-Serum & Urine Immunofixation to identify the monoclonal Ig & also to monitor response to Rx
2. Serum Free Light Chain Assay to identify free light chains & to monitor hematological response to Rx in Light Chain-associated kidney disorders
There are 2 different LC assays: Binding site & N-Latex assay
-Use same assay to follow LC levels
3. If the Clone cannot be detected in serum or urine by SPEP/IF, UPEP/IF, sFLC assay then do Immunoblot Analysis of the serum & urine as it can detect small amounts of monoclonal immunoglobulins i.e. it is more sensitive
4. Mass Spectrometry Assays are very sensitive in detecting monoclonal light chains & MS assay may replace Immunofixation
-MS assays also distinguish b/w therapeutic antibodies (which may be picked on Immunofixation: False +) from endogenous M-proteins
5. Determine the nature of the detected clone
Bone Marrow Aspiration/Biopsy:
-Immunohistochemistry & Flow cytometry to analyze lymphocyte & plasma cell markers
-FISH panel for cytogenetic abnormalities
-Molecular Biology to look for mutations
6. If Clone is detected on Bone Marrow aspirate/biopsy & nature of the clone has been determined then determine tumor burden: CRAB criteria/CT/PET/MRI
7. If Clone is not detected on Bone marrow aspirate/biopsy:
-Flow cytometry of blood lymphocytes to detect small circulating clone
-Whole body imaging to detect localized plasmacytoma/low grade B-cell lymphoma
8. There are newer techniques that can be used for detection of small clones in patients with MGRS
The most anticipated nephrology trial of the year has been published!
“Empagliflozin in Patients with Chronic Kidney Disease” #Kidneywk
@NEJM nejm.org/doi/full/10.10…
EMPA-KIDNEY trial is a randomized, parallel-group, double-blind, placebo-controlled trial designed to assess the effect of empagliflozin on progression of kidney disease & CV disease, & to examine safety profile of the drug in a wide range of pts. w/ CKD
The trial included patients without diabetes, patients with an eGFR of less than 30 ml per minute per 1.73 m2, and patients with low levels of proteinuria
📌 Tweetorial on “IgA Nephropathy: Approach to treatment” based on @goKDIGO webinar by Dr. Richard Lafayette
🔸First step in management of IgAN: Determine the risk of disease progression based on GFR, proteinuria, BP & kidney biopsy findings👇🏽 1/
📌 Approach to treatment of IgAN based on @goKDIGO guidelines👇🏽
🔸This Rx algorithm is NOT applicable to IgA deposition with minimal change disease, IgAN with AKI, IgAN with RPGN, IgA vasculitis, IgA-dominant post-infections GN & secondary forms of IgAN👇🏽 2/
📌 IgAN: All patients should receive supportive care:
🔸 Optimal BP management
🔸 Maximally tolerated ACEi/ARB
🔸 Lifestyle modification
🔸 Reduction of cardiovascular
risk👇🏽
3/
📌 Tweetorial on Diagnosis & Pathogenesis of IgA Nephropathy (IgAN) based on @goKDIGO webinar by @AgnesFogo & Dr. Jurgen Floege #IgAN
🔸Interesting fact: IgAN is not a new disease
First known case of IgAN was found in Prince Joseph of Austria (1776-1847) 1/
📌 IgAN is characterized by:
🔸Mesangial immune-complex deposits which sometimes can extend to the capillary loops & sub-endothelial locations
🔸 Dominant IgA deposits compared to the other immunoglobulins 2/
📌 IgA deposits in IgAN are typically polyclonal & lambda is more prominent than kappa
Dr. Carlos Flombaum from @MSK_Neph gave a holiday lecture full of historic pearls. We are so lucky to have Dr. Flombaum in our division!
Did you know how Cisplatin was ‘accidentally’ discovered?👇🏽 1/
Did you know that allopurinol was first studied as an anti-neoplastic agent. Well, it didn’t work as a cancer therapy but it was eventually used to treat gout and hyperuricemia
2/
In the 1970s, the Renal division at @sloan_kettering was called the Division of Clinical Physiology. Not too surprising as we all know that to be a good nephrologist you have to know physiology
3/