Acute glomerulonephritis (AGN) disease is mostly found in young adults. AGN term is caused by attack of immune system on the filtering unit glomeruli of kidney. Hippocrates found the AGN and symptoms like back pain and hematuria. Lately, these are known as anuria or oliguria. Richard Bright gave clinical presentations of AGN in 1827. So, it is known as Bright’s disease. Theodor Langhans observed some changes in pathology in glomeruli, which is caused by AGN in the microscope, and gave another clinical presentation. 

Glomerulonephritis is a glomerular disease. About 10 to 15 % of the cases of glomerular diseases and 25 to 30% of the cases of end-stage renal disease are found in the U.S. The most prevalent areas are Africa, India, the Caribbean, Pakistan, Malaysia, Papua, New Guinea, and South America.  

AGN can occur at any age but is common in children whose age is 5 years to 15 years old. Acute nephritis also occurs during infancy. AGN occurs more in males as compared to females. There is no racial or ethnic comparison. Higher rates are found in lower socioeconomic groups due to a compromised hygiene level. 

AGN disease causes the deposition of immune complexes or any other material, which may lead to enlargement or swelling in the kidney. This can lead to lesions in the glomerular. It has been found in severe diseases like PSGN and streptococcal products, which are involved in the formation of IgG or anti-IgG immune complexes that settle in glomeruli. Increased antibody titers to other antigens suggest a recent streptococcal infection. 

When glomerulonephritis occurs in association with staphylococcal infections, it is during active infection, and deposits are typical of immune complexes; immunofluorescence microscopy identifies deposits that stain for IgA and the complement component C3. The vascular endothelial cells transport circulating immune complexes from capillaries to peritubular interstitial space, where resident macrophages detect and remove them. This process includes the release of pro-inflammatory cytokines, which then triggers the migration of monocytes and neutrophils from the bloodstream into the kidney. 

Functional and structural changes 

Some important anatomic features of AGN include cellular proliferation in the glomerular tuft, that is, the existence of increased numbers of endothelial, mesangial, and epithelial cells. It can be endocapillary or extra-capillary proliferation. The latter leads to crescent formation. Proliferation of leukocytes is signaled by the existence of neutrophils and monocytes within the glomerular capillary lumen. 

The thickness of glomerular basement membrane is increased because of the deposition of electron dense material. This suggests the irreversible damage may be diffuse, focal, segmental, or global. 

From a functional standpoint, AGN is defined based on proteinuria, hematuria, decreased GFR, and red blood cells in urine sediment, along with casts. These functional changes, at times, lead to an increase in intravascular volume, edema, and quite commonly associated systemic hypertension. 

Poststreptococcal glomerulonephritis 

Previously, it was believed that an alpha helical coiled-coil in streptococcal M-protein mediated PSGN. Subsequently, the nephritis-associated streptococcal cationic protease was identified, and one of the protease substrates was shown to be identical to the host protein that activates plasminogen. A precursor for this protein, named nephritis-associated plasmin receptor (NAPlr), was found. Immuno-histochemical analysis of renal biopsy samples with anti-NAPlr antibodies showed NAPlr deposition in the glomeruli in the early phase of acute PSGN. The glomerular plasmin activity paralleled NAPlr deposition in the kidney biopsies of patients with acute PSGN. Studies have demonstrated that streptococcal infections which are associated with attacks of glomerulonephritis also have an increased level of antibodies to nephritis associated protease, NAPR as compared to those without glomerulonephritis. These kinds of antibodies can last for years and protect a person against another bout of PSGN. 

The factors which can cause AGN can be divided into non-infectious and infectious groups. 

Non-infectious groups: 

Non-infectious factors which can cause AGN are classified into systemic diseases, primary kidney diseases, and various miscellaneous agents or diseases. Multisystemic diseases which can lead to acute glomerulonephritis are like: 

Hypersensitivity vasculitis: This disease can include a wide range of diseases related to skin diseases and small vessels. 

Polyarteritis nodosa: This disease can lead to nephritis because of renal arteries, which are affected by vasculitis. 

Vasculitis: This disease can lead to glomerulonephritis which can cause inflammation in upper and lower granulomatous. 

Other diseases may include collagen, Vascular disease, Henoch, Schonlein purpura, goodpasture syndrome, cryoglobulinemia. 

Other factors which can cause AGN are COVID-19 vaccine, serum sickness, radiation treatment for Wilms tumor, Guillain- Barre syndrome, DPT vaccines, activation of EGFR. 

Infectious groups: 

Fungi, bacteria, parasites, or viruses can lead to non-streptococcal postinfectious glomerulonephritis. Bacteria instead of group A streptococci may cause AGN are like Diplococci, Brucella suis, Actinobacilli, Salmonella typhosa, Mycobacteria, Staphylococci, Other streptococci, Corynebacterium bovis, and Treponema pallidum. 

Hepatitis B virus, Epstein-Barr virus, cytomegalovirus, rickettsiae, rubella, mumps virus, and parvovirus B19 are the viral causes if there is no confirmation of group A beta-hemolytic streptococci infection.  

Assigning glomerulonephritis to a fungal or parasitic cause necessitates ruling out a streptococcal infection. Identified organisms include Coccidioides and following parasites: 

1. Toxoplasma gondii 
2. Plasmodium falciparum 
3. Wuchereria bancrofti 
4. Trypanosomes 
5. Schistosoma mansoni 
6. Plasmodium malariae 
7. Trichinella roundworms 

The important primary renal diseases that can present similarly to AGN are idiopathic rapidly progressive glomerulonephritis, Berger disease (IgA nephropathy), mesangial proliferative GN, and pure mesangial proliferative GN. Mesangial proliferative GN presents as proliferation and expansion of mesangial cells, probably in response to complement deposition, while in IgA nephropathy, there is a diffuse mesangial deposition of IgA and, to a lesser extent, IgG. Idiopathic rapidly progressive glomerulonephritis can be seen with the presence of glomerular crescents.  

Acute nephritis, specifically post-streptococcal glomerulonephritis, is the most common cause of chronic kidney disease (CKD). About 98% of the patients who have PSGN have no symptoms for up to 5 years. About 1 to 3 % may develop CKD. 

In a majority of patients, spontaneous resolution of fluid retention and hypertension ensues within a week, and the C3 levels normalize within eight weeks. Proteinuria may persist up to six months, while microscopic hematuria may last up to one year. 

Prognosis of non-streptococcal postinfectious glomerulonephritis depends on identification and treatment of the underlying agent. Other causes of nephritis, such as MRSA and chronic infections, often resolve with appropriate treatment. However, in a pooled analysis of post-staphylococcal glomerulonephritis, only 44.7% achieved remission, while 22.9% progressed to ESRD and 14.5% died. 

Other etiologies of acute glomerulonephritis range in course from complete recovery to complete renal failure; the prognosis worsens if there are cardiopulmonary or neurologic complications. 

AGN is common disease which has acute symptoms of puffiness in eyelids and swelling on face.  

Acute glomerulonephritis is a common disorder that points to acute onset of puffiness in the eyelids and facial swelling. This disease primarily affect the boys whose age is 2 to 14 years old and also middle ages and old men who have diabetes mellitus. 

The condition prevails in boys from 2 to 14 years, though it may affect middle-aged or older men, with special mention of those who have diabetes mellitus. Its onset often follows an infection, which can be visceral or related to the skin. Hematuria is nearly always present. The incubation period lasts up to three weeks, after which the symptoms develop abruptly. The possible causes are streptococcal throat or skin infection; predisposing factors are a recent history of fever, sore throat, arthralgia, hepatitis, recent travel, heart valve replacement, and intravenous drug abuse.  

Symptoms of this disease, like uremic symptoms and others, are like: 

Swelling on face 

Generalized itching 

Leg edema 

Nausea 

Loss of appetite 

Shortness of breath 

Bleeding from nose 

Brushing 

Tiredness 

Other conditions which are included are like oliguria, headache, dyspnea, hematuria. 

Patients may have normal blood pressure. The most common findings are a combination of hypertension, oliguria, and edema. The physician should particularly look for evidence of fluid overload, including:  

1. Increased jugular venous pressure 

1. Pleural effusion and ascites 

1. Crackles 

1. Hypertension and edema because of fluid overload 

1. Pedal or periorbital edema 

The physician should also examine for the following: 

1. Arthritis 
2. Renal angle tenderness or fullness 
3. Swelling of joints 
4. Abnormal neurological examination 
5. Rash 
6. Pallor 
7. Other possible signs involve: 
8. Impetigo 
9. Weight gain 
10. Back pain 
11. Pain in the abdomen 
12. Oral ulcers 
13. Pharyngitis 
14. Respiratory infection 
15. Heart murmur 
16. Pulmonary hemorrhage 

Differential diagnoses: 

1. Goodpasture syndrome 
2. Focal segmental glomerulosclerosis 
3. Crescentic glomerulonephritis 
4. Acute kidney injury 
5. Diffuse proliferative glomerulonephritis 
6. Lupus nephritis 
7. Rapidly progressive glomerulonephritis 
8. Poststreptococcal glomerulonephritis 
9. Glomerulonephritis related to nonstreptococcal infection 

• Abnormal urinalysis 
• Hypertension 
• Pulmonary edema 
• Chronic kidney disease (CKD) 
• Hypertensive retinopathy 
• Rapidly progressive glomerulonephritis 
• Hypertensive encephalopathy 
• Nephrotic syndrome 

Treatment of acute PSGN is largely supportive; there is no specific therapy for renal disease. Treatment of chronic infections involves management of the underlying infection.  

Renal treatment is needed in the presence of intensive care. Renal function, blood pressure, edema, urine protein, and serum albumin excretion rate must be monitored.  

 Pharmacologic therapy: 

Although antibiotics are indicated for symptom alleviation and prevention of infection spread to close contacts, they have no action on preventing the occurrence of glomerulonephritis if given in the first 36 hours.  

Streptococcal elimination may help to prevent post-streptococcal glomerulonephritis. Other treatments like loop diuretics who have edema and hypertension, vasodilators in severe hypertension or encephalopathy, and glucocorticoids and cytotoxic agents in the severe forms of PSGN. 

Nephrology

Diet and activity 

Fluid and Na intake must be avoided to manage the symptoms of fluid retention, like pulmonary edema or edema. Restriction in protein is recommended in cases of azotemia. Bed rest is suggested till the inflammation in glomerular and congestion in circulatory systems improves.  

Nephrology

Penicillin V: It is less susceptible to acidic gastric secretion than penicillin G. It is rapidly absorbed orally. 250 mg of penicillin V is the same as 400000 units of penicillin. 

Cephalexin: It is 1st generation of cephalosporin. It inhibits the replication of bacteria by the inhibition of cell wall synthesis of bacteria. It has bactericidal action and acts effectively against rapidly developing bacteria. 

Erythromycin: It is indicated in treating streptococcal pharyngitis. It is generally given in cases of allergy to cephalosporins or penicillin. 

Nephrology

Furosemide: It promotes water excretion by disrupting the chloride-binding cotransport system, thereby inhibiting the reabsorption of chloride and sodium in the distal renal tubule and ascending loop of Henle. 

Nephrology

Sodium nitroprusside: It is rapid acting and potent antihypertensive agent which is given intravenously. Due to rapid biotransformation, its effect usually seizes after stopping the infusion. 

Hydralazine: This is known to reduce blood pressure by directly relaxing the vascular smooth muscle, leading to peripheral vasodilation. To mitigate retention of sodium and over stimulation of heart, it is often used in conjunction with a beta-blocker and a thiazide diuretic. 

Nephrology

Nifedipine: It is a calcium channel blocker belonging to the class of dihydropyridine. It is believed to decrease blood pressure by producing a vasodilatory effect on the peripheral blood vessels. 

Nephrology

AGN is a chronic process requiring multi-phase treatment, including the acute phase, with only supportive care and monitoring for further complications, along with infection control. Diagnosis must, therefore, include the identification of the underlying cause, such as streptococcal infections or systemic diseases. The therapy is specific, depending on the etiology, and includes corticosteroids or immunosuppressive agents. Chronic management involves long-term follow-up of renal function and blood pressure is necessary, with advice regarding lifestyle modifications and diet to keep risk factors under control and to avoid further damage. Finally, there is a need for patient education and follow-up. This would normally be booked for regular appointments to check on progress and adjust treatment accordingly. All these phases are individualized according to the needs of the patient and characteristics of AGN. The approach ensures effective management and prevents further complications.