A landmark paper on membranous nephropathy was published by Beck et al in the most recent issue of NEJM. Ultimately we will have to see if the finding is reproducible, but based on the data presented this represents a major breakthrough in understanding the pathogenesis of membranous nephropathy and nephrotic syndrome.
There has long been strong evidence in support of a circulating factor which causes podocyte injury and resultant nephrotic syndrome. Additional evidence from the neutral endopeptidase story further suggested that an autoantibody directed again some podocyte antigen might be the culprit. In this issue, the researchers demonstrate that in 70% of patients with idiopathic membranous nephropathy (but 0% of patients with secondary membranous nephropathy or other forms of proteinuric kidney disease such as FSGS or diabetic nephropathy) contain an autoantibody against the podocyte antigen phospholipase A2 receptor. Furthermore, the autoantibody's presence appears to correlate with disease activity, suggesting a possible pathogenic role.
The work has a number of implications. First, it suggests that membranous nephropathy is indeed a separate disease than FSGS and other distinct forms of nephrotic syndrome. The common final pathway for proteinuria is the same (podocyte injury), but the ways in which to get there is likely different. Second, it suggests that detection of serum antibodies against phospholipase A2 receptor may be a useful part of the diagnostic workup for nephrotic syndrome--perhaps even making biopsies unnecessary--and perhaps could be used to follow disease activity in response to various therapeutic maneuvers. That is, this test may well become the "ANCA" of membranous nephropathy.
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ANCA of nembranous nephropathy
July 22, 2009
The Power of Pee?
Finally, I can sleep at night: scientists have discovered a way to turn urine into hydrogen. And you said I was crazy for collecting it in milk jugs!
From a group led by chemist Gerardine Botte of Ohio University comes a report (just published in the Royal Society of Chemistry's journal Chemical Communications) that hydrogen has been produced from urine.
According to a July 3, 2009 story on PhysOrg.com, "Urine's major constituent is urea, which incorporates four hydrogen atoms per molecule -- importantly, less tightly bonded than the hydrogen atoms in water molecules."
"Botte uses electrolysis to break the molecule apart, developing an inexpensive new nickel-based electrode to selectively and efficiently oxidise the urea. To break the molecule down, a voltage of 0.37V needs to be applied across the cell -- much less than the 1.23V needed to split water.
So, you know what this means, right? Wait for it....wait for it....the P-bomb. Thanks folks, I'll be here all week. Make sure to tip your bartender and maybe steal a bottle for me when they're not looking. *tap tap* Haha, is this still on?
Caveats for Using Renal Ultrasound to Diagnose Post-Renal Failure
Most would agree that the renal ultrasound is an invaluable tool in the workup of acute kidney injury. Although the renal ultrasound can give information regarding kidney echogenicity and presence of renal cysts, by and large its predominant utility is in determining the presence or absence of hydronephrosis, a marker for obstructive renal failure ("post-renal" failure when referring to the Holy Trinity of "pre-renal", "intrinsic renal", and "post-renal" categories of AKI).
However, there are important caveats to the use of the renal ultrasound to effectively rule-in or rule-out obstructive nephropathy. For instance, false-negatives (e.g., the renal ultrasound does not show hydronephrosis, but there actually is) can occur in the following scenarios:
1. very early obstruction: truly acute obstruction (e.g., with a kidney stone, for instance) may take some time to develop enough distension of the collecting system to detect with our current imaging tools.
2. obstruction in the setting of pre-renal failure: volume-depleted kidneys may not demonstrate significant hydronephrosis until after volume resuscitation, which expands the collecting system.
3. large retroperitoneal tumors: tumors which encase the kidneys may cause obstruction but not allow expansion of the collecting system enough to see hydronephrosis.
4. retroperitoneal fibrosis: this can occur in patients with past extensive GU surgery or prior chemotherapy or radiation therapy and can cause mechanical obstruction without allowing expansion of the collecting system.
In addition, false-positives (e.g., the renal ultrasound is read as "hydronephrosis" but this is probably not pathologic) can occur as well, most notably in pregnancy. It is also common that hydronephrosis detected on ultrasound is a chronic, long-standing issue and not the main culprit for the present episode of AKI.
This is taken from handout put up by Precious Body Fluids
Now a new study published in Circulation compared the blood pressure between individuals who ate vegetable protein (specifically glutamic acid along with 4 other amino acids which are relatively higher in vegetable than animal protein) with people who ate non-vegetable protein (read animal meat).
They found a difference of about -2.7/-2.0 mm Hg in blood pressure in people eating more vegetables. Although that may sound small, individual results may be different (and maybe higher for you).
H1N1 Death Rate Holds Steady
The latest update from the World Health Organization reveals the number of swine flu cases worldwide at 77,201—a nearly 50% increase from the June 22nd update. Deaths total 332 (up from 113) for an unchanged mortality rate of 0.43%.
H1N1 cases have now been reported in 120 countries or territories, and related deaths have occurred in 17. Countries disproportionately affected by new cases (where more than 500 cases have occurred) include Thailand, the United Kingdom, Brazil, Peru, and Spain. The number of swine flu deaths in the United States now surpasses those in Mexico.
Another Tool for anticoagulation
Medical management of T2DM
This review is a convenient reference and follows the “mainstream” recommendations. Note that the A1C target of 7%, which the authors advocate, is controversial number..