Nephrogenic Systemic Fibrosis-An Evolving Disease Entity

Check out this nice post from clinical correlations

Nephrogenic Systemic Fibrosis-An Evolving Disease Entity

Top Transplant Programs "by volume" in 2009, check out the list

http://nephronline.com/news.asp?N_ID=4188

Nephsap review: AKI and ICU Nephrology

We encountered a question on " osmotic Nephrosis" that led to a discussion.
What is that and what are its causes?
It is renal injury that is "tubular" in nature secondary to hyperosmolar substatnces
You will see vacuolization and swelling of the tubules and a finding that might look very similar to " CNI toxicity" to a certain extent. But CNI injury is different and there other findings in that case.

Why is it called "osmotic" Nephrosis? Who knows. Since the vacuoles are happening due to large amounts of hyperosmolar solutes but these solutes enter the tubular cell via pinocytosis and not osmotic forces.

Things that cause it:

Increased starch in "anything" usually older forms of IVIG
Hetastarch
Mannitol
Contrast dye
Dextran

Its usually reversible and most important preventable

Take a look at the following good references:
http://www.ncbi.nlm.nih.gov/pubmed/18295066
http://www.ncbi.nlm.nih.gov/pubmed/8074604
http://www.ncbi.nlm.nih.gov/pubmed/19435473
Image source:1.Nature.com
2.Renal Fellow Network

Nephsap review: AKI and ICU Nephrology

At Nephsap review of AKI, we came across a question regarding ischemic renal insult and its effect on the rest of the body organs.  AKI induces inflammation and functional changes in many organs and its worth noting the changes that happen in other organs due to AKI.

1. Brain: increased vascular permeability  and disruption of blood brain barrier
2. Lungs: increased vascular permeability and pulmonary edema, increased leukocyte trafficking and altered response to ventilator associated injury
3. Heart:- increased TNF- Alpha and increased apoptosis of heart muscle
4. Bone Marrow:- increased anemia, immune dysfunction and coagulation disorders
5. GI tract:- increased channel inducing factor, and increased k excretion
6. Liver:- increased oxidation products and decreased anti oxidants

Nephrocentric we are!

Minimal Change Disease

Minimal Change Disease

View more presentations from Nephrology, NSLIJ.

IN THE NEWS- CALMAG TRIAL

Calcium acetate/magnesium carbonate (CaMg) is a combination phosphate binder. 

Both can be used separately as binders.

What about using a combined Ca acetate with mg Carbonate binder?

Why ?

1. Less risk of hypercalcemia

2. Increased mg levels have been associated with benefits with vascular calcification and so forth.

A recent paper- nice prospective trial compared using a combination Ca and Mg product vs sevalemer HCL.

The study aim was to show non-inferiority of CaMg in lowering serum phosphorus levels into Kidney Disease Outcome Quality Initiative (K/DOQI) target level range after 24 weeks. Three hundred and twenty-six patients from five European countries were included. After a phosphate binder washout period, 255 patients were randomized in a 1:1 fashion. 204 patients finished the study. 

What did they find?

1. Serum phosphorus levels had decreased significantly with both drugs 25 weeks with equal effects in both arms.

2. Ionized serum calcium did not differ between groups.

3. An asymptomatic increase in serum magnesium occurred in CaMg-treated patients

4. There was no difference in the number of patients with adverse events.

HMM?

1. No cardiovascular risk benefit analysis, not followed long term

2. It seems ca didn't differ, so then why use CaMg combination?

3. Serum magnesium levels are largely dependent on dialysis fluid concentration as the only possibility to eliminate magnesium is via dialysis once residual renal function has disappeared Does that mean we have to monitor for hypermagnesemia more often in this case, the risk is there. 

4. What about the effects of Mg on bone disease? I think there is data that it might be beneficial in lowering pth?But worth a read as it might be important to see long term effects.

Reference: 

http://www.ncbi.nlm.nih.gov/pubmed/20530499

TOPIC DISCUSSION: Management of DKA in hemodialysis Patient

Diabetic patients tend to suffer from ketoacidosis less frequently after starting chronic dialysis than prior to it.The prolonged half life of insulin in advanced renal failure and frequent follow up of patients on chronic dilayis have been identified as reasons for the decreased frequency of ketoacidois in the dialysis population. The usual course leading to ketoacidosis is omission of one or more insulin doses, often due to an intercurrent illness. This is of prime importance as an underlying cause should always be looked for at presentation. The common ones being access related infections and myocardial ischemia.

The absence of osmotic diuresis distinguishes dialysis associated hyperglycemia from hyperglycemia observed in patients with normal renal function.The rise in plasma osmolality that is seen in diabetic ketoacidosis and non ketotic hyperosmolar coma is only in part due to the rise in serum glucose. The marked hyperosmolality is primarily due to the glucose osmotic diuresis that causes water loss in excess of sodium and potassium. The importance of effective plasma osmolality in the development of neurological symptoms are illustrated by observations in diabetic patients with end stage renal disease. These patients can develop severe hyperglycemia, with serum glucose concentrations that exceed 1000 to 1500 mg/dl . However because there is little or no osmotic diuresis, the rise in plasma osmolality is limited , hyponatremia is present, and there are few or no neurological symptoms.

Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation

Total body concentrations of potassium is unchanged, and they frequently have a high serum potassium level. Hyperglycemia has muliple effects on serum potassium: lack of insulin causes translocation of intracellular potassium to the extracellular compartment, a second hyperkalemic effect of hyperglycemia is the consequence of associated hypertonicity, which also leads to egress of potassium from the cells to the extracellular compartment

Insulin infusion is the only treatment required in majority of the patients. Emergency hemodialyis may be considered in severe pulmonary edema, profound metabolic acidosis and severe hyperkalemia with EKG mainfestations

http://www.ncbi.nlm.nih.gov/pubmed/18945331

 by

RIMDA WANCHOO, MD