Nephrotic Syndrome

Introduction to Nephrotic Syndrome

Nephrotic syndrome is a kidney disorder sometimes confused with glomerulonephritis because the pathophysiology, signs, and symptoms are similar. 

Nephrotic syndrome contains three main factors:

1. T-lymphocytes
2. Proteinuria or frothy urine
3. Fluid volume overload

T-Lymphocytes

T-lymphocytes (also known as T-cells) are responsible for nephrotic syndrome. They release chemical mediators which directly damage the glomeruli and the capillaries, increasing their permeability. That makes the glomeruli permeable to red blood cells and proteins.

Alternatively, the B-lymphocytes are responsible for glomerulonephritis. In glomerulonephritis, IgG and anti-IgG complexes are formed in what is called humoral immunity.

The glomerulus is a bundle of capillaries that filter waste products from the blood.

Related Video – What is Glomerulonephritis?

Etiologies

Following are the etiologies involved in nephrotic syndrome.

One etiology involved in nephrotic syndrome is glomerulonephritis. Glomerulonephritis that progresses and does not respond to treatment may turn into nephrotic syndrome involving the T-lymphocytes. The T-lymphocytes further damage the glomeruli.

Diabetic nephropathy is another etiology of nephrotic syndrome due to a process called focal segmental glomerulosclerosis (FSGS). That process is initiated with glomerulonephritis, but it ends up with the glomeruli becoming scarred. FSGS is the most common, primary cause of nephrotic syndrome.

Read: Glomerulonephritis

Proteinuria

The essential feature of nephrotic syndrome is proteinuria. Proteinuria results in frothy, tea-colored urine. Patients may lose up to three grams of protein per day via urine. Alternatively, glomerulonephritis causes hematuria, Coca-Cola-colored urine.

A hallmark sign of proteinuria is frothy urine. The frothiness is due to protein that has leaked out from the kidneys.

The huge protein loss resulting from proteinuria causes hypoalbuminemia. Neither oncotic pressure nor colloid osmotic pressure is holding onto fluid within the vessels. The fluids will leak out into the interstitial space, causing edema.

The edema will present in the periorbital area. There will also be peripheral edema. Hypertension will be present as edema, increasing systemic vascular resistance.

Related Video – Pathophysiology of Hypertensive Nephropathy

Fluid Volume Overload

All nursing interventions, assessments, monitoring, and medications are aimed at reversing fluid volume overload.

Providers also diligently assess for edema. Due to its size, providers must add meticulous skincare to their priority list because those edematous places are prone to skin tears and decubitus ulcers.

Edema is excess fluid in the body’s tissue. Edematous places are more prone to skin tears and ulcers.

Providers monitor for blood pressure, watching for edema and the daily weights, and lung sounds because fluid overload can impede breathing. They’ll also administer antihypertensives, particularly ACE inhibitors.

Similarly to treating glomerulonephritis, providers administer albumin to pull fluid back into the vascular space before administering diuretics to remove it. Clinicians give corticosteroids to suppress that immune response as well as antibiotics if the etiology is an infectious cause.

Summary

Nephrotic syndrome is a kidney disorder that affects the T-lymphocytes, causing proteinuria and fluid overload. Providers must monitor patients to prevent or manage fluid overload as it may cause large edemas or hypertension.