This document provides information about primary glomerular nephropathies from a medical school class. It defines primary glomerular nephropathies as renal diseases where the glomerulus is the main structure affected. Signs and symptoms can vary depending on location, aggressiveness and speed of histological damage, and may include hematuria, proteinuria, and hypertension. Diagnosis requires renal biopsy and examination under microscopy. Treatment options are detailed in Table 1, while classifications are shown in Table 2, according to each condition's clinical presentation. IgA nephropathy and membranoproliferative glomerulonephritis are discussed as examples.

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
PRIMARY
GLOMERULAR
NEPHROPATHIES
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. PRIMARY GLOMERULAR NEPHROPATHIES
Concept.- Renal diseases in which the glomerulus is the only structure or the
main structure affected. The glomerular basement membrane (MBG) is a
continuous laminar structure formed mainly by type IV collagen, proteoglycans
(heparansulfates), laminin and entactin.
Signs and Symptons.- According to the location, the aggressiveness and the
speed of establishment of the histological damage. There may be hematuria that
can be microscopic or macroscopic, the presence of blood cylinders or a high
percentage of dysmorphic red blood cells in the urinary sediment are highly
suggestive that the hematuria is of glomerular origin. The presence of proteinuria
is of great importance when it comes to cataloging the type and prognosis of
glomerulonephritis (GN). Hypertension (HT) is also a common clinical finding in
certain glomerular diseases, especially when renal failure coexists. On the
contrary, other glomerular diseases are characterized by an insidious and often
asymptomatic course.
Diagnosis, Classification and General Treatment.- The diagnosis of
glomerulonephritis requires the performance of the renal biopsy, with some
exceptions, after this examination the tissue should be examined with optical
microscopy (OM), by staining and immunohistochemical techniques,
immunofluorescence ( IF) and electron microscopy (ME). The treatment is

3. detailed in TABLE Nº, while the complete classification of them will be detailed
in TABLE Nº 2, according to the clinical presentation of each of them.
NEFROPATIA IG A
Concept.- It is the most common primary GN in the human population. The
disease is typical of adolescence and young adults.
Etiopathogenesis.- Although the etiology is unknown, the renal lesion is due to
the deposition in the glomerular mesangium of aggregates or circulating immune
complexes that contain mainly IgA1, but not IgA2.
Pathological Anatomy.- It is characterized by isolated or predominant deposits of
IgA1 in the glomerular mesangium, together with proliferation of mesangial cells
and increase of the mesangial matrix.
Signs and Symptons.- It is preferred in young adults between 16-35 years.
Nephropathy is manifested by macroscopic hematuria, recurrent or not, in almost
half of the cases, more frequently in children than in adults. In some cases,
macroscopic hematuria is accompanied by acute renal failure. High blood pressure
is frequent. In some cases malignant hypertension occurs during its evolution.
Another form of presentation consists of acute renal failure with hematuria that
shows in the renal biopsy crescents in more than 50% of the glomeruli.
TABLA 2. CLASIFICACIÓN DE LAS GLOMERULOPATÍAS PRIMARIAS.

4. Treatment and Prognosis.- The renal survival at 19 years of the beginning of the
disease is around 85% and at 20 years it is 75%. A conservative treatment is
recommended for most patients, with ACE inhibitors or ARAs. Glucocorticoids
could also be used for 6 months.
GLOMERULONEFRITIS MEMBRANOPROLIFERATIVA (GNMP)
Concept.- It is a rare condition
that is classified histologically
in two varieties: a) type l with
subendothelial capillaries of
IgG and C3; and b) type ll with
dense intramembranous deposits
exclusive of C3.
Etiopathogenesis.- Type 1
MPGN is a glomerular disease
caused by immune complexes
antigen-antibody. There are
many infectious diseases
(hepatitis C) that can cause it.
One of the most frequent
findings is
hypocomplementemia. Type II
MPGN less frequent, there is an
intense decrease of C3.
Pathological Anatomy.- It is characterized by intense proliferation of cells and
mesangial matrix. In IF, deposits of IgG and C3 are observed along capillary
walls and mesangium and the EM shows subendothelial deposits in type I and
intramembranous in type II.
Signs and Symptons.- Clinical presentation is nephrotic syndrome (50%),
nephritic syndrome (25%), asymptomatic microhematuria (25%). Serum levels of
C3 are reduced in 70-80% of cases of type I MPGN and in 90% of type II MPGN.
TABLA 1. TRATAMIENTO GENERAL DE LAS
GLOMERULONEFRITIS.

5. ACUTE GLOMERULONEFRITIS (GNA) POSTINFECTIOUS
Concept.- Acute glomerular inflammation preceded by an infectious process that
occurs with a nephritic syndrome in most cases and tends to spontaneous
recovery.
Etiopathogenesis .- is a disease caused by the deposit of immune complexes
related to specific antigens of the infectious agent responsible. In the post-
streptococcal GNA, the responsible germ is the b-hemolytic streptococcus of
group A of Lancefield or Streptococcus Piógenes.
Pathological Anatomy.- Diffuse endocapillary proliferation accompanied by
leukocyte infiltration.
Signs and Symptons.- Post-streptococcal GNA predominates in childhood. In the
adult it is more frequent in diabetic patients, alcoholics and drug addicts.
Macroscopic hematuria is recurrent (30%), edema is one of the most constant
signs (90%), as well as HBP (75%).
Prognosis and Treatment. - In the adult, oliguria or anuria can develop with
extracapillary proliferation being a little more unfavorable. The treatment is based
on antihypertensive agents; liquids; antibiotic therapy of responsible infection.
BIBLIOGRAPHIC REFERENCE
M, Prague Terente. 2016. "Primary glomerular nephropathies". In: Internal
Medicine of Farreras Valentino, Rozman Cricill. 18th Edition Barcelona, Spain.
pp. 832-841