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

SECONDARY GLOMERULAR NEPHROPATHIES
Several multiorgan diseases can cause glomerular injury and glomerulopathy may be
the predominant finding or a clinical manifestation that is not very relevant,
overlapped by the commitment of other organs and systems. This glomerular
condition is called "secondary", to differentiate it from the primary one in which the
condition is limited to the kidneys.
AUTOIMMUNE DISEASES
Systemic lupus erythematosus. Renal involvement is common in SLE and is one of
the main causes of morbidity
and mortality of this disease.
Lupus glomerulonephritis is
considered the prototype of
human diseases mediated by
circulating immunocomplexes,
consisting mainly of nuclear
antigens (native DNA), IgG
and complement that can be
demonstrated in renal biopsy
by immunofluorescence (IF).
The International Society of
Nephrology (2004) classifies
glomerular disorders in the
LES in six. Type I or minimal
mesonil disease is
characterized by the presence
of immune deposits identified
by IF and / or electron microscopy (EM) and by the absence of lesions in the
examination with optical microscopy (OM). Mesonil or type II proliferative lupus

glomerulonephritis is characterized by proliferation of mesangial cells and expansion
of the mesonil matrix in OM. Focal proliferative lupus glomerulonephritis or type III
is defined in OM due to the presence of endo- or extracapillary proliferation, which
affects less than 50% of the glomeruli. Lesions are associated with subendothelial
deposits in the ME and in this histological class, the chronicity index of the
glomerular lesions should always be evaluated. Diffuse proliferative or type IV lupus
glomerulonephritis is characterized by an endocapillary and / or extracapillary
proliferation that involves more than 50% of the glomeruli evaluated and thickening
of the capillary walls in wire loop, which is caused by the massive presence of
deposits predominantly subendothelial cells, infiltration by polymorphonuclear cells,
areas of necrosis, karyorrhexis, capillary thrombi and hematoxylin bodies.
Class IV should always be classified as segmental (IV-S) or global (IV-G) if more
than 50% of affected glomeruli have segmental or global lesions respectively, and the
assessment of the activity and chronicity indexes should always be added. the
injuries. Membranous or type V lupus glomerulonephritis is characterized by diffuse
thickening of the glomerular capillary wall in MO and by the presence of
subepithelial immune deposits in IF and ME accompanied in general by increased
mesonil proliferation and deposits also located in the glomerular mesangium. Finally,
type VI lupus nephropathy is characterized by global sclerosis of more than 90% of
the glomeruli evaluated.
The clinical manifestations of lupus nephropathy are very varied and are observed
in more than 75% of patients with SLE, not forgetting that cases of silent lupus
glomerulonephritis have also been described. The prevalence of nephrotic syndrome
in focal lupus glomerulonephritis is less than 20% and, in general, there is no
hypertension or renal failure. Diffuse proliferative lupus glomerulonephritis occurs
with moderate or severe proteinuria (100%), nephrotic syndrome (60% -90%),
microhematuria

(65% -80%), HBP (30% -60%) and renal failure (50% -60%). Membranous lupus
glomerulonephritis is characterized by proteinuria, usually accompanied by nephrotic
syndrome and microscopic hematuria.
The prognosis of patients with lupus nephropathy differs according to the type of
nephropathy they present, even independently of the treatment used. The treatment of
lupus nephropathy is based on the histopathological type. It consists of a first phase
of induction to the response and a second of maintenance of the response. In patients
with class I lupus glomerulonephritis, no specific treatment is indicated, and those
diagnosed with class II have a survival rate greater than 90% and are usually treated
with moderate doses of glucocorticoids, but sufficient to control the extrarenal
manifestations of the disease, with addition of antimalarials.
Systemic vasculitis.- are classified according to the size of the inflamed vessels.
Large vessel vasculitis is not usually accompanied by glomerular lesions and, in those
of a median vessel, the glomeruli collapse indirectly by ischemia, which may
manifest as non-nephrotic proteinuria and progressive renal failure, but with a urinary
sediment. normal.
Goodpasture disease. This renopulmonary syndrome is more frequent in males
between the third and seventh decades of life, with a reported incidence of 0.5-1 cases
per million white inhabitants. Patients usually come for consultation due to acute
renal failure, hematuria and non-nephrotic range proteinuria. The pulmonary affection
in the form of alveolar hemorrhage is present in 60% -70% of the patients, but other
signs of multiorganic affection are typically absent and their presence obliges us to
rule out the concurrence of a systemic vasculitis. The diagnosis requires the
demonstration of basal glomerular antimembrane antibodies (GBM), so, in addition
to performing the serological determination of these antibodies, it is highly
recommended to perform a renal biopsy to demonstrate the linear deposition of IgG
in the renal tissue. renal histological signs of activity and / or chronicity, which can
guide the treatment to be followed in each case. In untreated patients, mortality is

100% due to pulmonary hemorrhage or renal failure. The most rational therapeutic
approach consists of the elimination of anti-GBM antibodies and the blocking of their
synthesis.
Schönlein syndrome - Henoch (See Fig. 1) .-
This syndrome is characterized by cutaneous,
articular and digestive manifestations, often
accompanied by glomerulonephritis. Renal
disease is very frequent, greater than 50% in most
published series. However, if urine tests are
performed in the acute phase, the prevalence of
nephritis could reach 80%. Patients with renal
injury have proteinuria (70%), gross or
microscopic hematuria (60%) and, less frequently,
nephrotic syndrome (40%) and progressive renal
failure (25%). Serum complement is normal and, in half of the cases, elevated serum
levels of IgA have been observed. The etiology is unknown. In general, the disease is
considered to be a diffuse vasculitis of very small vessels due to circulating
immunocomplexes containing IgA. Its development could be favored by IgA1
glycosylation abnormalities. The disease has a recurrent course in about 40% of
cases. The prognosis is determined by the presence and severity of
glomerulonephritis and analogously to what happens in IgA nephropathy.
Treatment.- The majority of patients are completely cured or have only minor
anomalies, such as mild persistent proteinuria, after several years of clinical onset.
However, 5% -25% of patients with renal involvement develop progressive renal
failure and hypertension. It has not been shown that glucocorticoids,
immunosuppressants or anticoagulant therapy substantially modify the course of the
disease. However, an aggressive treatment with glucocorticoids, plasmatic and
immunomodulatory changes may be justified when it manifests as GNRP.
Recurrences of nephropathy have been described in transplant patients.
Fig. 1.- Rash e hinchazón de los pies
causados por la púrpura de Schönlein-
Henoch

Cryoglobulinemic vasculitis.- Mixed cryoglobulinemia is a disease mediated by
immune complexes with a systemic impact and very variable severity from one
individual to another. In milder cases, it may only present with cutaneous leukocyte
cutaneous vasculitis. The development of glomerulonephritis of variable intensity is
frequent and, in the most severe cases, a systemic necrotizing vasculitis with
involvement of small arteries may appear.
BIBLIOGRAPHIC REFERENCE
L. F. Quintana Porras, "Secondary Glomerular Nephropathies". In: Farreras, V.
Rozman, C. Internal Medicine, Barcelona-Spain Elsevier, 2016, Vol. 1, p. 842 - 845