Monday, January 30, 2012
Friday, January 27, 2012
Thursday, January 26, 2012
take a look
Wednesday, January 25, 2012
WHICH OF THE FOLLOWING ARE POTENTIAL CAUSES OF DEATH IN DIABETIC KETOACIDOSIS(DKA?)
Underlying lesion and complications
All of the above
Diabetic Ketoacidosis is a common entity that we encounter often leading to ICU level of care. Standard treatment is usually volume expansion, insulin to stop ketoacid production. As you give therapy with fluids and insulin, plasma glucose will fall, HCO3 will rise but slowly, ketoacids will decline, anion gap will close, plasma K will decrease, Na will increase and Phos will decrease.
by Rossmark Medical Publishers, 2004, Ontario, Canada.
Monday, January 23, 2012
1959: Adams et al described CPM as a potential disorder. They found it in alcoholics and malnourished and chronically ill individuals. They called it "new disease" and no cases reported prior to those years.
1963: Aleu and Terry noted that perhaps an iatrogenic agents were involved and that it happened predominately in the hospital setting.
1966: More lesions identified and not localized to the Pons. It became evident by observation that all had chronic conditions such as liver disease, sepsis, burns, and cancer.
1977: Burcar et al identified 15 cases and 12 had hyponatremia. Overall, 61% of cases of CPM were associated with hyponatremia.
1979: Messert et al made the most important observation that CPM was recognized only after the advent of IV fluids therapy in the late 1950s. ( reminds us of the MRI and gadolinium association )
1979: Kevin Leslie, a pathology resident was doing an autopsy case of CPM in a jaundiced patient. He noticed a striking green discoloration in the PONS- likely secondary to breakdown of BBB leading to albumin bound bile pigment to get there. Review of literature confirmed this in many CPM cases.
1979: Scott Venderberg, pathology resident was reviewing a CPM case. He mentioned; " could this discoloration be due to osmotic stress?". This bought to light if the correction of the Na was the factor and not the Na itself.
1980-82: 15 cases of CPM with hyponatremia were reviewed and found that all 15 cases had experienced a 20-30meq/L rise in serum sodium in 3-10 days ( mean of 6 days) before CPM developed.
1982: Similar findings were confirmed in rats made hyponatremic and then given hypertonic saline quickly.
1984: patients with hyponatremia for a short period of time( hours to a few days) did not develop CPM but patients with chronic hyponatremia did.
This is a fascinating history and great discovery. This points to a great observation power of these individuals and putting it together and what is now common knowledge in the Nephrology world.
For a complete reference: http://www.ncbi.nlm.nih.gov/pubmed/20182780
Sunday, January 22, 2012
Friday, January 20, 2012
"Trends in Acute Nonvariceal Upper Gastrointestinal
Bleeding in Dialysis Patients".
in this study the authors shed some light on why Hemodialysis patients have higher recurrence and 30-day mortality of acute Non-varecial upper Gi bleeding. it's an interesting approach from an epidemiologic point of view where they site Lenient and stringent definitions, and other ways of looking at outpatient management of GI bleed and including those to the total tally. however; they offer some added risk factors that Hemodialysis patients are especially exposed to which may explain the high recurrent and mortality of upper GI bleed that they face. these include; "
Advanced age, male sex, and certain medications (such as
antiplatelet or anticoagulant agents".
of note; they mention that some of the reported increased in GI Bleed in these patients may be due to vigilant coding of these occurrence Because of the added financial incentive of reporting GI bleed under the new billing system.
for the full text go to JASN . http://jasn.asnjournals.org/content/early/2012/01/18/ASN.2011070658.full.pdf+html]
Interestingly, this study suggests that there might be no secondary role for treatment of Lupus with rituximab if MMF and steroids are being used. Steroids were not spared in the rituximab arm, so its hard to see what would have happened if there were no steroids. Also, authors state that the power was not strong enough for better outcomes.
Judge for yourself. Does anti CD20 agents have a future in Lupus Nephritis?
Wednesday, January 18, 2012
This should be a resourceful drug for our patients; especially those who receive intrathecall/IV MTX and get kidney injury where we often have to do dialysis due to the toxic levels; so potentially saving patients from dialysis and it's complications.
sFLT1 are elevated in placental vascular dysfunction and pre eclampsia. sFLT1 is produced by placental cytotrophoblasts but also monocytes and endothelial cells and it inhibits VEGF. This study is interesting as it showed that sFLT1 was elevated in patients with PR3 ANCA vasculitis and this was due to monocyte activation activating the alternate complement components. They were increased in anti GBM and anti MPO disease but not significantly as in patients with anti PR3 related disease when compared to controls in their experiment. Interestingly, postulated that anti sFLT1 agents might be useful.
Take a look at the full reference
Tuesday, January 17, 2012
Saturday, January 14, 2012
Friday, January 13, 2012
8. C-ANCA Positive, MPO ++:-Active MPA and sometimes CS or WG
Thursday, January 12, 2012
Wednesday, January 11, 2012
Tuesday, January 10, 2012
Monday, January 9, 2012
Friday, January 6, 2012
A 45 y old male with Membranous Nephropathy moved to Nepal and started living in a high altitude region. Which of these statements regarding his kidney function at high altitudes are true?
His proteinuria will decrease
His renal blood flow will increase by 8-20%
He shall excrete less bicarbonate
Hypoxia inducible factor 2alpha is stimulated and that leads to decrease erythropoietin production
He is at low risk for cardiac complications at high altitudes from his CKD
Acute hypoxia generates acute hypocapnia. Over several days, the kidneys increase bicarbonate excretion to compensate for this respiratory alkalosis, thereby blunting the inhibitory effect of respiratory alkalosis on the hypoxic ventilatory response and improving oxygenation over time at altitude.
Check out the two really good references:
Thursday, January 5, 2012
1. 1313 patients were evaluated( different diagnosis- membranous, IgA, FSGS)
2. 63 month follow up was noted
3. The risk of venous thromboembolism was highest in Membranous GN followed by FSGS compared to IgA Nephropathy.
4. Gender, cancer, proteinuria and serum albumin were adjusted.
5. So instead of degree of proteinuria - it was associated with a specific disease type such as Membranous GN.
6. Why is that? and if so do we need to give anti coagulation?
take a look at the free KI paper for full review:
Monday, January 2, 2012
Sunday, January 1, 2012
A. This anti CD25 human/ mouse chimeric antibody is almost devoid of side effects. It does not increase the risk for malignancies or infections.
B. This antibody has been used in a recent trial to facilitate positive crossmatch transplantation in living donors by blocking the effector pathway of antibody mediated allograft injury.
C. This agent is used to treat antibody mediated rejection and as induction in sensitized individuals. It decreased the production of anti-HLA antibodies by targeting the CD 20 receptor on B cells and plasma cells.
D. This antibody targets CD 52. It is FDA approved for the treatment of CLL. It is often used in minimization protocols for kidney transplantation.
E. This agent when used as an induction agent may increase the risk of cellular rejection.
F. This polyclonal antibody preparation targets many different receptors on T cells. It increases the risk of PTLD, and CMV compared to no induction or anti-CD25 induction. However, it has been shown to be a superior agent in reducing rejection episodes and prolonging graft survival especially in high risk individuals.
G. This polyclonal antibody preparation came from horses. It has since been largely replaced by another polyclonal T cell preparation.
H. This agent was a humanized monoclonal antibody that targeted the alpha chain of the IL-2 receptor of T-cells. The manufacturer discontinued its use in January 2009.
I. This monoclonal antibody against the T-cell receptor was the first such antibody used for any clinical indication in the United States. Its current use has been minimized due to severe adverse reactions including serum sickness and pulmonary edema.
Alemtuzumab: D Alemtuzumab is FDA approved to treat CLL. It targets CD 52 and results in B and T cell depletion. It has been used as an agent to facilitate steroid free transplantation, and had similar outcome to Thymoglobulin in the recent INTACT trial (N Engl J Med. 2011 May 19;364(20):1909-19. PMID: 21591943).
Rituximab: E Rituximab is a monoclonal anti-CD 20 antibody that targets B cells. It has been used to treat antibody mediated rejection and in desensitization protocols. It does not however, target plasma cells (which is why answer C is incorrect). In non-sensitized patients, Clatworthy et al. found the risk of cellular rejection to be much higher when using rituximab as an induction agent compared to dacillizumab (83% vs. 14%) (N Engl J Med. 2009 Jun 18;360(25):2683-5. PMID: 19535812).
Thymoglobulin: F Thymoglobulin is the most common induction agent used in the USA. It is created by immunizing rabbits with human thymus. This results in a potent polyclonal T cell depleting agent which reduces the risk of rejection but also increases infectious and malignant complications.
Basiliximab: A Basilizimab and Daclizumab have been shown to reduce the risk of rejection in the first year post transplant (Lancet. 1997 Oct 25;350(9086):1193-8 PMID: 9652559). The anti-rejection effect is not as potent as anti-lymphocyte globulin however, basiliximab does not increase the risk for infections or malignancy.
Atgam: G Atgam has been largely replaced by Thymoglobulin in the U.S.
Eculizumab: B A recent trial by Stegall et al. found Eculizumab to help abrogate a positive flow cytometry crossmatch in living donor kidney transplantation(Am J Transplant. 2011 Nov;11(11):2405-13. PMID: 21942930). It is FDA approved to treat paroxysmal nocturnal hemoglobinuria (PNH) and works by blocking complement component C5.
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