Nephsap review: Glomerular, vascular and TI disease

In Nephsap review we learned that cancer following cytoxan carries risk due to total dosing amount

low dose of cytoxan usually means < 36gm of total cumulative cytoxan exposure
( this is artbitary)
<36gm group most common cancers were non melenoma skin and basal cell cancers
>36gm group most common cancers were non melenoma skin and basal cell but also saw bladder cancers, AML( which happened after many years)

Nephsap review: Glomerular, vascular and TI disease

In reviewing IgA Nephropathy:
Did you know that besides the pathology related prognostic signs, non traditional factors such as obesity, elevated nocturnal BP and increased uric acid levels and increased C4d mesangial depostion have been associated with a poorer prognosis in igA Nephropathy.  A mild alcohol consumption and mild elevation in bilirubin with a improved outcome.
Interesting ! Likely due to anti oxidant effects of both

Transplant Glomerulopathy

Transplant Glomerulopathy(TG) is a common biopsy finding that we see in kidney biopsies for proteinuria workup.The causes of TG are usually of similar to what causes secondary MPGN. Most of the time it turns out to be chronic antibody mediated rejection process. Pathologically, it is  defined by glomerular basement membrane duplication with peritubular capillary basement membrane multilayering (PTCML), and associated with anti-human leukocyte antigen antibodies and C4d. 
A recent study in Transplantation 2010 issue talks about possible predictors of long term outcomes of pure TG cases. 36 cases were noted. Only 33% were c4D positive. but the  C4d-positive cases also showed a trend toward rapid graft loss. Interstitial fibrosis, PTCML, and arteriolar hyalinosis were significant predictors of graft survival in TG. C4d positivity was associated with a more rapid rate of function decline. eGFR slope data showed significant deterioration in graft function well before the diagnostic biopsy.


References:
http://www.ncbi.nlm.nih.gov/pubmed/20838279
http://www.ncbi.nlm.nih.gov/pubmed/19594595

TOPIC DISCUSSION: Proximal Tubular Dysfunction

A nice discussion was done yesterday on Proximal Tubular function and then dysfunction.
A nice way that describes' the breakdown of these disorders : As suggested by Dr.A Bellucci.
Proximal Dysfunction can be:
1.Hemodynamically mediated
2.Altered Membrane Transport
3.Altered Intracellular Processes


So lets take them one by one.
1. Volume expansion decreases proximal tubular reabsorption (higher pcP and lower pcP): met acidosis (bicarbonaturia) & low BUN and leading to a physiologic prox tubular dysfunction. A pathologic example of this is renal vein thrombosis
2. Altered membrane transports are the ones that specifically lead to either bicarbonaturias or phosphaturias. Examples of these are: Osteopetrosis, Carbonic anhydrase inhibitor use, tumor induced osteomalacia or too much FGF 23
3. The last one is the ones we always encounter:- Myeloma, Ifosphomide toxicity, Heavy metal toxicity and in children: cystinosis, Dent's Diseases and Lowe's disease.

TOPIC DISCUSSION: FENA less than one causes!

“Crrap 'n' cheap” 

•Cardio-renal syndrome

• Renal Artery Stenosis

• Renal allograft rejection

• Acute interstitial nephritis

• Pre renal

• Non-oliguric ATN

•

• Contrast nephropathy

• Hepato-renal syndrome

• Early obstructive disease

• Acute Glomerulonephritis

• Pigment nephropathy 

Although the test was designed originally in Oliguric patients. So how much use we have of it. Who knows! but above list is usually where we see FeNa<1

Hypertension Review

https://www.pediatric-nephrology.com/home/2010/09/28/306-ipnaht.html

IN THE NEWS- Intestinal Dialysis

Recently in Connecticut, a whale was dialyzed and acute renal failure treated with intestinal dialysis. No catheter was needed. Mannitol was used and BUN and Crt came down.


You can check it out at the following website.
http://today.uchc.edu/features/2010/may10/whale.html

We think of mostly three modalities when it comes to Renal Replacement Therapy( HD, PD and Transplantation).  In some countries, they still use an another option as mentioned above. Intestinal dialysis, the patient is given soluble fibers such as mannitol, charcoal, acacia gum which then leads to increased nitrogenous fecal wasting leading to decreasing BUN and Crt.  One study in Argentina studied the combination of a low protein diet and oral activated charcoal to reduce serum urea and crea­tinine levels in very old ESRD patients who had refused to start chronic dialysis. Nine lucid, very old > 80 years, ESRD patients who had refused to start dialysis were prescribed a treatment based on a combination of a very low protein diet and oral activated charcoal (30 gram/day). None of the patients had anuria, oliguria, edema, significant metabolic acidosis or hyperkalemia. None of them had significant gastrointestinal symptoms. After one week and ten months of charcoal use signi ficant decrease in blood urea and creatinine levels was observed.  

Interesting that we don't offer this to someone with potential not wanting dialysis as a resort.

This should be looked into further.

Take a look at these references:

http://www.ncbi.nlm.nih.gov/pubmed/20061701
http://biomed.uninet.edu/2008/n1/musso-carta-en.html
Image source: Allrefer.com