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Emergency And Acute Medicine - Glomerulonephritis
Basics Description
Glomerulonephritis is a clinical syndrome characterized by hematuria, proteinuria, red blood cell casts, hypertension, and varying degrees of renal insufficiency. It represents a common final pathway of multiple disease processes that lead to intraglomerular inflammation and cellular proliferation. Contributing factors include genetic predisposition, infectious triggers, and rheumatologic or autoimmune conditions. Pathogenesis involves antibody deposition either by direct binding to glomerular antigens or deposition of circulating immune complexes, leading to activation of inflammatory mediators such as leukocytes, complement, and cytokines. Cell-mediated immune mechanisms further contribute to glomerular injury. Persistent inflammation may result in glomerular scarring and permanent renal damage.
Etiology
Postinfectious causes include poststreptococcal glomerulonephritis, which typically occurs 7–21 days after streptococcal pharyngitis or skin infection and is most common in children aged 2–14 years and in the elderly, with a male predominance. IgA nephropathy is common in men in the third and fourth decades and is often associated with increased IgA production following upper respiratory infections; Henoch–Schönlein purpura represents a systemic IgA-mediated disease affecting younger patients. Rapidly progressive glomerulonephritis can destroy renal function within days and is characterized by crescent formation in glomeruli. Pauci-immune vasculitides, often ANCA-positive, include granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis and may involve lungs or skin. Immune complex–mediated causes include postinfectious GN, endocarditis-associated GN, systemic lupus erythematosus, and Henoch–Schönlein purpura. Anti–glomerular basement membrane disease, such as Goodpasture syndrome, typically affects older adults and may involve pulmonary hemorrhage. Membranoproliferative glomerulonephritis is associated with complement deposition and conditions such as hepatitis C, non-Hodgkin lymphoma, or occult infection.
Diagnosis Signs And Symptoms
Core clinical features include hematuria, proteinuria, edema due to salt and water retention (periorbital edema, ascites, pleural effusions), hypertension, oliguria, azotemia, congestive heart failure, and renal failure. Nonspecific symptoms include fatigue, weight loss, abdominal pain, nausea, and vomiting. Autoimmune-related findings may include arthralgias, arthritis, rash, fever, and systemic inflammation. Goodpasture syndrome may present with hemoptysis. Granulomatosis with polyangiitis can cause purulent rhinorrhea, sinus pain, arthritis, and hemoptysis. Henoch–Schönlein purpura may present with abdominal pain, purpura, and arthritis.
In older adults, pauci-immune rapidly progressive glomerulonephritis is common and requires urgent diagnosis and biopsy due to high risk of progression to end-stage renal disease.
Essential Workup
Urinalysis is essential to identify hematuria, proteinuria, and red blood cell casts.
Diagnosis Tests And Interpretation
Laboratory evaluation includes electrolytes, BUN, creatinine, and GFR to assess renal function, as well as evaluation for hyperkalemia. Albumin and total protein levels may demonstrate hypoalbuminemia. CBC may show anemia related to chronic kidney disease, systemic illness, or pulmonary hemorrhage. Coagulation studies may be abnormal in select forms of GN. Additional tests guided by consultants include cultures, 24-hour urine protein measurement, antistreptolysin O titers, complement levels, ANA, ANCA, anti-GBM antibodies, ESR, CRP, hepatitis B and C serologies, and HIV testing.
Imaging may include renal ultrasound to assess kidney size and reversibility of disease and chest radiography to evaluate for pulmonary edema or hemorrhage.
Renal biopsy is the definitive diagnostic test to distinguish primary glomerular disease from secondary causes. Cystoscopy may be considered if bladder malignancy is suspected.
Differential Diagnosis
Hematologic disorders such as sickle cell disease and coagulopathies; renal causes including infection, malformation, neoplasm, ischemia, trauma, and vasculitis; postrenal causes such as obstruction or reflux; inflammatory genitourinary conditions; pigmenturia; factitious hematuria; and vaginal bleeding.
Treatment Pre Hospital
Provide supportive care with attention to airway, breathing, and circulation. Restrict fluids in stable patients with significant edema.
Initial Stabilization Therapy
Stabilize airway, breathing, and circulation.
Ed Treatment Procedures
Management is largely supportive and includes strict blood pressure control with a target below 125/75 mm Hg, loop diuretics for volume overload, and ACE inhibitors for maintenance therapy. Dialysis is indicated for fluid overload, hyperkalemia, or uremia.
Poststreptococcal glomerulonephritis is treated with supportive care and typically resolves spontaneously; antibiotics do not alter renal outcomes.
IgA nephropathy is managed supportively, with immunosuppressive therapy considered when biopsy shows active inflammation.
Rapidly progressive glomerulonephritis requires emergent nephrology consultation and early initiation of immunosuppressive therapy due to the risk of irreversible renal failure.
Membranoproliferative glomerulonephritis management focuses on treating underlying disease and may include plasma exchange, immunosuppressants, and steroids.
Medication
Therapeutic agents may include ACE inhibitors such as benazepril, loop diuretics such as furosemide, corticosteroids including methylprednisolone and prednisone, immunosuppressants such as cyclophosphamide or rituximab, vasodilators for hypertensive emergencies, and renal replacement therapy when indicated.
Follow-Up Disposition
Admission is required for patients with unstable vital signs, oliguria or anuria, uremia, acute renal failure, significant electrolyte abnormalities, hypertensive emergencies, congestive heart failure, or infectious causes of glomerulonephritis.
Selected patients with mild hematuria and proteinuria, stable vitals, no infection, and otherwise normal laboratory findings may be discharged with close follow-up.
Follow-Up Recommendations
All patients with glomerulonephritis require nephrology follow-up for monitoring, definitive diagnosis, and long-term management.
Key Clinical Insights And Avoidable Errors
Early nephrology consultation is critical when immunosuppressive therapy is being considered. Any finding of hematuria or proteinuria warrants appropriate follow-up, as progression to clinically significant glomerulonephritis may occur if overlooked.
Basics Description
Glomerulonephritis is a clinical syndrome characterized by hematuria, proteinuria, red blood cell casts, hypertension, and varying degrees of renal insufficiency. It represents a common final pathway of multiple disease processes that lead to intraglomerular inflammation and cellular proliferation. Contributing factors include genetic predisposition, infectious triggers, and rheumatologic or autoimmune conditions. Pathogenesis involves antibody deposition either by direct binding to glomerular antigens or deposition of circulating immune complexes, leading to activation of inflammatory mediators such as leukocytes, complement, and cytokines. Cell-mediated immune mechanisms further contribute to glomerular injury. Persistent inflammation may result in glomerular scarring and permanent renal damage.
Etiology
Postinfectious causes include poststreptococcal glomerulonephritis, which typically occurs 7–21 days after streptococcal pharyngitis or skin infection and is most common in children aged 2–14 years and in the elderly, with a male predominance. IgA nephropathy is common in men in the third and fourth decades and is often associated with increased IgA production following upper respiratory infections; Henoch–Schönlein purpura represents a systemic IgA-mediated disease affecting younger patients. Rapidly progressive glomerulonephritis can destroy renal function within days and is characterized by crescent formation in glomeruli. Pauci-immune vasculitides, often ANCA-positive, include granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis and may involve lungs or skin. Immune complex–mediated causes include postinfectious GN, endocarditis-associated GN, systemic lupus erythematosus, and Henoch–Schönlein purpura. Anti–glomerular basement membrane disease, such as Goodpasture syndrome, typically affects older adults and may involve pulmonary hemorrhage. Membranoproliferative glomerulonephritis is associated with complement deposition and conditions such as hepatitis C, non-Hodgkin lymphoma, or occult infection.
Diagnosis Signs And Symptoms
Core clinical features include hematuria, proteinuria, edema due to salt and water retention (periorbital edema, ascites, pleural effusions), hypertension, oliguria, azotemia, congestive heart failure, and renal failure. Nonspecific symptoms include fatigue, weight loss, abdominal pain, nausea, and vomiting. Autoimmune-related findings may include arthralgias, arthritis, rash, fever, and systemic inflammation. Goodpasture syndrome may present with hemoptysis. Granulomatosis with polyangiitis can cause purulent rhinorrhea, sinus pain, arthritis, and hemoptysis. Henoch–Schönlein purpura may present with abdominal pain, purpura, and arthritis.
In older adults, pauci-immune rapidly progressive glomerulonephritis is common and requires urgent diagnosis and biopsy due to high risk of progression to end-stage renal disease.
Essential Workup
Urinalysis is essential to identify hematuria, proteinuria, and red blood cell casts.
Diagnosis Tests And Interpretation
Laboratory evaluation includes electrolytes, BUN, creatinine, and GFR to assess renal function, as well as evaluation for hyperkalemia. Albumin and total protein levels may demonstrate hypoalbuminemia. CBC may show anemia related to chronic kidney disease, systemic illness, or pulmonary hemorrhage. Coagulation studies may be abnormal in select forms of GN. Additional tests guided by consultants include cultures, 24-hour urine protein measurement, antistreptolysin O titers, complement levels, ANA, ANCA, anti-GBM antibodies, ESR, CRP, hepatitis B and C serologies, and HIV testing.
Imaging may include renal ultrasound to assess kidney size and reversibility of disease and chest radiography to evaluate for pulmonary edema or hemorrhage.
Renal biopsy is the definitive diagnostic test to distinguish primary glomerular disease from secondary causes. Cystoscopy may be considered if bladder malignancy is suspected.
Differential Diagnosis
Hematologic disorders such as sickle cell disease and coagulopathies; renal causes including infection, malformation, neoplasm, ischemia, trauma, and vasculitis; postrenal causes such as obstruction or reflux; inflammatory genitourinary conditions; pigmenturia; factitious hematuria; and vaginal bleeding.
Treatment Pre Hospital
Provide supportive care with attention to airway, breathing, and circulation. Restrict fluids in stable patients with significant edema.
Initial Stabilization Therapy
Stabilize airway, breathing, and circulation.
Ed Treatment Procedures
Management is largely supportive and includes strict blood pressure control with a target below 125/75 mm Hg, loop diuretics for volume overload, and ACE inhibitors for maintenance therapy. Dialysis is indicated for fluid overload, hyperkalemia, or uremia.
Poststreptococcal glomerulonephritis is treated with supportive care and typically resolves spontaneously; antibiotics do not alter renal outcomes.
IgA nephropathy is managed supportively, with immunosuppressive therapy considered when biopsy shows active inflammation.
Rapidly progressive glomerulonephritis requires emergent nephrology consultation and early initiation of immunosuppressive therapy due to the risk of irreversible renal failure.
Membranoproliferative glomerulonephritis management focuses on treating underlying disease and may include plasma exchange, immunosuppressants, and steroids.
Medication
Therapeutic agents may include ACE inhibitors such as benazepril, loop diuretics such as furosemide, corticosteroids including methylprednisolone and prednisone, immunosuppressants such as cyclophosphamide or rituximab, vasodilators for hypertensive emergencies, and renal replacement therapy when indicated.
Follow-Up Disposition
Admission is required for patients with unstable vital signs, oliguria or anuria, uremia, acute renal failure, significant electrolyte abnormalities, hypertensive emergencies, congestive heart failure, or infectious causes of glomerulonephritis.
Selected patients with mild hematuria and proteinuria, stable vitals, no infection, and otherwise normal laboratory findings may be discharged with close follow-up.
Follow-Up Recommendations
All patients with glomerulonephritis require nephrology follow-up for monitoring, definitive diagnosis, and long-term management.
Key Clinical Insights And Avoidable Errors
Early nephrology consultation is critical when immunosuppressive therapy is being considered. Any finding of hematuria or proteinuria warrants appropriate follow-up, as progression to clinically significant glomerulonephritis may occur if overlooked.
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