B/ 71 The Nephritic syndrome

Question 1

Clinical manifestations of the clinical complex

Answer 1

Macroscopic hematuria
Mild hypertension
Mild proteinurea
Some degree of oliguria and azotemia

Question 2

Description of lesions

Answer 2

Involves proliferation of cells (such as mesangial and endothelial cells) along with infiltration of neutrophils and monocytes.

The inflammatory reaction leads to injuries of the capillary wall which can lead to leakage of RBCs into the urine (hematuria) along with reduction in GFR leading to oliguria and azotemia.

Question 3

Reasons for hypertension in Nephritic syndrome

Answer 3

1. Fluid retention due to the decreased GFR.
2. Ischemia of the kidney due to proliferation of cells which will lead to compression of the vessels. Renin is secreted and this augments the fluid retention.

Question 4

Acute post infectious (poststreptococcal) glomerulonephritis - etiology

Answer 4

Cellular proliferation and infiltration of leukocytes is the result of deposition of immune complexes within the walls of the glomerulus. It is also called “diffused proliferative GN”.

Question 5

Pathogenesis of PSGN

Answer 5

Due to streptococcal antigens (other bacterial and viral antigens can also cause the disease). Immune complexes are formed and deposited within the subepithelial area of the glomeruli. This activates the compliment system which recruits inflammatory cells which damage the cells stimulating the proliferation of cells.

Question 6

Morphology of PSGN

Answer 6

Granular deposition of immune complexes within the subepithelial area. Increased cellularity (inflammatory cells and proliferation of cells). Diffuse pattern of damage, as it affects all glomeruli.

Question 7

Clinical course of PSGN

Answer 7

Upper respiratory tract infection - abrupt onset of kidney disease after 2-3 weeks.
Malaise, fever, nausea, features of nephritic syndrome. Majority of patients recover by themselves due to functional macrophage system. Can transform into Rapidly progressive GN or chronic GN.

Question 8

Pathogenesis of IgA nephropathy (Berger disease)

Answer 8

Transient macroscopic hematuria. Occurs within 1-2 weeks of a nonspecific upper respiratory tract infection which leads to an increased production of IgA.
IgA can be deposited in the mesangium which activated the compliment system (alternative pathway) leading to inflammation and mesangial cell proliferation.

Question 9

Clinical course of IgA nephropathy (Berger Disease)

Answer 9

usually affects children and young adults. 30-40% if the cases only has microscopic hematuria. 10% shows nephritic syndrome. 15% show full recovery. 25-50% slowly progress to chronic liver disease.