Edema is a commonly observed sign in various renal diseases like nephrotic syndrome, acute nephritic syndrome and renal failure. The presence of edema implies an increase in interstitial fluid of 2.5 -3 litres. The pathogenetic mechanisms may be different in various types of renal diseases.




It is well known that the Starling forces control fluid movement between the vascular and interstitial compartments. Disturbances in these forces could account for abnormal development of edema in various renal diseases.

Fluid movement into the interstitial space is dependent on these factors:

LpS X ( ∆Hydrostatic pressure- ∆ Oncotic pressure)

∆Hydrostatic pressure = Intravasc pressure- interstitial pressure

∆ Oncotic pressure= s(P onc –Int onc)

Lp = Capillary surface area , S= Capillary permeability s= reflection coefficient of protein


Renal edema can be predominantly caused by two mechanisms  mainly salt retention ( Overfill theory) and hypoproteinemia(underfill theory) There can be overlap between these 2 causes of edema in several diseases with both contributing in different proportions.Activation o the RAAS(rennin angiotensin aldosterone system) could also contribute to salt and water retention and edema.



This classically is described in acute glomerulonephritis. Here there will be congestion  of the glomerular capillaries resulting in decreased glomerular filtration with resultant  accumulation of sodium and water. In renal failure also this could account for development of edema and breathlessness.


Symptoms would be edema, especially periorbital puffiness, dyspnoea, oliguria and hematuria.


Signs would include raised JVP. Basal crepitations and pitting pedal edema.


Investigations would reveal low  or normal urinary spot sodium, low Plasma renin activity(PRA) , high ANP(atrial natriuretic peptide) levels and nonnephrotic range proteinuria( upto 3 gms/ 24 hours).




This is classically described in minimal change glomerulonephritis where here is massive proteinuria(>3.5gm/1.73 sq m2), hypoalbuminemia with hypercholesterolemia. Due to alteration in the Starlings forces, there will be shift of fluid to the interstitial space.

Symptoms would be massive edema , often with anasarca.


Signs would include periorbital puffiness, ascites, pleural effusion and normal JVP with often normal or low BP, postural hypotension can occur.

Investigations would reveal nephrotic range proteinuria, hypoalbuminemia, hypercholesterolemia, high PRA and low ANP. Urinary Na is usually low.




Whether it is the overfill mechanisms or underfill mechanisms which predominate will influence the treatment modalities.

  1. Diet: Salt and water restriction is usually needed.  In acute nephritis, a salt free diet is ideal as it can control the edema, blood pressure and symptoms even negating the need for diuretics or antihypertensives. Fluid restriction is  based on the degree of edema, urine output, daily weight recording and signs like raised JVP, basal crepitations etc. In renal failure also this is needed. Nephrotics are generally advised a salt restricted diet as they may have intravascular depletion.

2.Diuretics:This may be needed if salt and fluid restriction is not sufficient.  However caution maybe needed in producing a profuse diuresis as this can cause intravascular depletion and can cause renal failure especially in nephrotics.

a)                  Loop diuretics ( Furosemide, Torsemide, Bumetanide, Ethacrynic acid) are the first line diuretics as they are the most potent.

b)                  If however they are not effective or if later diuretic resistance develops, thiazide diuretics, especially metalazone can be added.

c)                  As the renin angiotensin system is activated, aldosterone antagonists are also effective.

Often the various diuretics can be combined as additive effects are seen due to sequential nephron blockade. If they are still ineffective, then diuretic resistance has to be considered due to various factors like hypoalbuminemia or decreased oral GI absorption. Poor response to oral drugs can occur due to mucosal edema, poor perfusion of the GI tract due to hypovolemia etc. Here parenteral diuretics may be more effective. It has also been shown that slow infusion of diuretics may be more beneficial and also have a lesser incidence of ototoxicity than bolus injections.As the volume of distribution o diuretics is more in severe hypoalbuminemia, diuretic delivery may be affected. Adding diuretics to albumin infusions can be more effective.

3. Albumin / Plasma infusion

By correcting the altered Starlings forces it can decrease the edema. It can also make diuretics more effective.

4. Hemodialysis/Ultrafiltration/Peritoneal dialysis

This may be needed in renal failure or in severe resistant edema. If there is no renal failure, isolated ultrafiltration may suffice.

5. Head out water immersion.

This can mobilize fluid from the interstitial compartment to the intravascular compartment and can resulting  in a diuresis

6. Elastocrepe stockings/ bandages

This can also shift fluid from the interstitial compartment to the intravascular compartment and can resulting in a diuresis.

7. Specific therapy to decrease proteinuria:

Corticosteroids are highly effective in minimal change disease. Other alternatives are cyclophosphamide, cyclosporine, chlorambucil, mycophenolate mofetil etc

8. Nonspecific methods of decreasing proteinuria:

ACE inhibitors( captopril, enalapril ramipril), ARB blockers( losartan, telmisartan etc), NSAIDS can decrease proteinuria and can thus decrease edema.

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Posted on ตุลาคม 15, 2012, in บทความ. Bookmark the permalink. ใส่ความเห็น.


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