NurulHidayu: kanak-kanak

Nephrotic vs Nephritic Syndrome

Study is boring. But I need to study for the sack of human's life later. Hahaha. Okay so today Imma do some notes about nephrology (Had to!). Post posting examination is 9 days to go, and I'm so doomed! Dengan case write up tak start lagi. I need to go to the hospital quick. Oh btw, Kelantan cuti this Sunday, so yeaaaa I can sleep puas puas. But still ! Case write up tak siap lagi !

Okay so here we go, bismillah.
First of all, you can google about these thing easily, but I prefer to check out in youtube. More easier and clear. It's like having teacher inside the laptop. So there are two videos that I find it easier to understand the topic. Hope these can help you guys :D

N E P H R O T I C . V S . N E P H R I T I C . S Y N D R O M E

By Sarah Al Qubaiban (RSAU-HS)

Nephrotic vs Nephritic Syndrome Explained Clearly by MedCram.com

So both videos started with understanding about the components and layers that involved in gromerular filtration barrier (GFB).

GFB composed of 3 layers:

The endothelial layer of the gromerulus capillaries

Fenestrated cells

Contain pores 60-100nm
The basement membrane

Negatively charged because of Heparan Sulfate proteoglycans
The epithelial layer of Bowman capsule - the visceral part which contain podocytes and processes interdigitating with each other forming filtration slit.

Any molecule that has to enter the tubules, it need to pass through two barriers:

Charge barrier

Can be gromerular basal membrane
Physical (Size) barrier

Can be pore or slits of epithelial layer.

<4nm - All charged molecules can pass

4-8nm - Only positive charges can pass

>8nm - No filtrations

Type of proteinuria:

Mild Proteinuria

Selective proteinuria - only Albumin
Moderate Proteinuria

Non-selective proteinuria : Albumin + Globulin

<3.5g/day

Sub-nephrotic range
Severe Proteinuria

Non-selective proteinuria : Albumin + Globulin

>3.5g/day

Nephrotic range

Image result for mechanism of nephrotic syndrome

Despite the production of protein, it is leaking into the urine.
Hydrostatic and oncotic pressure disturbed
Fluids leaks out to the interstitiam
Hypovolemia develops -perfusion of the blood to the kidney decrease
Renin-Angiotensin-System will be activated and ADH will be produced in large amount because of increase in osmolality which will be sensed by hypothalamus as will as aldosterone. All of these will retain water in kidney.
Protein concentration is still low so more edema will develop.

Nephrotic Syndrome Triad

Proteinuria
Hypoalbuminaemia
Edema

Nephrotic syndrome

Proteinuria (>3.5g in 24hrs)

++++ Protein

Urine looks frothy

Tip: Nephrotic & Protein both have an “O” which may help you remember!

Hypoalbuminaemia

Albumin is lost in the urine.

Gaps in podocytes allow proteins to leak into the urine.

Oedema

Albumin is lost into the urine.

Hypoalbuminemia results in decreased intravascular oncotic pressure.

As a result fluid moves out of the intravascular compartment and into the surrounding tissues causing oedema.

Hyperlipidemia

Due to hypoalbuminaemia, the liver compensates and increases production, however this has the side effect of also increasing the production of lipids, hence causing hyperlipidaemia.

Nephritic syndrome

Haematuria

+++ Blood – microscopic or macroscopic haematuria

Red cell casts – distinguishing feature, form in nephrons and indicate glomerular damage

Haematuria occurs due to podocytes developing large pores which allows blood and protein to escape into the urine.

Proteinuria

++ Protein (small amount)

Hypertension

Usually only mild

Low urine volume <300ml/day

Due to reduced renal function.

Differential diagnosis of Nephrotic and Nephritic syndrome

Nephrotic syndrome – associated diseases

Primary causes

Minimal change glomerulonephritis

Focal segmental glomerulosclerosis

Membranous glomerulonephritis

Secondary causes

SLE

Hep B and C

HIV

Diabetes mellitus

Malignancy

Nephritic syndrome – associated diseases.

Post-streptococcal glomerulonephritis – appears weeks after upper respiratory tract infection (URTI)

IgA nephropathy – appears within a day or two after a URTI

Rapidly progressive glomerulonephritis (crescentic glomerulonephritis)

Goodpasture’s syndrome – anti-GBM antibodies against basal membrane antigens
Vasculitic disorder – Wegener’s granulomatosis / Microscopic Polyangiitis / Churg Strauss disease

Membranoproliferative glomerulonephritis – primary or secondary to SLE / Hepatitis B/C

Henoch-Schönlein purpura – systemic vasculitis – deposition of IgA in the skin and kidneys