Introduction:
Post-infectious acute glomerulonephritis (GNA) is defined by acute non-suppurative inflammation of the glomerular capillaries.They have in common the occurrence of infections, immune complex pathogenicity and potentially curable treatment with anti-infectives. They are characterized most often by the sudden onset of an acute nephritic syndrome associating hematuria, proteinuria,
edema, hypertension (hypertension) and renal insufficiency, all occurring after a free interval of variable duration according to the infection in question. Morphologically, the fundamental lesion is a proliferation of the endocapillary cells. The possible association with extracapillary proliferation gives a more noisy picture and a less favorable evolution dominating oligoanuria and renal insufficiency. Poststreptococcal GNAs are the most frequent and best known; other postinfectious GNAs are more rare.
Poststreptococcal acute glomerulonephritis:
EPIDEMIOLOGY:
Incidence:
The actual incidence of postinfectious GNA is difficult to assess because subclinical cases are probably more frequent than clinically relevant cases. However, the incidence of NEGs has declined significantly in developed countries over the past 40 years. This decline in incidence is likely due to improved living standards and improved medical coverage.It is still important in some regions of the world such as Africa, India, Pakistan, Malaysia, New Guinea and South America. In our experience, over a 15-year period, the study of adult biopsied glomerular nephropathies showed a marked regression of pure endocapillar proliferative glomerulonephritis, which increased from 27.7% in 1975- 1980 to 9.4% during the period 1985-1990.
Poststreptococcal GNA occurs either sporadically or through epidemics. These occur in communities where there is strong promiscuity with poor hygiene conditions (epidemics in Trinidad, Maracaibo and Minnesota) and low socioeconomic status. They occur seasonally: in winter and spring for GNA secondary to nasopharyngeal infections and in summer for those secondary to skin infections. In our experiment, we observed an autumnal dominance in 64% of cases.
Poststreptococcal GNA cases may occur in the siblings of affected individuals. Dodge et al reported a 20% incidence of GNA (patent or subclinical forms) in the siblings of patients. Rodriguez-Iturbe found a nephropathy in 37.8% of the subjects outside the epidemics, but the study of the groupings human leukocyte antigen (HLA) did not find particularities in the affected subjects.
Age and sex:
The age of onset of poststreptococcal GNA is variable. They are mostly common between 2 and 12 years. In large series, 5% of patients are under 2 years of age and 5 to 10% are over 40 years of age.
Both sexes are affected, but there is a male predominance with a ratio of 2/1. This male predominance tends to fade when subclinical cases are taken into account.
Initial streptococcal infection:
The role of certain types of beta-hemolytic group A streptococci has long been well established, particularly type 12, but also many others such as 1, 3, 4, 6 and 25 for nasopharyngeal infections, 2, 49, 55, 57 and 60 for skin infections.Exceptionally, a streptococcus from another group was incriminated (group C: Streptococcus zooepidermicus).
These streptococci consistently contain, among the antigens of their wall, the antigen M. This M protein confers a lasting immunity, which explains the absence of recurrence. Other antigens are likely to explain nephrogenicity, such as endostreptosin and zymogen.
Nasopharyngeal infection is the most common cause, especially in sporadic forms, but a skin infection such as impetigo or superinfected mange can be observed in epidemic forms. A superinfected scab was incriminated in ten of our patients. Infection is more rarely otitis, sinusitis, dental abscess, scarlatina or pyoderma.
PHYSIOPATHOLOGY:
Immunopathogenesis of glomerular disease:
Poststreptococcal glomerulonephritis is a disease by immune complexes. The arguments in favor are:
– the existence of a free interval between infection and the onset of clinical signs; time required for the formation of immune complexes;
– a decrease in serum complement (93% of patients), presence of circulating immune complexes (in two thirds of patients) in serum, and cryoglobulins (in two thirds of patients) in the first 2 weeks;
– the existence of immunoglobulin (Ig) deposits and the C3 fraction of the complement at the kidney level in immunofluorescence;
– the great similarity with the experimental glomerulonephritis induced in the rabbit by the injection of bovine albumin (acute serum sickness).
Streptococcal antigens:
Currently, three antigenic fractions isolated from the nephritigene streptococcus have been identified and found in the glomeruli of the patients. In addition, high levels of antibodies to each of these antigens were detected in most patients. It is an antigen isolated from the New York Medical College Group, with a molecular weight (MW) of 40,000 to 50,000 d, referred to as endostreptosin.
Villareal, in 1979, isolated a protein fraction quite similar to endostreptosin. Vogt, in 1983, isolated a cationic protein that has common epitopes with the glomerular basal membrane (MBG). This protein easily crosses the MBG and is localized in the subepithelial region, where humps are usually observed.
Autoimmune reaction:
Streptococcal neuraminidase (sialidase) has been shown to alter host IgG by exposing antigenic sites. This altered IgG can induce an autoimmune response with formation of endogenous antigen-antibody complexes.
Seat of the immune reaction:
The seat of the immune reaction has been a subject of controversy. The role of circulating immune complexes captured secondarily by glomeruli was suggested because of the similarity between poststreptococcal GNA and acute serum sickness. At present it is established that an in situ reaction between the positively charged cationic antigen and the corresponding antibody occurs initially in the subepithelial region. Likewise, the production of a GNA using preformed immune complexes can only be carried out with immune complexes having a cationic antigen. But nephrogenicity is not reserved for cationic molecules, since electrostatic repulsion can be blocked or minimized by mechanisms that reduce the negative charge of the walls of the capillaries. Streptococcal neuraminidase can free the MBG from its sialic acid and cause a defect in charge and permeability.
Role of cells infiltrating glomeruli:
Glomerular infiltration of monocytes and T lymphocytes has been demonstrated in poststreptococcal GNA. This is correlated with the severity of proteinuria. The accumulation of these cells may be due to their binding to the Fc fragment of Ig deposited in the glomerulus or to lymphokines.
Direct nephrogenicity of the terminal complement components:
The chemotactic properties of complement components such as C5a explain that the majority of lesions caused by complement are mediated by neutrophils. The production of C3a and C5a can result in a release of histamine which increases the permeability of the capillaries. The complement end-products (C5b, C9 [MBG attack complex]) may have a direct effect on the basal membrane of the glomerular capillary. Parra demonstrated the deposition of this attack complex along the glomerular capillaries in prostrate post-capillary endocapillary glomerulonephritis.
Mechanisms of edema:
It has been well demonstrated that edema and hypertension are due to hydrosodic retention. The inflammatory reaction at the level of the glomerulus decreases the rate of glomerular filtration by reduction of the effective surface area of filtration and by a shunt of the circulation between the glomerular capillaries. Renal plasma flow is normal and even high. Glomerular filtration is lowered. Thus, the filtration fraction is decreased. Classically, an imbalance of the glomerulotubular balance is invoked; the tubular reabsorption of salt and water does not decrease in parallel with the decline in glomerular filtration. This results in decreased diuresis and hydrosodic retention.
SYMPTOMATOLOGY:
Clinic:
There is a free interval between infection and the clinical onset of nephropathy of 1 to 2 weeks in case of nasopharyngeal infection and more than 15 days in case of skin infection.
The most characteristic clinical presentation remains acute nephritic syndrome, of sudden onset, associating edema, macroscopic haematuria, hypertension and oliguria. Forty percent of children have a complete picture and about 96% have at least two of these symptoms.
Macroscopic hematuria is common and may be the only symptom of GNA. Urine is rare, dark colored called “Coca-Cola” or dirty broth. Thirty percent of our patients have macroscopic hematuria.
Edema is very common and is often the reason for consultation. They sit on the face and lower limbs of the adolescent and are readily generalized in young children. They are due to a hydrosodic retention.
Ascites and pleural effusion are more rare. Ninety-three percent of our patients presented with edema.
HTA is present in more than 80% of patients. It is found in 74% of our adult series and in 80% of a pediatric series of 114 cases. It is systolic-diastolic. It may be moderate or severe, and may be complicated by hypertensive encephalopathy with somnolence, convulsions or sometimes also congestive heart failure, especially in children with dyspnea, cough, galloping, or even acute edema of the lung. It is voluntary and its severity is a function of the importance of the hydrosodic retention.
Nonspecific symptoms may be seen in the initial stages, such as general discomfort, nausea with or without vomiting, abdominal pain, or low back pain (5-10%). There are no extrarenal signs. The systematic search for an infectious outbreak is often negative at this stage.
Biology:
Urinary tract signs:
Proteinuria is constant and variable in abundance, less than 500 mg / 24 hours in 50% of cases and 3 g / 24 h in 75% of cases. It sometimes exceeds 3 g / 24 h and is then accompanied by a nephrotic syndrome.
Microscopic haematuria is virtually constant. The study of the urinary sediment finds hematic cylinders and a deformed aspect of the red blood corpuscles, witnessing the glomerular origin of haematuria.
The urinary ionogram shows a decrease in natriuresis and an increase in urinary urea.
Blood Signs:
Protid electrophoresis may show normal or lowered protidemia, with hypoalbuminemia in cases of nephrotic syndrome which is often transient. Our personal data show that nephrotic syndrome is present in 33.3% of adult cases and in only 6.3% of pediatric cases, with moderate hypergammaglobulinaemia in 62% of adults and 81.8% of children.Moderate and transient renal insufficiency can be observed with an increase in blood urea, while serum creatinine is often subnormal.
There is also a discrete inflammatory syndrome with normocytic normocytic anemia and polynuclear leucocytosis. The rate of sedimentation is increased, as well as fibrinemia. C-reactive protein was found to be elevated experimentally during acute serum sickness. It is probably elevated in humans during GNA. However, there are no data in the literature.
Concerning the complement, there is a decrease of CH5O and especially of C3 which shows a deep drop and returns to normal in 6 to 8 weeks. The C4 level is normal. A preferred observation reported by Strife concluded that complement activation is anterior and probably participates in the immunological reaction leading to the observed renal lesions.
Mixed cryoglobulinemia (IgG-C3) as well as circulating immune complexes can be seen in the acute phase.
Stigma of streptococcal disease:
– Direct: culture of throat or cutaneous specimens consistently show a group A streptococcus.
– Indirect: antibodies directed against certain streptococcal antigens:
– antistreptolysins O (ASLO) rise in the serum during the first 2 weeks after infection and then return to normal within a few months. It is mainly the increase of ASLO at 2 weeks interval which strongly suggests a recent streptococcal infection. In the GNA following a skin infection, the increase in ASLO is less frequent, but that of antideoxyribonuclease B (B-DNAase) is high in 90% of the cases. ASLOs are the best indicators of respiratory tract infections, whereas B-DNAs are the best indicators for respiratory tract infections;
– zymogen: the level of anti-zymogen antibodies appears to be currently the best marker of streptococcal infection associated with GNA.
Other complementary examinations:
– Radiography of the thorax, if done, may show signs of pulmonary overload, rarely a pleural effusion. The heart is of normal volume.
– The electrocardiogram is usually normal.
– Renal ultrasound shows normal or slightly enlarged kidneys with good corticomedullary differentiation, indicating the recent character of nephropathy.
– In the case of severe hypertension, the fundus can show a papillary blur but no sign of crossing, indicating the recent character of this hypertension.
EVOLUTION:
Immediate:
Evolution is judged clinically on weight, diuresis, blood pressure curves, urine test strips and biologically on serum creatinine, 24-hour proteinuria, the Addis count, and the study of CH5O and the C3 fraction of the complement.
In the child, the unfavorable immediate evolution is very rare, often less than 1%, and this even in the oligoanuric forms requiring an extrarenal purification. Spontaneous healing may occur without specific treatment. It is the same in adults. Indeed, of our 72 cases of ANG in adults, we observed no deaths. In the elderly, early mortality can reach 25%.
Almost constantly, with appropriate therapeutic measures including rest during the edematous phase, a diet low in salt, diuretics, antihypertensives in case of need and antibiotics, the signs fade in 1 week. At the end of the second week, diuresis increases and the edema disappears, with crossing of weight and diuresis curves.
Biological abnormalities persist longer. Proteinuria disappears first, whereas microscopic haematuria disappears in 6 months in 90% of cases. The serum levels of CH5O and C3 standardized at the eighth week. The persistence of hypocomplementemia suggests the existence of chronic glomerulonephritis with acute onset.
Early age, the existence of an associated tare, the presence of persistent nephrotic syndrome and renal insufficiency, and the existence of a proliferation of renal histology extracapillary and hump.
Long-term:
The assessment of long-term trends is still controversial. The populations studied are rarely homogeneous, in particular, the proof of the streptococcal origin and the histological criteria are not constantly brought. This is probably explained by the great variability of the conclusions drawn from the study of numerous series.
Forty-nine of our patients (60%) were able to be properly monitored. They had no clinical or biological abnormalities after 6 months.
The epidemic form in adults and children seems to be very favorable, except in cases where histological examination initially shows the presence of numerous epithelial crescents.
The sporadic form, in children, is also favorable prognosis distant. It appears to be incapable of causing chronic renal failure, although abnormalities (proteinuria, hematuria) may persist for several years after clinical cure.
In adults, the prognosis of sporadic form is variously estimated. Twenty percent of the patients were considered to have urinary abnormalities after 10 to 20 years of evolution. Healing is less frequent in adults than in children. It is defined by the absence of proteinuria, haematuria, renal insufficiency and hypertension. It can only be pronounced after at least 1 year of evolution.
HISTOLOGY:
When the clinical picture is typical and the progression rapidly favorable, renal biopsy is not indicated, especially in children. It is done in case of abundant proteinuria in the acute phase, if the renal function degrades quickly, if the serum complement is normal initially, or if it does not return to normal in 6 to 8 weeks. After the usual precautions, it shows, in typical cases, an exudative pure endocapillary proliferative glomerulonephritis.
Optical microscopy study:
The glomeruli appear enlarged and are the site of cellular proliferation mainly made up of mesangial cells, but also endothelial cells, monocytes, T lymphocytes, polynuclear cells. The existence of a large number of polymorphonuclears in the lumen of the capillaries confers the exudative character of this glomerulonephritis. On early biopsies, eosinophilic conical, “hump” or “gendarme hat” deposits are often observed on the epithelial slope of basal membranes called humps. MBGs are normal.
In some cases, there is an interstitial edema with some mono- or polynucleate infiltrates and hematic cylinders. In our own experience, of the 81 cases of pure endocapillar proliferative glomerulonephritis, the endocapillary proliferation is very intense, with obstruction of the capillary lumen and exudation in 42% of the cases.
When the biopsy is done late, the capillary lumens are permeable and the polymorphonucleuses, as well as the humps, disappear. Only diffuse or focal mesangial proliferation persists.
Immunofluorescence study:
Deposits are essentially made of C3, with or without IgG. There is no fixation of C1q.
The distribution of deposits is variable. They are often diffuse and granular, of irregular size, sitting along the glomerular capillaries corresponding to the humps and in the mesangium, giving a “starry sky” appearance. Two other aspects have been described: one corresponds to contiguous deposits of IgG along glomerular capillaries without mesangial deposits producing a “garland” aspect, testifying to confluent humps, and often accompanied by abundant proteinuria; the other, where deposits, essentially made of C3, predominate in the mesangium.
Electron microscopy study:
It shows the presence of subepithelial deposits, sometimes subendothelial, as well as the proliferation of mesangial and circulating cells. Extramembrane conical deposits (humps) are typical of poststreptococcal GNA, but are not very specific.
The study by electron microscopy is not of diagnostic interest.
SPECIFIC FORMS:
Asymptomatic forms:
They are very common. Epidemiological surveys have demonstrated this. It all comes down to mere urinary abnormalities: proteinuria and microscopic haematuria.
In Japan, asymptomatic forms of poststreptococcal GNA were estimated to be 25%. Moreover, in a prospective study in New York of children with streptococcal infection, 21.8% developed urinary abnormalities, with or without complement decrease.
The asymptomatic forms, considered by Rodriguez as having an excellent immediate prognosis, may, for others, evolve towards chronicity. This should emphasize the need to look for urinary abnormalities in the course of any streptococcal infection.
Severe forms: subacute or malignant glomerulonephritis or rapidly progressive
Their frequency is low: nine cases out of 126 in the Baldwin series, one case out of 35 in the Hinglais series and seven cases out of 61 in our experiment. The picture is dominated by persistent oligoanuria and severe renal insufficiency, which is sometimes irreversible, whereas hypertension is less frequent than in pure endocapillar glomerulonephritis.
Nevertheless, all of them do not evolve towards chronic terminal renal insufficiency at the outset, and their prognosis is considered better than that of idiopathic extracapillary proliferative glomerulonephritis.
They are characterized by a high percentage of epithelial crescents reaching more than 50% of the glomeruli. The prognosis depends on the proportion of the glomeruli, the seat of croissants. Endocapillary proliferation often makes morphological analysis more difficult. Mesangial proliferation is usually clear, but humps are not easy to recognize by optical microscopy. Immunofluorescence binding revealed deposits of C3, with or without IgG, at the level of the floccus and fibrinogen on the croissants. Tubulo-interstitial lesions are more severe and diffuse than in pure endocapillary proliferative glomerulonephritis and may contribute to the persistence of chronic renal insufficiency.
Forms occurring during other nephropathies:
A GNA may be superimposed on a pre-existing glomerular nephropathy. Thus, a few cases have been reported in patients with nephropathy with mesangial deposits of IgA or diabetic nephropathy.
DIAGNOSTIC:
Positive diagnosis:
This diagnosis is based on:
– the notion of a recent streptococcal infection, usually otolaryngologic (ENT) or cutaneous;
– the existence of a free interval between infection and onset of symptoms;
– the sudden appearance of an acute nephritic syndrome without extrarenal signs;
– elevation of the antibody titer against streptococcal antigens, in particular ASLOs and antizymogens;
The transient decrease in the serum complement CH5O and C3;
– the rapid progression of renal signs.
Differential diagnosis:
This diagnosis can be made in the presence of any glomerular nephropathy with acute onset, whether primary or secondary. In these cases, the complement dosage is of great utility. Indeed, before an acute nephritic syndrome with a low complement one can evoke, either the diagnosis of the other postinfectious GNAs (bacterial endocarditis, shunt nephrite …) (cf infra), or a membranoproliferative glomerulonephritis, systemic lupus erythematosus or cryoglobulinemia .
If the complement is normal, the diagnosis of an IgA nephropathy or of a vasculitis is mentioned. The existence of extrarenal signs, specific biological or immunological signs, and renal biopsy make it possible to correct the diagnosis.
TREATMENT:
Treatment of acute episode:
It is essentially symptomatic, based on:
– hygiene measures;
– bed rest during the edematous phase;
– a diet low in salt;
– reduction of beverages;
– in cases of major edema, a diuretic treatment is indicated, either orally or intravenously, in emergency if there is a table of circulatory overload, the dosage being dependent on the importance of renal insufficiency;
– if the HTA is moderate, it is easily reduced by rest and diet without salt and diuretics. If it is severe, antihypertensive therapy is associated with diuretics. In case of resistance with presence of encephalic manifestations, injectable antihypertensive agents are prescribed.
Certain medicinal products should be avoided in these patients, such as digitalis, as they are ineffective in cases of heart failure with a risk of poisoning, inefficient and hyperkalaemic spironolactones, ACE inhibitors for their risk of hyperkalaemia, propranolol because it can precipitate heart failure and alphamethyldopa because ineffective at low doses and source of drowsiness at higher dose.
In severe forms with prolonged oligoanuria and severe renal insufficiency, extrarenal scrubbing by peritoneal dialysis or hemodialysis may become necessary.
In diffuse crescent forms, corticosteroid treatment with or without immunosuppressants and plasma exchange may be necessary.
As for antibiotic treatment, it is mainly prescribed whenever an infectious focus is detected or an identified germ.However, several authors recommend a systematic antibiotic treatment in all patients for ten days by penicillin G or erythromycin in case of allergy to penicillin.
Remote processing:
The regime is gradually expanded under medical supervision.
The activity can be resumed after 4 to 6 weeks after the onset of the disease. Infectious foci are removed under antibiotic coverage. Antibiotherapy in principle is not justified.
In children, it is recognized that it is necessary to wait several months after the disappearance of the urinary abnormalities to carry out the anti-tetanus and diphtheria vaccination, whereas vaccinations with the bacillus Calmette-Guérin (BCG) and against polio can be carried out without special precautions.
Preventive treatment:
The parallel reduction in the incidence of acute rheumatic fever (RA) and poststreptococcal GNA, well established by epidemiological studies, highlights the effectiveness of antibiotic treatments in any ENT infection, especially angina.However, since streptococcal infection provides lasting immunity and recidivism is exceptional, prophylactic antibiotic therapy with benzathine benzylpenicillin does not appear to be warranted.
Other acute post-infectious glomerulonephritis:
Several other infections can be the cause of the GNA. They can be bacterial, viral or parasitic infections.
ACUTE GLOMERULONEPHRITIS DURING BACTERIAL INFECTIONS:
Bacterial endocarditis:
The frequency of glomerular involvement in bacterial endocarditis is difficult to assess. It is observed whatever the valvular location and whatever the germ. Before the era of antibiotics, the organism was Streptococcus viridans;currently, Staphylococcus aureus is the most frequently found germ, but other germs may be involved.
Clinically, there is usually proteinuria and hematuria. Immunological abnormalities are almost always present: circulating immune complexes, cryoglobulinemia and rheumatoid factor.
Morphologically, it is a proliferative glomerulonephritis that can be segmental and focal or diffuse and global.
Sometimes, necrotic lesions and segmental epithelial crescents can be noted.
In immunofluorescence, there are deposits of IgG and complement (C1q + C3), mesangial and subendothelial sites.
Under the effect of the early treatment of endocarditis, the evolution is generally favorable. The renal signs disappear, with improvement, even histological healing.
We observed 32 cases of glomerular nephropathy complicating bacterial endocarditis, 23 patients had proteinuria, 24 had hematuria and 10 were oligoanuria. Nephrotic syndrome was present in 12 patients and renal insufficiency in 20 patients.
Renal biopsy in 18 patients resulted in pure endocapillary glomerulonephritis in five cases, endo- and extracapillary glomerulonephritis in seven cases, type I membranoproliferative glomerulonephritis in five cases, and segmental and focal glomerulonephritis in one case.
The vital prognosis is mainly related to cardiac involvement.
In practice, renal involvement should be sought in any patient with bacterial endocarditis and, conversely, any renal abnormality (proteinuria, hematuria, renal failure) in a patient with valvulopathy should seek endocarditis.
Deep Suppurations:
Glomerulonephritis can be observed in Gram positive and negative bacterial infections. Suppuration is variable, often pulmonary. Sometimes it is a subphrenic abscess or infection of a vascular prosthesis.
Clinically, it is usually a rapidly progressive glomerulonephritis, with acute renal failure, hypertension, macroscopic haematuria. The serum complement is normal. There are circulating immune complexes and cryoglobulinemia.
Histological lesions are variable. It may be diffuse endocapillary proliferative glomerulonephritis, endo- and extracapillary glomerulonephritis, type I membranoproliferative glomerulonephritis, and inflammatory infiltration of the interstitium.
The appearance of glomerular lesions appears to be correlated with duration of infection. Endocapillary proliferation is observed in infections lasting less than 2 months, whereas a lingering infection for more than 2 months is associated with a crescent glomerulonephritis. Complete eradication of the infection can result in the cure of kidney symptoms.The prognosis is not related to renal damage.
Ventriculoatrial Derivations:
These “shunt nephritis” glomerulonephritis occur in about 4% of patients treated for hydrocephalus by ventriculoatal shunt and with prolonged bacteremia.
Coagulase-negative staphylococcus is the most frequently responsible cause, but many other germs can be detected.They are mostly observed in children.
The delay between shunt placement and the appearance of renal signs varies from a few months to several years.Fever may be absent.
Renal involvement can be revealing, with haematuria sometimes macroscopic, proteinuria, or even nephrotic syndrome, hypertension and renal insufficiency often moderate. The complement fractions C1q, C3 and C4 are lowered.
Morphologically, it is most often a type I membranoproliferative glomerulonephritis, or more rarely an endocapillary proliferative glomerulonephritis.
Some cases of segmental and focal glomerulonephritis or crescent glomerulonephritis have been reported.
In immunofluorescence, IgM diffuse granular endomembranous deposits with less intense deposits of IgG, C3 and C1q are noted.
The antibiotic treatment associated with the removal of the shunt leads to the cure of glomerular nephropathy.
We observed a shunt nephritis in three adults.
Renal histology showed a type I membranoproliferative glomerulonephritis in all three cases. Two patients had a cure of their nephropathy, 7 and 12 months after removal of the prosthetic material and antibiotic treatment. The third patient developed chronic terminal renal failure after 15 years.
Septicemia:
Rarely, it is a picture of glomerular nephropathy with proteinuria and hematuria. Renal manifestations are most often those of acute functional renal failure, tubulo-interstitial nephropathy or partial or total cortical necrosis. All germs may be responsible for nephropathy during septicemia, with predominance of Gram-negative germs. The entrance doors are diverse. In the case of glomerular involvement, lesions can be of three types: segmental and focal glomerulonephritis, diffuse endocapillary proliferative glomerulonephritis, or, more rarely, thrombosis of the glomerular capillary loops.
Pneumonia:
Pneumonia, regardless of the organism involved (pneumococcus, Klebsiella pneumoniae, Mycoplasma pneumoniae, Legionella pneumophila, Staphylococcus aureus), may be accompanied by glomerulonephritis with immune complexes. It is usually a diffuse endocapillary proliferative glomerulonephritis and more rarely a focal form or a crescent glomerulonephritis. In some cases, the pneumococcal antigen has been found in glomerular deposits.
Typhoid:
Typhoid fever is still common, posing a public health problem in some countries. The frequency of renal involvement varies according to the authors: Nasrallah finds 6% in a series of adults; Katz finds a frequency of 2.5% in a pediatric series. For some authors, 60% of patients present proteinuria with moderate microscopic hematuria during the febrile phase which disappear after about 2 weeks. Histologically, it is an endocapillary proliferative glomerulonephritis with mesangial deposits of IgG and C3.
Salmonella antigen could in some cases be detected in glomeruli.
This glomerulonephritis usually cures under antibiotic treatment.
Meadow:
Several studies have reported glomerular nephropathies other than amylose in patients with lepromatous leprosy.
Their frequency varies from 6 to 50% in studies with renal biopsies. Other authors found urinary abnormalities in only 11 of their 636 patients.
Morphologically, the lesions described are very variable, but mainly to diffuse endocapillary glomerulonephritis or mesangial proliferative glomerulonephritis, sometimes with crescent glomerulonephritis.
In immunofluorescence, granular deposits of IgG, C3 and less often IgM or IgA are observed.
Other cases of GNA have been reported, with a multitude of infections such as leptospirosis, brucellosis, syphilis, meningococcal meningitis, rickettsioses, etc.
ACUTE GLOMERULONEPHRITIS DURING PARASITIC INFECTIONS:
The fact that parasitosis patients are often poly-infected requires a cautious interpretation of the role of parasitoses in the occurrence of GBN.
Schistosomiasis:
Acute glomerular nephropathies have been reported during schistosoma mansoni bilharziasis, particularly in its hepatosplenic form, especially when associated with salmonella infection. This has been well described by Egyptian and South American authors. It manifests itself in a nephrotic syndrome with hematuria, but without hypertension or hypertension. There is usually hypergammaglobulinemia and a decrease in C3.
The lesion may be a mesangial proliferative glomerulonephritis or a membranoproliferative glomerulonephritis.
This glomerular nephropathy responds to antiparasitic and antibiotic treatments.
Malaria:
In the course of Plasmodium falciparum infections, GNAs clinically characterized by weak proteinuria with microscopic haematuria have been reported in 20-50% of cases. Fractions C3 and C4 are lowered and the circulating immune complexes are present.
In optic microscopy, the lesions observed are mesangial-like with thickening of the mesangial tissue, associated with irregular thickening of the MBG. In immunofluorescence, deposits of IgM, C3, are observed at the level of the mesangium and along the MBG.
These lesions are transient and disappear within 4 to 6 weeks after antimalarial treatment, unlike the chronic glomerular nephropathies that occur during Plasmodium malariae infections.
Leishmaniasis:
Leishmaniasis is a common disease in Latin America, Asia and Africa. Renal involvement is rare and moderate. It manifests itself as proteinuria, hematuria and leucocyturia (30% of patients), without hypertension or nephrotic syndrome. There is hypergammaglobulinemia and hypoalbuminemia. Immunologically, circulating immune complexes are frequently detected, as well as a rheumatoid factor and cryoglobulinemia.
Morphologically, there is a mesangial proliferation, with a moderate mesangial expansion associated with an interstitial inflammatory infiltrate.
In immunofluorescence, there are granular IgG and C3 deposits, mesangial seating and along the MBG and IgM at the mesangium.
The mechanism of this glomerulonephritis is very probably immune, although the antigen in the kidney could not be demonstrated.
Renal involvement is benign and regresses entirely under pest control.
Renal involvement was observed in four patients with visceral leishmaniasis: three children and one young adult. All three had proteinuria, hematuria and normal blood pressure. The adult had macroscopic hematuria with two large kidneys, normal blood pressure. In all four cases, the biopsy revealed an endocapillary proliferative glomerulonephritis.Pest control resulted in clinical and biological recovery in all cases. An iterative renal biopsy performed 1 year later in the adult patient confirmed histological healing.
Hydatidose:
Very few cases of glomerulonephritis have been reported during hydatidosis. These are extramembraneous glomerulonephritis, amyloidosis or membranoproliferative glomerulonephritis.
A preliminary observation was able to demonstrate the regression of a mesangial glomerulonephritis after ablation of the hydatid cyst and its reappearance with the recurrence of it. Three cases of pure endocapillar proliferative glomerular nephropathy, two cases of type I membranoproliferative glomerulonephritis, three cases of extramembraneous glomerulonephritis, and two cases of proliferative glomerulonephritis, croissants associated with liver hydatid cysts. Two patients developed favorably after surgical removal of the cyst (amyloidosis: one case; extramembraneous glomerulonephritis: one case).
VIRAL INFECTIONS:
Several sporadic cases of glomerular nephropathy have been reported in the course of viral diseases. These are mainly cases of GNA occurring during an infectious mononucleosis.
Nephropathy occurred at the same time as the other symptoms of virosis. Histology revealed pure endocapillary glomerulonephritis and mononuclear interstitial cell infiltrates.
Rarely, cases of GNA have been reported with other viruses such as varicella, Epstein-Barr virus, cytomegalovirus, coxsackies, echovirus and Guillain-Barré syndrome.
Conclusion:
Post-infectious GNAs, if they are endangered in developed countries, remain sadly common in Third World countries.
Their incidence is inversely proportional to the socio-economic level.
The main form is the poststreptococcal GNA. His clinical picture is most often acute nephritic syndrome with a transient decrease of C3 which is of great diagnostic interest. The criterion of the streptococcal attack is the increase of the ASLO rate, but especially of anti-zymogenic antibodies. Renal biopsy is not routinely indicated. The most characteristic lesion is an exudative pure endocapillar proliferative glomerulonephritis, with granular and parietal fixation of C3. The evolution is generally favorable. However, prolonged monitoring for 1 year is required.
Other post-infectious GNAs, if less frequent, need to be recognized. Their clinical picture is less stereotyped.
Histological lesions are more polymorphic. The development is favorable in case of early diagnosis and appropriate treatment.
Postinfectious GNAs are preventable. Their prophylaxis involves improving hygiene, detection and early treatment of any infectious focus.
