GLOMERULONEFRITIS MEMBRANOSA TRATAMIENTO PDF

¿Cuándo y cómo tratar a los pacientes con glomerulonefritis membranosa? Visits . .. Praga M. Tratamiento de la glomerulonefritis membranosa. Tables v. KDIGO Board Members vi. Reference Keys vii. Abbreviations and Acronyms viiii. Notice. Foreword. Work Group Membership. Abstract. Palabras clave: nefropatía lúpica, lupus eritematoso sistémico, tratamiento. . se presenta en dos tercios de los pacientes con glomerulonefritis membranosa.

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Los botones se encuentran debajo. To the right is a diagram of just one glomerular capillary. Within the lumen of that capillary are red blood cells, white blood cells, and protein molecules, as well as other important components of the blood. Those elements need to be retained within the capillary.

The pressure gradient across that capillary will cause fluid and very tiny molecules to cross into the filtrate that enters the urinary space. This glomerulus has relatively normal appearance here, and you can see what it looks like in an actual tissue section that would be examined by the pathologist who was determining what the cause for renal disease might be in that patient.

You can see a small artery, an arteriole, coming in over in the right- hand bottom corner. You can even see some red blood cells in the lumen, and then the little capillaries with their delicate walls, and the arteriole exiting over at about 7 o’clock in that photomicrograph.

You can have mesangial proliferation, as we will discuss. There is this glomerular basement membrane, the GBM, which is the main barrier.

There is the endothelial cell, which at real high magnification actually has holes in it, fenestrations in it, so it is not much of a barrier. The epithelial cell actually has what are called foot membraonsa. They are tratamienti extensions that come down to the surface of the capillary.

If you cut them in cross section, they look like little feet. Actually we ylomerulonefritis see that they are fused when there is proteinuria, so there is a change in those cells.

But the major barrier to proteinuria is that basement membrane. What factors normally glomrulonefritis us from losing too much protein? Toto pointed out, one thing is the size of the protein molecules relative to the functional pore size of this glomerular basement membrane. If you look at that glomerular basement membrane, you really can’t see the pores in it. But by testing whether certain sized molecules can go through it, you can determine there is a functional pore size.

The proteins in the circulation are mostly too large to go through those functional pore sizes.

Also, there is an electrical charge on protein molecules and cells and tissues. It is mainly a negative charge.

Like charges repel each other. So the plasma proteins are negatively charged, and the capillary wall is negatively charged. That tends to repel the proteins from getting into these pores and getting through.

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This pore size and negative charge normally keep proteins from crossing. Nota espuma en la orina. Anteced, de HTA leve Sin antec familiares de enf. Peso 72 Kg, Talla 1. This is a year old African-American woman who is a lab technician who presented with swelling of her feet and ankles for the past one to two weeks. She noted that her urine had become bubbly recently.

Her past medical history was significant only for mild high blood pressure, controlled with a thiazide diuretic. Her review of systems was otherwise negative and there was no history of kidney disease in her family. Her head and neck exam was negative, her heart was regular with a normal S1 and S2 and there were no murmurs, rubs nor gallops appreciated. Her lungs were clear.

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Her abdomen was obese, non-tender and otherwise unremarkable.

Lupus nephritis. Clinical presentation, classification and treatment

Urinalysis and laboratory data Her urinalysis demonstrated a specific gravity of glmerulonefritis a pH of 6. Under microscopy red blood cells were noted as well as white traramiento cells. There were moderate epithelial cells but no dysmorphic red cells or red cells casts were noted. Laboratory data included a white count of 7. Membrannosa ultrasound her kidneys were 12 cm bilaterally and noted to be somewhat echogenic. It is due to certain circumstances that cause the capillary of the glomerulus to leak protein.

They are normal effects of living in our environment. So, for instance, excessive exercise, stress of excessive heat or excessive cold, can lead to increases in the amount of protein that is filtered and excreted into the urine. This is generally not considered a disease phenomenon because it is short lived, goes away, and really has no significant clinical consequences.

The mechanism by which this takes place is believed to be due to a transient increase in the permeability, that is the membrane allowing protein to pass through it. Changes in urine protein excretion on standing postural proteinuria Postural proteinuria is a relatively common phenomenon. As far as its pathological significance is concerned, it glomeruulonefritis kind of controversial. It is a problem because some individuals have this condition.

It becomes scary glomerulonrfritis it goes on for a long period of time. It is not a transient phenomenon, and we really don’t know exactly what the mechanisms membrranosa. What it means glomerulonefritos, that during the daytime when an individual is in the upright position and the urine is collected, we find abnormal amounts of albumin in the urine.

The glomerulus is leaking albumin. But when the subject with this condition lies down and goes to sleep at night, the excess protein filtration and excretion by the kidney seems to go away. At least it is dampened substantially. Although the mechanism has not been clear, it is presumably due to some partial temporary obstruction of the veins to the kidney, which is where the blood goes out of the kidney.

Jennette will show you that in a minute. The condition is generally not a serious one.

Children or adults who have this condition don’t seem to have any long-term consequences from it in terms of kidney disease. I said it is scary because it doesn’t seem to go away in a lot of people. You worry–does this harbinger a kidney disease? But individuals can have this condition for a long, memmbranosa time, and it doesn’t seem to lead to kidney damage or tratameinto going on a dialysis machine or needing a kidney transplant.

Cambios en la membraa basal causan proteinuria. You could surmise from what I have must said a decrease in that negative charge, which is observed in many causes of nephrotic syndrome. There is a loss of that negative charge in the capillary wall which allows protein to get to the wall. There is also an increase in that functional pore size. There is damage to that wall by different factors in different types of disease, which make bigger pores in the wall and allows the protein to spill through.

Also, sometimes glomerulonefrjtis the glomerular level, and maybe even in the whole body, there is an increase in blood pressure that can force more protein across the wall, which may be why certain antagonists of increased pressure, such as ACE inhibitors, can reduce the proteinuria in certain patients. There are structural changes that take place within the glomerulus when this happens in different glomerulonefritks, and this is what we are going to focus on to identify the different types of disease that cause the nephrotic syndrome.

One change you can tratamieento in this particular diagram, on the right, the normal capillary has the membranosx foot processes intact On the right-hand side some of those little foot processes have fused together. It is just a structural marker that proteinuria has taken place. You see foot process fusion in all patients who have proteinuria, so it is not specific for a particular cause. You may or may not have hypoalbuminemia, edema, hyperlipidemia, and hypercoagulable state. But nephrologists are fond of talking about nephrotic range proteinuria because if you have 10 grams of albuminuria, whether you have these manifestations or not, you will tratxmiento develop them.

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Moreover, the diseases that give you 10 grams of proteinuria are the same regardless of whether you have the manifestations. But we are going to focus on these manifestations now, the edema, the glmerulonefritis, the hypercoagulable state.

What can you do in general for your patient with nephrotic syndrome? Light microscopy involves taking a thin section of a kidney biopsy, which is usually obtained by inserting a needle into the back, a hollow needle, and removing a trtamiento core of kidney tissue.

It is fixed with a fixative and sliced very thinly and stained with textile dye basically. You get a pattern similar to what we see on the far left.

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Immunofluorescence microscopy allows the specific identification of, in particular, abnormal antibodies that can cause certain kinds of glomerular disease but don’t cause others. So this immunofluorescence stains these abnormal antibodies. Electron microscopy allows you to look at a very high magnification that you can’t see by standard microscopy. For example, on the far right–that is just one capillary loop.

You can see on the far right just one capillary loop; on the left, you can see there are many loops there. So the rightmost picture was taken at much higher magnification. I have put it up there because I believe it is becoming increasingly important, and that is persistent proteinuria. Persistent proteinuria in many of our recent large clinical trials that have been ongoing within the United States has really been shown to be what we call an independent risk factor for progression of renal disease.

That means independent of all the other things that we can look at and measure and check and watch. So we are becoming more and more concerned that proteinuria itself may have some significant implications to the kidney in terms of its ability to actually cause damage and injury and thus be what we call a progression promoter or promoter of progressive renal disease.

Dyslipidemia The second group of complications that I would like to talk about is the area of dyslipidemia: Altered cholesterol levels, high cholesterol levels, changes in the amounts of fats and lipids in the body.

A large part of this, as I will show you in a moment, is driven by changes in the glomerular filter and the leaking of protein into the urine. But they changes in blood lipid levels in themselves have significant implications. They have implications for cardiovascular disease, and there is now a growing body of scientific evidence to suggest that this may be an important and yet overlooked complication that we have in our adult population. There is also a fair amount of clinical data from prospective trials to look at lipids as a progression promoter for renal disease.

So not only do the lipids appear to be potentially injurious to the coronary arteries, giving us heart disease, but they may also be injurious to the kidney.