Friday, April 27, 2012
Thursday, April 26, 2012
In the News: It's not the kidney, It's the environment it's in!
A recent report in the NEJM describes a case of recurrent FSGS. A patient with FSGS was given a kidney from his sister and developed recurrent FSGS. Recurrent FSGS occurred within days after transplantation with over 10 grams of proteinuria. That kidney was removed and then re transplanted in another individual with known diabetic nephropathy. The kidney functioned very well and months out had normal renal function and no proteinuria.
This single case can be very enlightening in terms of the pathophysiology of FSGS post transplant. This might suggest that sUPAR is a major player. It enlightens us to the fact that the problem lies in the environment the kidney is placed in and not the kidney itself.
The once challenged thought of permeability factor causing FSGS is becoming more and more a reality of this disease entity.
This single case can be very enlightening in terms of the pathophysiology of FSGS post transplant. This might suggest that sUPAR is a major player. It enlightens us to the fact that the problem lies in the environment the kidney is placed in and not the kidney itself.
The once challenged thought of permeability factor causing FSGS is becoming more and more a reality of this disease entity.
Wednesday, April 25, 2012
Isotretinoin and the Kidney
Is Acutane (Isotretinoin) Nephrotoxic?
Post by
Acutane has been used for severe acne in cases. In certain dermatology practices, aside from monitoring serial pregnancy tests due to the severe teratogenicity of this product, they check monthly UA to monitor for proteinuria.
After a long literature search I found one letter to the editor, in NDT in 2000 describing a case of nephrotic syndrome(minimal change disease) in someone treated with acutane.
There was also mention that “mild proteinuria had been reported 60 times, in most cases with a temporal relationship. “ And they also stated that the “international product information lists proteinuria as a potential complication.” In the FDA product labeling, all I could find was to monitor “urine for white blood cells, proteinuria, gross or microscopic hematuria.”
But there are rat models which demonstrate some antiproliferative effects and amerioration of renal damage using these agents.
So should we be stopping our patients with proteinuria from taking this medication? Or can this medication be beneficial to our patients with chonic kidney disease?
Post by
Mala Sachdeva, MD
Monday, April 23, 2012
Clinical Case 55: Answers and Summary
WHICH TWO KIDNEY BIOPSY FINDINGS ARE MOST ASSOCIATED WITH CLINICAL FINDINGS OF CLL?
Friday, April 20, 2012
International Nephrology Education Foundation(INEF)
The international nephrology education foundation or INEF was founded in 2010 by Dr. Meguid El Nahas from United Kingdom. Its a charitable foundation to fund and support training, education and leadership in Nephrology and Medicine in emerging countries.
It is the same leadership as for the Global Kidney Academy website. Have a look at this excellent resource for many.
Thursday, April 19, 2012
Predictors of Membranous GN in cancer
The strongest predictors of cancer as a cause of Membranous GN are:
1. Smoking
2. Advanced Age
3. Leukocytic infiltration of the glomeruli( eight leukocytes per glomerulus has a sensitivity of 75% and specificity of 92%)
For an interesting case discussion regarding this, visit CJASN's attending Rounds on Nephrotic Syndrome in an older patient
1. Smoking
2. Advanced Age
3. Leukocytic infiltration of the glomeruli( eight leukocytes per glomerulus has a sensitivity of 75% and specificity of 92%)
For an interesting case discussion regarding this, visit CJASN's attending Rounds on Nephrotic Syndrome in an older patient
Wednesday, April 18, 2012
Diabetes with Icodextrin Peritoneal Dialysis: Hypo- or Hyper-glycemia?
A 56 year-old male with a past medical history of insulin-requiring DM2, hypertension and ESRD on peritoneal dialysis with icodextrin was hospitalized for viral gastroenteritis. His GI symptoms were improving with symptomatic management but his glycemic control was worsening, with random capillary blood glucose values ranging from 180 to 300 mg/dL. He was maintained on regular insulin coverage based on a sliding-scale, with subsequent capillary blood glucose values between 150-180 mg/dL. The patient complained of recurrence of vague GI symptoms, which were attributed to the primary diagnosis of viral gastroenteritis. On the third day of hospitalization, he developed seizures and a 'code' was called. Bedside capillary blood glucose was 90 mg/dL. His venous blood glucose was measured by the central laboratory as a part of the seizure work-up during the code, and was found to be 15 mg/dL. Administration of glucose led to resolution of his symptoms.
Point-of-care testing with standard glucometers used in hospitals (Accucheck) results in spurious elevations in blood glucose levels in icodextrin-treated patients. Icodextrin may be absorbed in the systemic circulation and is hydrolyzed into maltose and maltotriose. Maltose accumulates in the systemic circulation because humans are deficient in maltase. Many bedside glucometers like Accucheck use the glucose dehydrogenase with pyrroquinolinequinone (PQQ) in their test strips, which identify the free reducing group of glucose at the end of the maltose molecule and thus overestimate the blood glucose levels. This overestimation, however, is not seen with the glucometers based on the glucose-oxidase enzymatic system (One-touch)
Overestimation of blood glucose levels could mask true hypoglycemia, or can result in inappropriate administration of insulin, leading to hypoglycemia, and if severe, even death. Therefore, patients on PD with icodextrin should either undergo central laboratory determination of blood glucose or should be allowed to use their own home glucometers.
References:
Post by,
Ritu Soni, MD
University of Pittsburgh Medical Center
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