Nephrotoxicity from Chemotherapy There are many different mechanisms of nephrotoxicity from chemotherapeutic drugs. These include indirect and direct renal toxicity. Indirect mechanisms Prerenal AKI due to hypovolemia from chemo induced nausea, vomiting, and diarrhea Ischemic acute tubular necrosis (ATN) from neutropenic sepsis or cytokine release syndrome (seen in CAR-T therapy) Direct mechanisms Nephrotoxic
Arteriovenous access is the preferred access for hemodialysis (as opposed to use of a catheter). There are 2 types of arteriovenous access Arteriovenous fistula (AVF) - native artery transposed to native vein. Native vein hypertrophies under increased arterial pressure. This becomes fistula. This is the preferred dialysis access (over both catheters and arteriovenous
Membranous nephropathy is an important cause of nephrotic syndrome in adults. This condition is exciting in nephrology because the pathogenic antibody for the majority of cases of primary idiopathic membranous nephropathy has been discovered. This is the phospholipase A2 receptor (PLA2R) antibody. Clinical Presentation Often presents as full blown nephrotic syndrome with severe
Two parts of trusting your gut: If something doesn’t make sense it probably isn’t right. Take a step back and look again. Don’t go along with something you don’t believe. What is the FeNa? The FeNa is the percent of sodium filtered by the kidneys (glomeruli) that is excreted in the urine. What
Dialysis access is the lifeline for patients on dialysis. The goal is to have a durable arteriovenous access (ideally an arteriovenous fistula). However, this is not always possible. The majority of patients initiate dialysis with a catheter and there may be complications that impair the use of the arteriovenous access in prevalent patients.
FSGS is a pathologic description meaning a part (segment) of some of the glomeruli (focal) are scarred (sclerosis). Since scarring is the end result of most glomerular injury, anything that is severe enough for long enough will end up causing sclerosis. It’s like minimal change disease, but worse. It is a more common
This is a topic that is often given as a reason by students and residents for choosing a nephrology elective, wanting to understand acid base disorders. There are multiple ways to assess acid base status. Physiologic Approach Base Excess Approach Stewart Method Nephrologists use the Physiologic approach. What is this? There is an
How do we decide the treatment time or duration of dialysis? How do we assess if a patient is getting sufficient dialysis? Dialysis adequacy refers to the clearance of uremic toxins. Although we use BUN, creatinine and eGFR to assess the degree of kidney function, we don’t use these parameters to assess the
Minimal change disease is a glomerular disease that causes nephrotic syndrome and the first one I’ll be reviewing in this series. Called minimal change as the glomeruli look normal (there are minimal glomerular changes) on light microscopy. Also referred to NIL disease, not sure why they called it that. NIL might be an
Just like in hyperkalemia A useful framework for evaluating nephrology electrolyte issues like hypokalemia is: Too little in Cellular shifts Too much out Before we get to that there also can be artifactual hypokalemia. This happens when the potassium in the body is normal, but enters the cells ex vivo, in the collection
