6/18/2012

Nephrotic syndrome


Nephrotic syndrome


   

Definition

Nephrotic syndrome Is a clinical syndrome associated with proteinuria in the nephrotic range (3.5mg/m2/24hrs), edema and hyperlipidemia.
Nephrotic syndrome is not due to inflammatory processes but due to direct action of the membrane attack unit of complement on the glomerulus.

Clinical suspicion

It should be suspected when a patient presents with generalized oedema, protein detected in urine, hypoalbuminemia.



Diagnosis

The diagnosis maybe established with proteinuria in the nephrotic range alone without the other criteria.
1.  Proteinuria > 3.5 g/m2/day:
On detection of protein in urine a 24 hour urinary protein test is in order. There are two cut off values for this test: 1. increased urinary protein <1.5g/day; this is refered to as isolated proteinuria. 2. >3.5g/day; this establishes nephrotic syndrome.

2.  Hypoalbuminaemia
3.  Hyperlipidaemia:
As albumen in serum is lost through the kidneys, the liver increases its production of albumen and concomitantly increases the production of cholesterol.

4.  Oedema: resulting from loss of intravascular fluid to the extravascular space due decreased intravascular oncotic pressure (decreased albumen).
However, the presence of proteinuria in the nephrotic range (3.5g/day) establishes the diagnosis.
Differential diagnosis: proteinuria

Causes

Once the diagnosis of nephrotic syndrome is established the cause of the syndrome is sought in order to treat accordingly.

Nephrotic syndrome with active sediment (mixed nephrotic/ nephritic)

This denotes the presence of RBC casts (active sediment). Causes include:
1ry glomerular diseases as MPGN (main cause), and 2ry glomerular diseases as SLE (most common presentation of SLE), vasculitis such as Henoch Schonlein purpura, mixed essential cryoglobulinemia.

Nephrotic syndrome with bland sediment (Pure nephrotic)

1ry glomerular diseases such as MCNS, Membranous glomerulonephritis, Focal glomerulosclerosis. As well as 2ry glomerular diseases that result from Diabetes (Klemelsteli-Wilson syndrome) and amyloidosis.

Treatment

Treatment of nephrotic syndrome depends primarily on the cause, however, it frequently involves the use the glucorticoids given over long periods of time. Especially in cases of minimal change disease. Here the role of steroids is to suppress the autoimmune basis for this disease. The use of cytotoxic agents maybe required in some cases (e.g. cyclophosphamide).
Dietary salt control, treatment of hypertension and hypercholestrolemia is also recommended. ACE inhibitors, in addition to controlling blood pressure have also been found to decrease the protein loss. Diuretics may help control the edema and the hypertension.

Acute Renal Failure Causes Diagnosis and Treatment


Acute Renal Failure Causes Diagnosis and Treatment  

Acute Renal Failure

Definition

Renal failure depicts a group of diseases that may be associated with decreased GFR and manifested by retention of BUN and creatinine. Acute renal failure is defined as a rapidly (over a period of days) increasing creatinine level or decreasing urine output.

Causes

Causes of acute renal failure is caused by failure of the kidneys to perform their normal functions due to:
  • Prerenal - Problems affecting the flow of blood before it reaches the kidneys
  • Postrenal - Problems affecting the movement of urine out of the kidneys
  • Renal - Problems with the kidney itself that prevent proper filtration of blood or production of urine 

Prerenal failure

This is by far the most common type of acute renal failure. Your kidneys do not receive enough blood to filter. Prerenal failure can be caused by the following conditions:
  • Dehydration - From vomiting, diarrhea, water pills, or blood loss
  • Disruption of blood flow to the kidneys - From a variety of causes
    • Drastic drop in blood pressure - From major surgery, severe injury or burns, or infection in the bloodstream (sepsis)
    • Blockage or narrowing of a blood vessel leading to the kidneys
    • Heart failure or heart attacks
    • Liver failure
There is no actual damage to the kidneys with prerenal failure. With appropriate treatment, it usually can be reversed. 

Postrenal failure

Postrenal renal failure is sometimes referred to as obstructive renal failure, since it is often caused by something blocking elimination of urine produced by the kidneys. This problem also can be reversed.
At the ureter level, this condition can be caused by the following:
  • Kidney stone
  • Cancer
  • Medications
At the bladder level, the following conditions can cause obstruction:
  • Kidney stone
  • Enlarged prostate (the most common cause)
  • Blood clot
  • Bladder cancer
  • Neurologic disorders of the bladder
Treatment consists of relieving the obstruction. Once the blockage is removed, the kidneys usually recover in 1-2 weeks if there is no infection or other problem.

Renal damage

Primary renal damage is the most complicated cause of renal failure. Renal causes of acute kidney failure can be subdivided into those affecting the filtering system of the kidney, those affecting the blood supply in the kidney, and those affecting kidney tissue.
Some of the kidney problems that can cause kidney failure include the following:
  • Blood vessel diseases
  • Blood clot in a vessel in the kidneys 
  • Injury to kidney tissue and cells
  • Glomerulonephritis
  • Acute interstitial nephritis
  • Acute tubular necrosis

Clinical manifestations

ARF passes through two phases 1. Destructive phase: oliguric and non-oliguric 2. Reconstructive phase: could be polyuric.
ARF due to pre-renal or renal causes (esp. ATN) usually presents as oliguric renal failure passing through the 3 phases of pathology:
  1. Intitiation phase: due to the initiating insult on the kidney.
  2. Maintenance phase: maintenance of oliguria (1-2 weeks).
  3. Recovery phase: due to recovery of renal function (polyuria).
ARF due to other causes as partial obstruction may present as polyuria.
ARF due to postrenal obstruction may present as anuria.

Diagnosis

Renal failure is manifested by the rise of serum creatinine. The next step is to identify if chronic or acute renal failure. Then exclude if postrenal then identify if pre-renal or renal. If renal identify what type of intrisic renal disease ? if no diagnosis is reached then by exclusion the diagnosis is ATN.

1. Prerenal azotemia

  • Urine/plasma creatinine ratio > 40
  • Urinary Na decreased < 20
  • Fractional excretion of Na is <1%
  • Urine osmolarity is > 500

2. Renal azotemia

  • Urine/plasma creatinine ratio < 20
  • Urinary Na decreased > 40
  • Fractional excretion of Na is >1%
  • Urine osmolarity is > 350
?        These findings can be altered by diuretic use and urine sample should be taken before institution of diuretic use.

3. Postrenal azotemia

Post-renal azotemia develops only if the obstruction is bilateral or affects a solitary functioning kidney. During the early stages of obstruction, continued glomerular filtration leads to increased intra-luminal pressure proximal to the site of obstruction. As a result, there is gradual distension of the proximal ureters, renal pelvis and calyces and fall in glomerular filtration which will be evident by renal ultrasound.
N.B.: the level of creatinine in serum has nothing to do with whether the ARF is oliguric, anuric or non-oliguric: it is an indication that tubular function is lost as creatinine is not filtered- it is secreted. K+ and H+ are retained even in nonoliguric renal failure due to the same principal (they are both secreted and not filtered).

Treatment  

Treatment of acute renal failure usually should be conservative and largely supportive. It requires careful and precise management. All patients will require close monitoring, many of them within intensive care settings.

Supportive care includes stabilizing the patient, monitoring input and output strictly, weighing daily, determining electrolyte values frequently, preventing sepsis via reducing the number of intravenous lines and removing an indwelling urinary.

Therapy for prerenal failure

Rapid volume replacement and treatment of the underlying condition that resulted in prerenal failure are the cornerstones of therapy. Initial fluid administration of isotonic saline (0.9%) or 5% albumin (10 to 20 mL/kg per dose) should be used to restore intravascular volume. This can be both a diagnostic and a therapeutic trial. Fluid administration also can convert oliguric to nonoliguric renal failure in its early stage.

Therapy for postrenal failure

Therapy for postrenal failure includes removal of obstruction by decompression or diversion of the urinary tract, stabilization of electrolyte abnormalities, management of postobstructive diuresis, and therapy for voiding dysfunction and for urinary tract infection. Surgical intervention will require urologic consultation. The site of the obstruction will determine the approach: placement of a Foley catheter, vesicostomy, ureteral catheters (stents), or nephrostomy tubes.

Therapy for established renal failure

Maintaining Balance of Fluid and Electrolytes

In a euvolemic state, fluid intake, including water generated from endogenous metabolism (insensible fluid gain), is balanced by fluid output.

Treating Hypertension

Kidney failure in any form can present as hypertension and hypertensive encephalopathy. It is essential to lower the blood pressure quickly and safely. The blood pressure should be reduced by at least 25% within 1 hour with an antihypertensive medicine whose onset of action is rapid. It is advisable to start with one antihypertensive medicine and increase the dose to its maximum recommended level. Therapy is individualized and needs titration. In most cases, hypertension is the result of sodium and fluid retention, but other factors, such as activation of the renin-aldosterone-angiotensin II and/or the alpha-adrenergic system, may have roles in kidney failure.

New drugs and research for Alzheimer's disease

New drugs and research for Alzheimer's disease 






New drugs and research for Alzheimer's disease  



This month witnessed the discovery of two drugs that may help in treating Alzheimer's disease. On the other hand, it has been announced that a large-scale study will be launched next April with the aim of better understanding this disease.

Alzheimer's disease (AD) affects approximately 4.5 million Americans. It is considered the most common cause of dementia in western countries. Approximately 10% of all persons over the age of 70 have significant memory loss; in more than half, the cause is AD. AD is a progressive dementia (that is the dementia keeps getting worse).
The most important risk factors for AD are old age and a positive family history. The frequency of AD increases with each decade of adult life to reach 20 to 40% of the population over the age of 85. A positive family history of dementia suggests a genetic cause of AD.

Mechanism

AD is characterized in the brain by abnormal clumps (amyloid plaques) and tangled bundles of fibers (neurofibrillary tangles) composed of misplaced proteins. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD.
The management of Alzheimer's disease is difficult and frustrating, because there is no specific treatment and no way to slow the progression of the disease. The primary focus is on long-term amelioration of associated behavioral and neurologic problems. Currently there are five FDA-approved drugs that may benefit some people in the early or middle stages of the disease. Tacrine (Cognex) may alleviate some cognitive symptoms. Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) may keep some symptoms from becoming worse for a limited time.
"In recent studies, the benefit of  these medications were shown to be more effective in the early and middle stages of Alzheimer's and less effective in the last stage", comments Carolyn Merritt, LPN of The Doctors Lounge. "The studies seemed to show it delayed the onset of the third and final stage".
The fifth drug, memantine (Namenda), was recently approved for use in the United States.

US launches major study

In April 2005, researchers will begin recruiting about 800 Americans, ranging from 55 to 90 years old, in an effort to gain a better understanding of the early stages of the disease. This will be part of a major government study to track early Alzheimer's disease.
Researchers will use MRIs of the brain and other tests to track people who have either early-stage disease or a milder type of memory loss known as "mild cognitive impairment." Over the course of five years, they will compare the biological changes that occur within those patients' brains to the aging that takes place in the brains of healthy seniors.
The goal is to find early warning signs that can identify people at highest risk, and markers to help test the effectiveness of new therapies. The study, which will cost approximately $60 million (mostly funded by the government), was unveiled Wednesday by the National Institute on Aging.

How to Improving brain cell survival after brain injury

How to Improving brain cell survival after brain injury







How to Improving brain cell survival after brain injury

Scientists at Melbourne's Howard Florey Institute have found a protein in the brain that can save neurons from dying after experiencing traumatic brain injury from incidents such as stroke, car accidents and falls.

The team, led by Professor Seong-Seng Tan, has discovered that this naturally occurring protein, called BP5, is produced more than usual in brain cells after they have experienced traumatic injury.
Prof Tan said that because this protein is "over-expressed", it can prevent the neuron's cells from dying, thus reducing brain damage.
"BP5's pattern of expression indicates that it allows neurons to survive in a stressed environment," Professor Tan said.
"We have tested this hypothesis in mice by expressing BP5 in stressed neurons and this proof-of-principle experiment showed that BP5 can prevent neurons from undergoing cell death.
"BP5 works by using the cell's waste disposal system to flush away toxic and damaged proteins produced after injury, which appears to tip the balance towards nerve cell survival, instead of death," he said.
Professor Tan is the first to show that this mechanism can be fruitfully manipulated to prevent brain cells from dying. For this reason, his work has been published by the Journal of Neuroscience, the peak body journal of the American Society for Neuroscience.
"Now our challenge is to understand how BP5 performs it neuron-saving function and develop drugs that can do the same thing," Professor Tan said.
"Ultimately, we want to deliver the drug to patients suffering brain injury from stroke or trauma so save as many neurons as possible.
"Such a drug would limit damage to the brain after the injury, as well as the subsequent few days when injured nerves release 'suicide factors' that cause surrounding, healthy neurons to die en masse.

6/17/2012

Watch Portugal vs Netherlands Euro 2012


Watch Portugal vs Netherlands Euro 2012


Watch Portugal vs Netherlands Euro 2012 

 

Portugal vs Netherlands, the heavyweight match of Group B (Group of Death) will be on air today from OSK Metalist Stadium where A win can lead them into the quarter final of Euro 2012. But, for, Netherlands it’s quiet tough as they have to beat Portugal by scoring 2-0 goals depending on the results of Germany vs Denmark where Germany have to win.

For Portugal, It’s quiet easy to go into the knockout stage of Euro 2012 as they have already in the second position of Group B. A normal win will turn Portugal into the Quarterfinal of Euro 2012 where top eight teams will be fought with each other.

It’s a great news that both teams have no injury concerns. Portugal coach Paulo Bento might have field that squad which they have field against Denmark and got a win by 3-2. Netherlands boss Bert van Marwijk will be named their top-level squad to beat Portugal and secure them into the safe stage of Euro 2012. Netherlands can do magic as like Greece have done it last night by defeating Russia 1-0.





6/15/2012

Watch France vs Ukraine Euro 2012


Watch France vs Ukraine Euro 2012 


Watch France vs Ukraine Euro 2012 


Ukraine vs France Live Stream Euro 2012 Online - 14 June 2012Ukraine have a great match and they were ready to France . The first match is drawn between the two of the best teams England and France in the last match. Ukraine have some of the best players and they have done well in the last match and win their match against the team of the Sweden. This week France will have to win their match to win the game against the Ukraine.Ukraine the Group D team have 3 points in the Group table and they have no issues to lose this match because if they win the match they will qualified for the Euro 2012 Quarter Finals. France have show a good performance...