induced AKI
2.       Significant reduction in post-procedural rise of creatinine.
3.       Study demonstrated a strong trend toward improved clinical outcomes when ACEi/ARB was held before angiography.
4.       No adverse events were reported in the hold ACEi/ARB group
5.       Safety: no rise in CHF or HTN with holding ACEi/ARB therapy

This randomized trial does suggest that in CKD patients, it might be beneficial to hold the ACEI/ARB pre cardiac cath for some potential benefit.  A larger N would have perhaps been important to do to get a better sense of this protective effect. A multi center study would have been useful as well. 

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